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Vitamin E, like progesterone and aspirin, acts within the cellular regulatory systems, to prevent inflammation and inappropriate excitation. Since uncontrolled excitation causes destructive oxidations, these substances prevent those forms of oxidation.

维生素E，像孕酮和阿司匹林一样，在细胞调节系统中起作用，防止炎症和不适当的兴奋。由于不受控制的兴奋会导致破坏性的氧化，这些物质会阻止这些形式的氧化。

Molecules that can easily be oxidized and reduced can function as antioxidants, and vitamin E does function as that kind of antioxidant in many chemical environments. But it is highly misleading to consider that as the explanation for its many beneficial biological effects. That kind of reasoning contributed to the use of the antioxidant carcinogens BHT and BHA as food additives and “antiaging” supplements, and many other chemicals are being promoted on the basis of their abstract antioxidant function.

容易被氧化和还原的分子可以充当抗氧化剂，而维生素E在许多化学环境中确实发挥了这种抗氧化剂的作用。但是，如果认为这是对其许多有益的生物学效应的解释，就会产生极大的误导。这种推理有助于使用抗氧化剂致癌物质BHT和BHA作为食品添加剂和“抗衰老”补充剂，以及许多其他化学物质正在推广的基础上抽象的抗氧化功能。

*Becoming aware of the real value of vitamin E will have far reaching implications in nutrition and medicine. *

认识到维生素E的真正价值将在营养和医学方面产生深远的影响。

In determining criminal or civil legal responsibility, the concept “should have known” is recognized and used. In science, which is all about knowing, there is certainly a responsibility to be informed when the subject involves the life and health of millions of people. The science establishment of government and industry should be held responsible for the information it hides, destroys, or ignores for its own benefit. The US government has an agency for prosecuting research fraud, but the concept is applied so narrowly as to be meaningless, when deception has become the rule. And since it controls the court system, govenment agencies and their functionaries won't be prosecuted, even when their crimes become well known.

在确定刑事或民事法律责任时，承认和使用了“应当知道”的概念。在科学中，一切都是关于知识的，当一门学科涉及到数百万人的生命和健康时，人们当然有责任被告知。政府和工业的科学机构应该为其为了自身利益而隐藏、破坏或忽视的信息负责。美国政府有一个负责调查研究欺诈的机构，但这个概念的应用范围太过狭窄，以至于在欺骗已成为规则的情况下，它变得毫无意义。由于它控制着法院系统，政府机构及其工作人员不会被起诉，即使他们的罪行众所周知。

“Vitamin E was advocated as an effective treatment for heart disease by Dr. Evan Shute of London, Ontario more than 50 years ago. His pioneering claims, which were unacceptable to the medical community at large, have been confirmed by recent findings from epidemiologic studies and clinical trials.”

50多年前，安大略省伦敦市的埃文·舒特(Evan Shute)医生提倡维生素E作为一种有效的心脏病治疗方法。他的开拓性的主张不被整个医学界所接受，但最近的流行病学研究和临床试验结果证实了他的主张。

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Political scientists have recognized the process in which big corporations “capture” the governmental agencies that were created to regulate them. The editorial boards of professional journals can be captured even more cheaply than the agencies of government, and their influence can be even more valuable to industry.

政治学家已经认识到，大公司“俘获”了为监管它们而设立的政府机构。专业期刊的编辑委员会比政府机构更容易被抓住，他们的影响力对行业来说甚至更有价值。

If science impinges upon the plans of an industry, it can be managed into compliance, when the industry controls the journals and the agencies that fund research.

如果科学影响到一个行业的计划，当行业控制期刊和资助研究的机构时，它可以被管理成合规。

In the 1940s, it had already become clear to the estrogen industry that vitamin E research was impinging on its vital interests.

在20世纪40年代，雌激素产业已经清楚地认识到维生素E的研究正影响着他们的重要利益。

The Manhattan Project, that created the atomic bomb, also created a generation of scientific and bureaucratic zealots who ignored public health and safety to advance their projects and their careers, and changed the way science was done. At exactly the same time, the pharmaceutical industry was using its financial and political power to change the way medicine was practiced and taught, and the consequences for world health rivalled those of the nuclear industry.

创造了原子弹的曼哈顿计划，也造就了一代科学和官僚主义狂热分子，他们无视公共健康和安全，以推进他们的项目和事业，并改变了科学研究的方式。与此同时，制药工业利用其财政和政治力量改变医学的实践和教学方式，其对世界健康的影响与核工业不相上下。

In 1933 the physician R.J. Shute was aware of the problems associated with toxemia of pregnancy or preeclampsia. Especially among poorly nourished women, many pregnancies were complicated by circulatory problems, including cyclic bleeding, thrombosis, stroke, and hypertension, and these difficult pregnancies often ended in miscarriage or premature delivery, resulting in many serious health problems among the babies that survived.

1933年，医生R.J.舒特意识到与妊娠毒血症或先兆子痫相关的问题。特别是在营养不良的妇女中，许多怀孕伴随着循环系统问题，包括循环出血、血栓形成、中风和高血压，这些困难的怀孕往往以流产或早产告终，给幸存的婴儿造成许多严重的健康问题。

At that time, both estrogen and vitamin E were being widely studied, though the exact structure of the tocopherol molecule wasn't defined until 1936-37. Vitamin E had been found to improve fertility of both male and female animals, and to prevent intrauterine death of the embryo or fetus, so it was called the “antisterility vitamin.” Using it to prevent women from having miscarriages must have occurred to many people.

当时，雌激素和维生素E都被广泛研究，尽管生育酚分子的确切结构直到1936-37年才被确定。人们发现维生素E可以提高雄性和雌性动物的生育能力，并防止胚胎或胎儿宫内死亡，因此它被称为“抗不育维生素”。用它来防止妇女流产的人肯定很多。

Animal research in the 1930s was also showing that estrogen had many toxic effects, including causing infertility or intrauterine death, connective tissue abnormalities, and excessive blood clotting. Dr. Shute and his sons, Wilfred and Evan, were among those who considered vitamin E to be an antiestrogen. They found that it was very effective in preventing the clotting diseases of pregnancy.

20世纪30年代的动物研究也显示雌激素有许多毒性作用，包括导致不孕或宫内死亡、结缔组织异常和过度凝血。舒特医生和他的儿子威尔弗雷德(Wilfred)和埃文(Evan)都认为维生素E是一种反雌激素。他们发现它对预防妊娠期间的凝血疾病非常有效。

Other researchers, who knew that progesterone protected against the toxic effects of estrogen, described vitamin E as the “progesterone-sparing agent,” since so many of its antiestrogenic effects resembled those of progesterone.

其他研究人员知道黄体酮可以抵抗雌激素的毒性作用，他们把维生素E描述为“黄体酮保护剂”，因为它的许多抗雌激素作用与黄体酮类似。

The Shute brothers began using vitamin E to treat circulatory diseases in general, rather than just in pregnant women–blood clots, phlebitis, hypertension, heart disease, and diabetes all responded well to treatment with large doses.

舒特兄弟开始使用维生素E治疗一般循环系统疾病，而不仅仅是孕妇——血凝块、静脉炎、高血压、心脏病和糖尿病都对大剂量治疗有良好反应。

Vitamin E, as its name indicates, was the fifth type of “vitamin” factor to be identified, and it received its name in 1922, even though its chemical structure hadn't been identified. The public quickly understood and accepted that certain substances in food were essential for life and health, so by 1940 practically all physicians were recommending the use of nutritional supplements.

维生素E，顾名思义，是第五种被识别的“维生素”因子，它在1922年被命名，尽管它的化学结构还没有被识别出来。公众很快就理解并接受了食物中的某些物质对生命和健康是必不可少的，所以到1940年，几乎所有的医生都建议使用营养补充剂。

If vitamin E was essential for human health, and achieved at least some of its amazing effects by opposing estrogen, then the synthetic estrogen industry had a problem.

如果维生素E对人类健康至关重要，并且通过对抗雌激素至少取得了一些惊人的效果，那么合成雌激素产业就有问题了。

Edward L. Bernays had already been in business for decades, teaching corporations and governments how to “engineer consent.” After his work for the government to engineer support for entering the first world war, Bernays' next big job was for the tobacco industry. To convince women to smoke cigarettes, to achieve equality with men, he organized an Easter parade, Torches of Freedom, in which thousands of women marched smoking their freedom torches. In association with the American Medical Association (the editor of JAMA actually helped the tobacco industry design its campaigns), Bernays ran a campaign to convince Americans that smoking was good for the health.

爱德华·L·伯内斯(Edward L. berays)已经从商几十年了，他教企业和政府如何“策划同意”。伯奈斯在政府公司工作，为参加第一次世界大战提供支持，之后他的下一个重要工作是烟草工业。为了说服女性吸烟，实现男女平等，他组织了一场复活节游行，“自由火炬”，数千名女性在游行中点燃她们的自由火炬。伯奈斯与美国医学协会(American Medical association，《美国医学会杂志》的编辑实际上帮助了烟草行业设计其宣传活动)合作，发起了一场让美国人相信吸烟对健康有益的运动。

The drug industry began using his techniques in sometimes crude but always effective ways. Estrogen was named “the female hormone;” natural hormones, including estrogen and progesterone, were claimed, without any research, to be inactive when taken orally. Physician-shills were created to claim wonderful effects for estrogen. The vitamin status of the tocopherols was denied; as recently as the 1970s (and maybe later), university professors of dietetics were flatly saying “no one needs vitamin E.”

制药业开始使用他的技术，有时很粗糙，但总是很有效。雌激素被称为“女性荷尔蒙”;未经任何研究，包括雌激素和黄体酮在内的天然激素口服后被认为是无效的。医生希尔斯被创造出来，声称对雌激素有奇妙的效果。生育酚的维生素地位被否认;就在20世纪70年代(可能更晚)，大学营养学教授还直截了当地说:“没人需要维生素e。”

Very little research showing the curative effects of vitamin E in human diseases was allowed to be published, so it was only occasionally necessary to openly denounce vitamin E as worthless or dangerous. In 1981, the journal of the AMA published an article reviewing the “toxic” effects of vitamin E. Since I had read all of the articles cited, I realized that the author was claiming that whenever vitamin E changed something, the change was harmful, even though the original publication had described the effect as beneficial.

很少有研究表明维生素E对人类疾病的疗效被允许发表，所以只有偶尔有必要公开谴责维生素E毫无价值或危险。在1981年,《美国医学协会杂志》上发表了一篇文章审查的维生素E 的“有毒”效果。自从我读过的所有文章引用,我意识到作者是声称只要维生素E改变些什么,改变是有害的,尽管最初的出版物描述效果是有益的。

Although JAMA was eventually forced to give up its revenue from cigarette advertising, it didn't suffer at all, because of the vast advertising campaigns of the estrogen industry. JAMA obviously wouldn't want to publish anything suggesting that vitamin E, or progesterone, or thyroid, might be beneficial because of its antagonism of the harmful effects of estrogen.

尽管《美国医学会杂志》最终被迫放弃了香烟广告收入，但由于雌激素行业的大规模广告宣传，它根本没有受到影响。显然，《美国医学会杂志》不想发表任何关于维生素E、黄体酮或甲状腺可能有益的文章，因为它们能对抗雌激素的有害影响。

Estrogen causes changes in the uterus that prevent implantation of the embryo, and that impair support for its development if it has already implanted. It decreases the availability of oxygen to the embryo, while vitamin E increases it.

雌激素引起子宫的变化，阻止胚胎着床，如果胚胎已经着床，则会损害对胚胎发育的支持。它减少了胚胎获得氧气的机会，而维生素E则增加了氧气的机会。

My dissertation adviser, A.L. Soderwall, did a series of experiments in which he showed that providing hamsters with extra vitamin E postponed the onset of infertility in middle age. In my experiments, vitamin E increased the amount of oxygen in the uterus, correcting an oxygen deficiency produced either by supplemental estrogen or by old age. Progesterone has similar effects on the delivery of oxygen to the uterus.

我的论文导师索德沃尔(A.L. Soderwall)做了一系列实验，他证明给仓鼠提供额外的维生素E可以延缓中年时不孕的发生。在我的实验中，维生素E增加了子宫内的氧气量，纠正了由于补充雌激素或年老而产生的氧气不足。孕酮在向子宫输送氧气方面也有类似的作用。

In the 1940s, the official definition of vitamin E's activity was changed. Instead of its effectiveness in preventing the death and resorption of embryos, or the degeneration of the testicles or brain or muscles, it was redefined as an antioxidant, preventing the oxidation of unsaturated oils.

20世纪40年代，官方对维生素E活性的定义发生了改变。它没有有效地防止胚胎的死亡和吸收，或睾丸、大脑或肌肉的退化，而是被重新定义为一种抗氧化剂，防止不饱和油的氧化。

Although some people continued to think of it as a protective factor against thrombosis, heart attacks, diabetes, and infertility, the medical establishment claimed that the prevention or cure of diseases in animals wasn't relevant to humans, and that a mere antioxidant couldn't prevent or cure any human disease.

尽管一些人仍然认为它是防止血栓形成、心脏病、糖尿病和不孕的保护性因素，但医疗机构声称，对动物疾病的预防或治疗与人类无关，仅仅抗氧化剂不能预防或治疗任何人类疾病。

The experiments that led to the identification of vitamin E involved feeding rats a diet containing rancid lard and, as a vitamin A supplement, cod liver oil. Both of these contained large amounts of polyunsaturated oils.

在研究维生素E的实验中，研究人员给老鼠喂食含有腐臭猪油和鱼肝油的食物，作为维生素a的补充。这两种都含有大量的多不饱和油。

From 1929 to the early 1930s, other researchers were claiming to have demonstrated that the polyunsaturated fatty acids were nutritionally essential. These experiments, like the vitamin E experiments, were done on rats, but the medical establishment was satisfied that rat experiments proved that humans need linoleic or linolenic acid, while they refused to accept that vitamin E was essential for humans. When, in the 1940s, a group of vitamin B6 researchers showed that the supposed “essential fatty acid deficiency” could be cured by a supplement of vitamin B6, it became apparent that the polyunsaturated fatty acids slowed metabolism, and reduced all nutritional needs. The thyroid hormone was powerfully suppressed by the “essential” fatty acids.

从1929年到20世纪30年代初，其他研究人员声称已经证明多不饱和脂肪酸是营养必需品。这些实验，就像维生素E实验一样，是在老鼠身上进行的，但医疗机构对老鼠实验证明人类需要亚油酸或亚麻酸感到满意，而他们拒绝接受维生素E对人类是必要的。在20世纪40年代，一组维生素B6的研究人员表明，所谓的“必需脂肪酸缺乏”可以通过补充维生素B6来治愈。很明显，多不饱和脂肪酸减缓了新陈代谢，减少了所有的营养需求。甲状腺激素受到“必需”脂肪酸的有力抑制。

When we consider the two sets of experiments together, their outstanding feature is the toxicity of the polyunsaturated oils, which in one kind of experiment suppressed metabolism, and in the other kind of experiment created a variety of degenerative conditions.

当我们把这两组实验放在一起考虑时，它们的突出特点是多不饱和油脂的毒性，在一种实验中抑制了代谢，在另一种实验中创造了各种退化的条件。

By the late 1940s and early 1950s, estrogens of various sorts had been synthesized from hydrocarbons, and were being recommended to prevent miscarriages, because “estrogen is the female hormone.” The meat industry had found that the polyunsaturated oils were valuable in animal feed, since they suppressed metabolism and made it cheaper to fatten the animals, and these antithyroid oils were next marketed as “heart protective” human foods, though by suppressing the thyroid and destroying vitamin E, they actually contributed to both heart disease and cancer. (Giving estrogen to livestock to improve their feed efficiency, and to people “to prevent heart attacks,” was an interesting parallel to the oil promotional campaigns.)

到20世纪40年代末和50年代初，各种各样的雌激素已经从碳氢化合物中合成出来，并被推荐用来防止流产，因为“雌激素是女性荷尔蒙”。肉类工业发现，多不饱和油脂在动物饲料中很有价值，因为它们抑制新陈代谢，使动物增肥的成本更低，这些抗甲状腺油随后被作为“保护心脏”的人类食品出售，尽管通过抑制甲状腺和破坏维生素E，它们实际上会导致心脏病和癌症。(给牲畜注射雌激素是为了提高饲料效率，给人注射雌激素是为了“防止心脏病发作”，这与石油宣传活动是一个有趣的平行。)

The influence of the food oil industry kept researchers away from the idea that these oils were not safe for food use, and instead tended to support the idea that vitamin E is just an antioxidant, and that the seed oils were the best way to get vitamin E in the diet.

食用油行业的影响使研究人员远离“这些油当做食品食用是不安全”的想法，而是倾向于支持这样的想法：“维生素 E 只是一种抗氧化剂，种子油是在饮食中获取维生素E的最佳方式”。

The antifertility effects of the polyunsaturated oils, demonstrated in the vitamin E experiments, weren't at the time understood to have anything to do with estrogen's antifertility effects. But to understand vitamin E, I think we have to consider the close interactions between estrogen and the polyunsatured fatty acids (PUFA). Their actions are closely intertwined, and are antagonized by a variety of energizing and stabiliizing substances, including saturated fats, progesterone, thyroid, vitamin E, and aspirin.

在维生素E实验中显示的多不饱和油脂的抗生育作用，当时并不被认为与雌激素的抗生育作用有任何关系。但要理解维生素E，我认为我们必须考虑雌激素和多不饱和脂肪酸(PUFA)之间的密切相互作用。它们的作用紧密地交织在一起，并被包括饱和脂肪、黄体酮、甲状腺、维生素E和阿司匹林在内的多种激活和稳定物质拮抗。

Generally, chemicals that inhibit enzymes are toxic, producing some sort of symptom or deterioration. But a group of enzymes related to estrogen and PUFA are inhibited by these protective substances. Although under our present diet, these enzymes metabolize the PUFA, in the fetus and newborn they act on our endogenous fats, the series related to the Mead acids. The Mead acid is antiinflammatory, and broadly protective. The dietary PUFA interfere with these natural protective substances.

一般来说，抑制酶的化学物质是有毒的，会产生某种症状或恶化。但与雌激素和多不饱和脂肪酸相关的一组酶被这些保护性物质抑制。虽然在我们目前的饮食中，这些酶代谢多不饱和脂肪酸，但在胎儿和新生儿中，它们作用于我们的内源性脂肪，即与米德酸相关的系列脂肪。米德酸具有抗炎和广泛的保护作用。膳食中的多不饱和脂肪酸会干扰这些天然保护物质。

The enzymes that, if we didn't eat PUFA, would be regulating the Mead series, being activated in response to stress, would be producing antistress substances, which would limit the stress reaction. But as we become increasingly saturated with the anti-vitamin E fats, these enzymes, instead of stopping inflammation, promote it and cause tissue injury. The remaining stress limiting factors, such as progesterone, by correcting the distortions caused by stress, tend to eliminate the conditions which activated the enzymes–in a very indirect form of inhibition.

这些酶，如果我们不吃多不饱和脂肪酸，会调节米德系列，在应激反应中被激活，会产生抗应激物质，这将限制应激反应。但当我们体内的抗维生素E脂肪越来越多时，这些酶非但不能阻止炎症，反而会促进炎症，导致组织损伤。剩下的压力限制因素，如孕酮，通过纠正压力造成的扭曲，倾向于消除激活酶的条件——以一种非常间接的抑制形式。

Many of the events involved in inflammation are increased by estrogen, and decreased by vitamin E. Estrogen causes capillaries to become leaky; vitamin E does the opposite. Estrogen increases platelet aggregation, and decreases a factor that inhibits platelet aggregation; vitamin E does the opposite.

许多与炎症有关的事件因雌激素而增加，因维生素E而减少。

雌激素导致毛细血管渗漏;维生素E则相反。

雌激素增加血小板聚集，减少抑制血小板聚集的因素;维生素E则相反。

Excess clotting is known to be caused by too much estrogen, and also by a vitamin E deficiency.

众所周知，过多的凝血是由过多的雌激素和维生素E缺乏引起的。

Clotting leads to fibrosis, and there is clear evidence that vitamin E prevents and cures fibrotic diseases, but this still isn't generally accepted by the powerful medical institutions. Estrogen and polyunsaturated fats increase fibrosis.

凝血导致纤维化，有明确的证据表明维生素E可以预防和治疗纤维化疾病，但这仍然没有被强大的医疗机构普遍接受。雌激素和多不饱和脂肪会增加纤维化。

Estrogen increases progstaglandin synthesis, vitamin E decreases their synthesis; estrogen increases the activity of the enzymes COX and LOX, vitamin E decreases their activitiy. (Jiang, et al., 2000; Ali, et al., 1980; Parkhomets, et al., 2001.) Estrogen releases enzymes from lysosomes, vitamin E inhibits their release. Beta-glucuronidase, one of these enzymes, can release estrogen at the site of an inflammation.

雌激素增加黄体酮的合成，维生素E减少其合成;雌激素会增加COX和LOX酶的活性，维生素E则会降低它们的活性。(江等，2000;阿里等人，1980年;Parkhomets等，2001。)雌激素从溶酶体中释放酶，维生素E抑制它们的释放。葡萄糖醛酸酶是这些酶中的一种，可以在炎症部位释放雌激素。

Estrogen often increases intracellular calcium and protein kinase C, vitamin E has generally opposite effects.

雌激素通常会增加细胞内的钙和蛋白激酶C，维生素E一般有相反的作用。

The polyunsaturated fatty acids and their derivatives, the prostaglandins, act as effectors, or amplifiers, of estrogen's actions.

多不饱和脂肪酸及其衍生物前列腺素作为雌激素作用的效应器或放大器。

If vitamin E is acting as a protectant against the polyunsaturated fatty acids, that in itself would account for at least some of its antiestrogenic effects.

如果维生素E可以作为抗多不饱和脂肪酸的保护剂，那么它本身至少可以解释它的一些抗雌激素作用。

Besides antagonizing some of the end effects of the toxic fatty acids, vitamin E inhibits lipolysis, lowering the concentration of free fatty acids (the opposite of estrogen's effect), and it also binds to, and inactivates, free fatty acids. The long saturated carbon chain is very important for its full functioning, and this saturated chain might allow it to serve as a substitute for the omega -9 fats, from which the Mead acid is formed. The unsaturated tocotrienols have hardly been tested for the spectrum of true vitamin E activity, and animal studies have suggested that it may be toxic, since it caused liver enlargement.

除了拮抗一些有毒脂肪酸的末端作用外，维生素E还能抑制脂解，降低游离脂肪酸的浓度(与雌激素的作用相反)，它还能结合游离脂肪酸并使其失活。长长的饱和碳链对它的完整功能非常重要，这条饱和碳链可能使它可以作为形成米德酸的omega -9脂肪的替代品。不饱和的生育三烯醇几乎没有测试过真正的维生素E活性谱，动物研究表明它可能是有毒的，因为它会导致肝脏增大。

One possibly crucial protective effect of vitamin E against the polyunsaturated fatty acids that hasn't been explored is the direct destruction of linolenic and linoleic acid. It is known that bacterial vitamin E is involved in the saturation of unsaturated fatty acids, and it is also known that intestinal bacteria turn linoleic and linolenic acids into the fully saturated stearic acid.

维生素E对多不饱和脂肪酸的一个可能至关重要的保护作用尚未被探索，那就是对亚麻酸和亚油酸的直接破坏。已知细菌维生素E参与不饱和脂肪酸的饱和，也知道肠道细菌将亚油酸和亚麻酸转化为完全饱和的硬脂酸。

“No metabolic function is known for alpha-tocopherolquinol or its quinone other than as a cofactor in the biohydrogenation of unsaturated fatty acids that can be carried out by only a few organisms.”

• P.E. Hughes and S.B. Tove, 1982.*

生育酚或其醌没有已知的代谢功能，除了作为仅能由少数生物体进行的不饱和脂肪酸生物氢化的辅助因子。

“Linoleic acid was significantly decreased (P &lt; 0.001) and there was a significant rise (P &lt; 0.05) in its hydrogenation product, stearic acid. Linolenic acid was also significantly decreased. . . .”“The study provides evidence that bacteria from the human colon can hydrogenate C18 essential polyunsaturated fatty acids.*” 亚油酸显著降低(P &lt; 0.001)，其氢化产物硬脂酸显著升高(P &lt; 0.05)。亚麻酸也显著减少. . . .”“这项研究提供了证据，证明来自人类结肠的细菌可以氢化C18必需的多不饱和脂肪酸。”* F.A. Howard &amp; C._ Henderson, 1999* Because of the way in which the decision to call vitamin E a simple antioxidant was conditioned by the historical setting, there has been a reluctance, until recently, to give much weight to the pathogenicity of lipid peroxidation and free radicals, partly because lipid peroxidation is only a minor part of the toxicity of the polyunsaturated oils, and there was little support for the investigation of the real nature of their toxicity. This environment has even distorted the actual antioxidant value of the various forms of vitamin E. (For example, see Chen, et al., 2002.) 因为叫维生素E的方式决定一个简单的抗氧化剂是历史条件的设置,有不愿意,直到最近,给了一些份量在致病性脂质过氧化自由基方面,部分原因是脂质过氧化是只有一小部分的多不饱和油脂的毒性,而且几乎没有人支持对它们毒性的真实性质进行调查。这种环境甚至扭曲了各种维生素E的实际抗氧化价值。 The people who say that vitamin E is nothing but an antioxidant sometimes take other antioxidants, with, or instead of, vitamin E. BHT, BHA, and many natural compounds (derived from industrial and agricultural wastes) are often said to be “better than vitamin E” as antioxidants. Anything that can be oxidized and reduced (melatonin, estrogen, tryptophan, carotene, etc.) will function as an antioxidant in some system, but in other circumstances, it can be a pro-oxidant. 说维生素E只是一种抗氧化剂的人，有时服用其他抗氧化剂，与维生素E，或代替维生素E, BHT, BHA，和许多天然化合物(从工业和农业废料中提取)经常被认为是“比维生素E更好的”抗氧化剂。任何可以被氧化和还原的物质(褪黑素、雌激素、色氨酸、胡萝卜素等)在某些系统中都能起到抗氧化剂的作用，但在其他情况下，它可能是一种促氧化剂。 The people who think there is benefit in the abstract “antioxidant” function seem to be thinking in terms of something that will, like a ubiquitous fire department, put out every little fire as soon as it starts. I think it's more appropriate to think of the biological antioxidant systems as programs for controlling the arsonists before they can set the fires. 那些认为抽象的“抗氧化剂”功能有好处的人，似乎是在考虑某种东西，比如无处不在的消防部门，一旦发生小火灾，就会把它扑灭。我认为把生物抗氧化系统看作是在纵火犯纵火之前控制他们的程序更合适。 Since the requirement for vitamin E decreases as the consumption of unsaturated fats decreases, the requirement, if any, would be very small if we didn't eat significant quantities of those fats. 由于对维生素E的需求随着不饱和脂肪的消耗而减少，如果我们不吃大量的不饱和脂肪，对维生素E的需求就会非常小。 In the years since the tocopherols were identified as vitamin E, the material sold for research and for use as a nutritional supplement has changed drastically several times, even when it has been given a specific chemical identity, such as mixed tocopherols or d-alpha tocopherol. Variations in viscosity and color, caused by changes in the impurities, have undoubtedly influenced its biological effects, but the ideology about its antioxidant value has kept researchers from finding out what a particular batch of it really is and what it really does. 在生育酚被鉴定为维生素E之后的这些年里，这种用于研究和营养补充的物质已经发生了好几次巨大的变化，即使它被赋予了特定的化学特性，比如混合生育酚或d- α生育酚。由杂质的变化引起的粘度和颜色的变化，无疑影响了它的生物效果，但关于它的抗氧化价值的意识形态，一直让研究人员无法找出某一批它到底是什么，以及它到底有什么作用。 “We compared the effect of a mixed tocopherol preparation with that of alpha-tocopherol alone on superoxide dismutase (SOD) activity and iNOS expression in cultured myocytes exposed to H-R.” “Both tocopherol preparations attenuated cell injury. . . .” “However, mixed-tocopherol preparation was much superior to alpha-tocopherol in terms of myocyte protection. . . .” “Lack of efficacy of commercial tocopherol preparations in clinical trials may reflect absence of gamma- and delta-tocopherols.” Chen H, Li D, Saldeen T, Romeo F, Mehta JL,Biochem Biophys Res Commun 2002 “Mixed tocopherol preparation is superior to alpha-tocopherol alone against hypoxia-reoxygenation injury.”* “我们比较了混合生育酚制剂与单独α -生育酚制剂对接触H-R培养的心肌细胞超氧化物歧化酶(SOD)活性和iNOS表达的影响。”“两种生育酚制剂都能减轻细胞损伤. . . .”“然而，在保护肌细胞方面，混合生育酚制剂比α -生育酚要好得多. . . .”“临床试验中商业生育酚制剂缺乏功效可能反映了gamma-和delta-生育酚的缺乏。”来自“复合生育酚制剂在抗缺氧-复氧损伤方面优于单用-生育酚制剂” Keeping our diet as free as possible of the polyunsaturated fats, to create something like the “deficiency” state that is so protective (against cancer, trauma, poison, shock, inflammation, infection, etc.) in the animal experiments, seems preferable to trying to saturate ourselves with antioxidants, considering the imperfectly defined nature of the vitamin E products, and the known toxicity of many of the other antioxidants on the market. 在动物实验中，让我们的饮食尽可能不含多不饱和脂肪，从而产生一种类似于“缺乏”状态的东西(对癌症、创伤、中毒、休克、炎症、感染等)，似乎比试图让我们自己充满抗氧化剂更可取，考虑到维生素E产品的不完全定义，以及市场上许多其他抗氧化剂的已知毒性。 The carcinogenic properties of the polyunsaturated fats have been known for more than 50 years, as has the principle of extending the life span by restricted feeding. More recently several studies have demonstrated that the long lived species contain fewer highly unsaturated fats than the short lived species. Restriction of calories prevents the lipids in the brain, heart, and liver from becoming more unsaturated with aging. (Lee, et al., 1999; Laganiere, et al., 1993; Tacconi, et al., 1991; R. Patzelt-Wenczler, 1981.) 多不饱和脂肪的致癌特性在50多年前就已为人所知，通过限制喂养延长寿命的原则也已为人所知。最近的几项研究表明，长寿物种比短命物种含有更少的高不饱和脂肪。限制卡路里可以防止大脑、心脏和肝脏中的脂质随着年龄增长而变得更加不饱和。 When cells are grown in tissue culture without the “essential fatty acids,” they become “deficient,” and in that state are very resistant to chemical injury, and can be grown indefinitely. Besides being a simple demonstration of the way in which the polyunsaturated fats sensitize cells to injury (Wey, et al., 1993), these experiments must be an embarrassment to the people who base their argument for the oils’ essentiality on a supposed requirement for “making cell membranes.” Since the cells can multiply nicely in their deficient state, we have to conclude that the oils aren’t needed for “membranes,” or maybe that cells resist injury better “without membranes.” 当细胞在没有“必需脂肪酸”的组织培养中生长时，它们就会“缺乏”，在这种状态下，细胞对化学损伤具有很强的抵抗力，可以无限生长。除了简单地证明了多不饱和脂肪是如何使细胞对损伤敏感之外(Wey等人，1993年)，这些实验肯定会让那些把油脂的必要性建立在“制造细胞膜”的假设要求上的人感到尴尬。由于细胞在有缺陷的状态下可以很好地繁殖，我们不得不得出这样的结论:“膜”不需要油，或者“没有膜”的细胞更能抵抗损伤。 In the opposite direction, an excess of insulin or prolactin, or a deficiency of vitamin E, increases the activity of the enzymes that convert linoleic acid into the more highly unsaturated fatty acids. Excess insulin and prolactin are crucially involved in many degenerative diseases. 相反，过量的胰岛素或催乳素，或缺乏维生素E，会增加将亚油酸转化为不饱和脂肪酸的酶的活性。过量的胰岛素和催乳素与许多退行性疾病密切相关。 The highly unsaturated fats suppress respiration in many ways, and these trends toward increased unsaturation with aging, endocrine stress, and vitamin E deficiency parallel the life-long trend toward lower energy production from respiration. Many studies show that vitamin E can protect and improve mitochondrial energy production. (Kikuchi, et al., 1991; Donchenko, et al., 1990, 1983; Guarnieri, et al., 1981, 1982.) But the state of so-called essential fatty acid deficiency not only makes mitochondria very resistant to injury, it greatly intensifies their energy production. Vitamin E supplementation is seldom as effective as the absence of the toxic oils. 高不饱和脂肪以多种方式抑制呼吸，而随着年龄增长、内分泌压力和维生素E缺乏，不饱和脂肪增加的趋势与呼吸产生能量的终生趋势相平行。许多研究表明，维生素E可以保护和改善线粒体能量的产生。(菊池等人，1991;东琴科等，1990,1983;Guarnieri等，1981,1982)。但是，所谓的必需脂肪酸缺乏状态不仅使线粒体非常抗损伤，还极大地增强了它们的能量生产。补充维生素E很少能像没有有毒油脂那样有效。 Many nutrition charts no longer list liver as a good source of vitamin E, but a large portion of an animal's vitamin E is in its liver. This bias in the dietetic literature can be traced to various sources, but a major influence was the campaign in the 1970s by the drug companies that had patented new forms of synthetic “vitamin A.” They had physicians and professors fabricate stories about the great toxicity of natural vitamin A, and placed the stories in national magazines, to clear the field for their supposedly non-toxic products, which have turned out to be disastrously toxic. The result is that many people have fearfully stopped eating liver, because of its vitamin A. The other vitamins in liver, including vitamin K, function very closely with vitamin E, and the stably stored forms of vitamin E are likely to be a good approximation for our needs. 许多营养图表不再将肝脏列为维生素E的良好来源，但动物的维生素E的很大一部分在肝脏中。这种偏见在饮食文学可以追溯到各种来源,但运动的主要影响是在1970年代的制药公司专利新形式的合成维生素a。“他们医生和教授制造天然维生素a的毒性的故事,并把故事在国家杂志,为他们所谓的无毒产品扫清障碍，而这些产品却被证明是灾难性的有毒产品。结果是，许多人害怕地停止吃肝脏，因为它含有维生素a。肝脏中的其他维生素，包括维生素K，与维生素E的功能非常密切，维生素E的稳定储存形式很可能是我们需要的一个很好的近似。 There is still a strong division between what people can say in their professional publications, and what they believe. A man who was influential in designating vitamin E as an antioxidant, M.K. Horwitt, complained when the government raised its recommended vitamin E intake by 50%, because it wasn't supported by new data, and because millions of people get only ten milligrams per day and “are healthy.” But he has been taking 200 mg daily (plus aspirin) for many years. He apparently doesn't have very much confidence in the ideas he advocates publicly.
人们在专业出版物上的言论和他们的信仰之间仍然存在很大的分歧。在将维生素E确定为抗氧化剂方面有影响力的M.K. Horwitt抱怨政府将推荐的维生素E摄入量提高了50%，因为它没有新的数据支持，因为数百万人每天只摄入10毫克维生素E，而且“是健康的”。但多年来，他每天服用200毫克(外加阿司匹林)。显然，他对自己公开倡导的理念没有太多信心。 </markdown> Edit:2021.08.25<markdown> REFERENCES Prostaglandins Med 1980 Feb;4(2):79-85. Inhibition of human platelet cyclooxygenase by alpha-tocopherol. Ali M, Gudbranson CG, McDonald JW. Alpha-tocopherol, an inhibitor of platelet aggregation, was evaluated for its effects on the synthesis of thromboxane and prostaglandins. A dose-dependent reduction in thromboxane B2 and prostaglandin D2 synthesis was observed with approximately 60% inhibition at 5.0 IU or alpha-tocopherol. Alpha-tocopherol produced a time-dependent, irreversible inhibition. Int J Vitam Nutr Res 2001 Jan;71(1):18-24. Vitamin E and the prevention of atherosclerosis. Bron D, Asmis R. “Recent new findings have shed new light on the physiological role of vitamin E and suggest that it has a much broader array of biological activities than originally expected. In addition to its well described role as an antioxidant, it is becoming evident that vitamin E also can modulate the immune system, suppress local and chronic inflammation, reduce blood coagulation and thrombus formation, and enhance cell function and survival.” Plast Reconstr Surg 1981 Nov;68(5):696-9. The effectiveness of alpha-tocopherol (vitamin E) in reducing the incidence of spherical contracture around breast implants. Baker JL Jr. Vitamin E appears to be a safe, simple, and inexpensive means of reducing the number of postoperative capsular contractures following breast augmentation. The synthetic form of vitamin E (alpha-tocopherol) is recommended to avoid nausea or skin eruptions in patients with oily skin, which are frequently encountered when the natural form is taken. No harmful side effects have been noted in any of the patients to date. Vitamin E has no effect on coagulation systems and does not cause excessive bleeding either during or after surgery. The recommended dosage of synthetic vitamin E is 1000 IU, b.i.d., for 2 years beginning 1 week before surgery. If no contracture exists at that time, the dosage may be reduced to 1000 IU daily thereafter. Carcinogenesis 1999 Jun;20(6):1019-24. Decrease in linoleic acid metabolites as a potential mechanism in cancer risk reduction by conjugated linoleic acid. Banni S, Angioni E, Casu V, Melis MP, Carta G, Corongiu FP, Thompson H, Ip C. Mech Ageing Dev 1978 Nov;8(5):311-28. Anomalous vitamin E effects in mitochondrial oxidative metabolism. Baumgartner WA, Hill VA, Wright ET. Three different vitamin E effects, suggestive of specific antioxidant effects, were discovered in the protective action of vitamin E against respiratory decline (a decrease in mitochondrial respiration attributed to a “leakage” of electron transport radicals). No correlation was found between respiraotry decline and random lipid peroxidation. The mechanisms behind two of the three atypical vitamin E effects were defined. Both involve an artifact in the TBA assay for lipid peroxidation. This artifact occurs when TBA assays are carried out in the presence of sucrose and acetaldehyde; the latter is produced from ethanol, the solvent used to add vitamin E to preparations. The artifact in the TBA assay for peroxidations appears also to be responsible for differing interpretations of the hepatotoxic effect of ethanol. Eur J Biochem 1990 Mar 10;188(2):327-32. Polychlorinated biphenyls increase fatty acid desaturation in the proliferating endoplasmic reticulum of pigeon and rat livers. Borlakoglu JT, Edwards-Webb JD, Dils RR. Nutr Cancer 2000;38(1):87-97. Effects of topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice. Burke KE, Clive J, Combs GF Jr, Commisso J, Keen CL, Nakamura RM. “Results showed that the skin concentrations of Eol, as well as levels in the adipose tissue, were increased after topical application. Mice treated with each form of vitamin E showed no signs of toxicity and had significantly less acute and chronic skin damage induced by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.” Am J Physiol 1991 Jun;260(6 Pt 2):R1235-40. Acute phase response in exercise. II. Associations between vitamin E, cytokines, and muscle proteolysis. Cannon JG, Meydani SN, Fielding RA, Fiatarone MA, Meydani M, Farhangmehr M, Orencole SF, Blumberg JB, Evans WJ. Vrach Delo 1990 Dec;(12):6-8. [The effect of tocopherol and nicotinic acid on the microcirculation and blood coagulability in patients with ischemic heart disease] Chernomorets NN, Kotlubei GV, Vatutin NT, Zhivotovskaia IA, Gnilitskaia VB, Alifanova RE, Lobach EIa, Mal'tseva NV, Mitrofanov AN. “Complex treatment using tocopherol acetate produced a positive effect on the coagulation properties of the blood and did essentially influence the fibrinolytic activity and microcirculation. Tocopherol plus nicotinic acid resulted in normalization of the blood coagulation process, favoured activation of fibrinolysis and improvement of the microcirculatory bed.” Free Radic Biol Med 1991;10(5):325-38. Oxidative status and oral contraceptive. Its relevance to platelet abnormalities and cardiovascular risk. Ciavatti M, Renaud S. INSERM Unit 63, Bron, France. “Oral contraceptive (OC) use is a risk for thrombogenic events.” “From these data we conclude that: 1. OC use modifies slightly but significantly the oxidative status in women and in animals by decreasing in plasma and blood cells the antioxidant defenses (vitamins and enzymes). 2. The changes in the oxidative status are related to an increase in plasma lipid peroxides apparently responsible for the hyperaggregability and possibly the imbalance in clotting factors associated with the OC-induced prethrombotic state. 3. These effects of OC appear to be increased by a high intake of polyunsaturated fat and counteracted by supplements of vitamin E. 4. The risk factors acting synergistically with OC, have all been shown to increase platelet reactivity.” Bol Med Hosp Infant Mex 1980 May-Jun;37(3):457-67. [Jaundice caused by microangiopathic hemolysis associated to septicemia in the newborn] Covarrubias Espinoza G, Lepe Zuniga JL. “These infants with over 3% fragmented cells were found to have a significant association with: sepsis, jaundice, crenated RBC's, low levels of hemoglobin, increased reticulocyte count, and low vitamin E levels.” Endocrinology 1992 Nov;131(5):2482-4. Vitamin E protects hypothalamic beta-endorphin neurons from estradiol neurotoxicity. Desjardins GC, Beaudet A, Schipper HM, Brawer JR. “Estradiol valerate (EV) treatment has been shown to result in the destruction of 60% of beta-endorphin neurons in the hypothalamic arcuate nucleus. Evidence suggests that the mechanism of EV-induced neurotoxicity involves the conversion of estradiol to catechol estrogen and subsequent oxidation to free radicals in local peroxidase-positive astrocytes. In this study, we examined whether treatment with the antioxidant, vitamin E, protects beta-endorphin neurons from the neurotoxic action of estradiol. Our results demonstrate that chronic vitamin E treatment prevents the decrement in hypothalamic beta-endorphin concentrations resulting from arcuate beta-endorphin cell loss, suggesting that the latter is mediated by free radicals. Vitamin E treatment also prevented the onset of persistent vaginal cornification and polycystic ovarian condition which have been shown to result from the EV-induced hypothalamic pathology.” Free Radic Biol Med 2000 Dec 15;29(12):1302-6. Hyperinsulinemia: the missing link among oxidative stress and age-related diseases? Facchini FS, Hua NW, Reaven GM, Stoohs RA. “Other proaging effects of insulin involve the inhibition of proteasome and the stimulation of polyunsaturated fatty acid (PUFA) synthesis and of nitric oxide (NO). The hypothesis that hyperinsulinemia accelerates aging also offers a metabolic explanation for the life-prolonging effect of calorie restriction and of mutations decreasing the overall activity of insulin-like receptors in the nematode Caenorhabditis elegans.” J Bacteriol 1982 Sep;151(3):1397-402. Occurrence of alpha-tocopherolquinone and alpha-tocopherolquinol in microorganisms. Hughes PE, Tove SB. “Both alpha-tocopherolquinol and alpha-tocopherolquinone were found in 56 of 93 strains of microorganisms examined.” “Those microorganisms that did not contain alpha-tocopherolquinol or alpha-tocopherolquinone tended to fall into two groups. One group consisted of gram-positive, anaerobic or facultative bacteria with a low content of guanine and cytosine, and the second group encompassed all of the filamentous microorganisms studied.” “No metabolic function is known for alpha-tocopherolquinol or its quinone other than as a cofactor in the biohydrogenation of unsaturated fatty acids that can be carried out by only a few organisms.” J Biol Chem 1980 Dec 25;255(24):11802-6. Identification of deoxy-alpha-tocopherolquinol as another endogenous electron donor for biohydrogenation. Hughes PE, Tove SB. J Biol Chem 1980 May 25;255(10):4447-52. Identification of an endogenous electron donor for biohydrogenation as alpha-tocopherolquinol. Hughes PE, Tove SB. “The ratio of alpha-tocopherolquinone produced to fatty acid reduced was 2:1 when the tocopherol derivatives were extracted aerobically. When the extraction was carried out anaerobically, the ratio was 1. It is suggested that the oxidation of 2 molecules of alpha-tocopherolquinol, each to the semiquinone, provides the electrons required for the reduction of the cis-bond of the conjugated dienoic fatty acid.” Lett Appl Microbiol 1999 Sep;29(3):193-6. Hydrogenation of polyunsaturated fatty acids by human colonic bacteria. Howard FA, Henderson C. Emulsions of the fatty acids linoleic (C18:2 n-6), alpha-linolenic (C18:3 n-3) and arachidonic acid (C20:4 n-6) were incubated for 4 h under anaerobic conditions with human faecal suspensions. Linoleic acid was significantly decreased (P &lt; 0.001) and there was a significant rise (P &lt; 0.05) in its hydrogenation product, stearic acid. Linolenic acid was also significantly decreased (P &lt; 0.01), and significant increases in C18:3 cis-trans isomers (P &lt; 0.01) and linoleic acid (P &lt; 0.05) were seen. With each acid, there were non-significant increases in acids considered to be intermediates in biohydrogenation. The study provides evidence that bacteria from the human colon can hydrogenate C18 essential polyunsaturated fatty acids. However, with arachidonic acid there was no evidence of hydrogenation. Prostaglandins Leukot Essent Fatty Acids 1998 Dec;59(6):395-400. Modulation of rat liver lipid metabolism by prolactin. Igal RA, de Gomez Dumm IN, Goya RG. Clin Chim Acta 1994 Mar;225(2):97-103. Vitamin E and the hypercoagulability of neonatal blood. Jain SK, McCoy B, Wise R. “There was a significant correlation between plasma vitamin E and whole blood clotting time (r = 0.54, P &lt; 0.04) of cord blood. The addition of standard vitamin E to cord blood in vitro resulted in prolongation of whole blood clotting time. This suggests that a deficiency of plasma vitamin E can shorten whole blood clotting time in newborns, which may have a role in the disseminated intravascular coagulation frequently experienced by newborn infants.” Proc Natl Acad Sci U S A 2000 Oct 10;97(21):11494-9. gamma-tocopherol and its major metabolite, in contrast to alpha-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells. Jiang Q, Elson-Schwab I, Courtemanche C, Ames BN. “Cyclooxygenase-2 (COX-2)-catalyzed synthesis of prostaglandin E(2) (PGE(2)) plays a key role in inflammation and its associated diseases, such as cancer and vascular heart disease. Here we report that gamma-tocopherol (gammaT) reduced PGE(2) synthesis in both lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and IL-1beta-treated A549 human epithelial cells with an apparent IC(50) of 7.5 and 4 microM, respectively.” “The inhibitory effects of gammaT and gamma-CEHC stemmed from their inhibition of COX-2 activity, rather than affecting protein expression or substrate availability, and appeared to be independent of antioxidant activity.” “The inhibitory potency of gammaT and gamma-CEHC was diminished by an increase in AA concentration, suggesting that they might compete with AA at the active site of COX-2. We also observed a moderate reduction of nitrite accumulation and suppression of inducible nitric oxide synthase expression by gammaT in lipopolysaccharide-treated macrophages. These findings indicate that gammaT and its major metabolite possess anti-inflammatory activity and that gammaT at physiological concentrations may be important in human disease prevention.” Biosci Biotechnol Biochem 1992 Sep;56(9):1420-3. Effects of alpha-tocopherol and tocotrienols on blood pressure and linoleic acid metabolism in the spontaneously hypertensive rat (SHR). Koba K, Abe K, Ikeda I, Sugano M. Both alpha-tocopherol and a 1:1.7 mixture of alpha-tocopherol and tocotrienols at a 0.2% dietary level significantly depressed the age-related increase in the systolic blood pressure of spontaneously hypertensive rats (SHRs) after 3 weeks of feeding. The aortic production of prostacyclin was increased 1.5 times both by alpha-tocopherol and a tocotrienol mixture, suggesting a possible relevance to their hypotensive effect. These vitamins did not influence the delta 6- and delta 5-desaturase activities of liver microsomes, but fatty acid profiles of the liver phospholipids predicted a reduction of linoleic acid desaturation. These effects were in general more clear with tocotrienols than with alpha-tocopherol. Platelet aggregation by 5 microM ADP remained uninfluenced. Thus, tocotrienols may have effects on various lipid parameters somewhat different from those of alpha-tocopherol. Gerontology 1993;39(1):7-18. Modulation of membrane phospholipid fatty acid composition by age and food restriction. Laganiere S, Yu BP. H.M. “Phospholipids from liver mitochondrial and microsomal membrane preparations were analyzed to further assess the effects of age and lifelong calorie restriction on membrane lipid composition.” “The data revealed characteristic patterns of age-related changes in ad libitum (AL) fed rats: membrane levels of long-chain polyunsaturated fatty acids, 22:4 and 22:5, increased progressively, while membrane linoleic acid (18:2) decreased steadily with age. Levels of 18:2 fell by approximately 40%, and 22:5 content almost doubled making the peroxidizability index increase with age.” “We concluded that the membrane-stabilizing action of long-term calorie restriction relates to the selective modification of membrane long-chain polyunsaturated fatty acids during aging.” Free Radic Biol Med 1999 Feb;26(3-4):260-5. Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake. Lee J, Yu BP, Herlihy JT. “The fatty acid composition of the mitochondrial membranes of the two ad lib fed groups differed: the long-chain polyunsaturated 22:4 fatty acid was higher in the older group, although linoleic acid (18:2) was lower. DR eliminated the differences.” “Considered together, these results suggest that DR maintains the integrity of the cardiac mitochondrial membrane fluidity by minimizing membrane damage through modulation of membrane fatty acid profile.” Lipids 2001 Jun;36(6):589-93. Effect of dietary restriction on age-related increase of liver susceptibility to peroxidation in rats. Leon TI, Lim BO, Yu BP, Lim Y, Jeon EJ, Park DK. Jpn J Pharmacol 1979 Apr;29(2):179-86. Effect of linoleic acid hydroperoxide on liver microsomal enzymes in vitro. Masuda Y, Murano T. “Rat liver microsomes incubated with linoleic acid hydroperoxide (LAHPO) lost cytochrome P-450 specifically among the enzymes of microsomal electron transport systems. The loss of cytochrome P-450 content and glucose-6-phosphatase activity by LAHPO was accompanied by an increase in malondialdehyde (MDA) production.” “These results suggest the possibility that the loss of microsomal enzyme activities during lipid peroxidation may be attributed largely to a direct attack on enzyme proteins by lipid peroxides rather than indirectly to a structural damage of microsomal membranes resulting from peroxidative breakdown of membrane lipids.” Ukr Biokhim Zh 2001 Jan-Feb;73(1):43-7. [Effect of alpha-tocopherol, tocopheryl quinone and other complexes with tocopherol-binding proteins on the activity of enzymes metabolizing arachidonic acid] Parkhomets' VP, Silonov SB, Donchenko HV. Palladin Institute of Biochemistry, National Academy of Science of Ukraine, Kyiv. alpha-Tocopherol, tocopherylquinon jointly with the proteins tocopherol acceptors from cytosole were identified to inhibit the activity of 5-lipoxigenase and so the synthesis of leukotriene A4 at the early stages providing for A4 hydrolase activation and C4 synthesase, as well as accelerate leukotrienes B4 and C4 synthesis at the further stages respectively changing the final spectrum of leukotriens in the organism tissues. Firstly, the leading role of proteins complexes capable to strengthen the effect of alpha-tocopherol and tocopherylquinon on arachidonic acid oxidative metabolism was determined. Int J Vitam Nutr Res 1981;51(1):26-33. [Effect of vitamin E on the synthesis of polyunsaturated fatty acids] Patzelt-Wenczler R. The formation of polyunsaturated fatty acids is influenced by vitamin E. The enzyme of the endoplasmic reticulum isolated from rat liver responsible for chain elongation and desaturation showed higher activity under vitamin E-deficiency. The activity was raised both per mg protein and per mg DNA. The application of alpha-Tocopherol to the vitamin E-deficient animals caused the normalization of the enzyme activity within 48 hours. This indicates a regulatory function of alpha-Tocopherol in the process of oxidation. Lipids 2001 May;36(5):491-8. Correlation of fatty acid unsaturation of the major liver mitochondrial phospholipid classes in mammals to their maximum life span potential. Portero-Otin M, Bellmunt MJ, Ruiz MC, Barja G, Pamplona R. Free Radic Biol Med 1999 Oct;27(7-8):729-37. Age-dependent increase of collagenase expression can be reduced by alpha-tocopherol via protein kinase C inhibition. Ricciarelli R, Maroni P, Ozer N, Zingg JM, Azzi A. “Our in vitro experiments with skin fibroblasts suggest that alpha-tocopherol may protect against skin aging by decreasing the level of collagenase expression, which is induced by environmental insults and by aging.” Prostaglandins Leukot Essent Fatty Acids 1991 Oct;44(2):89-92. Inhibition of PGE2 production in macrophages from vitamin E-treated rats. Sakamoto W, Fujie K, Nishihira J, Mino M, Morita I, Murota S. Int J Vitam Nutr Res 1990;60(1):26-34. The influence of vitamin E on rheological parameters in high altitude mountaineers. Simon-Schnass I, Korniszewski L. “The erythrocyte filterability was unaltered in the vitamin E group in comparison with baseline but was significantly impaired in the control group.” Neurobiol Aging 1991 Jan-Feb;12(1):55-9. Aging and food restriction: effect on lipids of cerebral cortex. Tacconi MT, Lligona L, Salmona M, Pitsikas N, Algeri S. In experimental animals dietary restriction reduces the body weight increase due to aging, increases longevity and delays the onset of age-related physiological deterioration, including age-related changes in serum lipids. Little is known about the influence of food restriction on brain lipids, whose concentration and composition have been shown to change with age. We studied whether some biochemical and biophysical parameters of rat brain membranes, known to be modified with age, were affected by a diet low in calories, in which 50% of lipids and 35% of carbohydrates have been replaced by fibers. The diet was started at weaning and maintained throughout the animal's entire life span. Animals fed the low calorie diet survived longer and gained less body weight than standard diet fed rats. Age-related increases in microviscosity, cholesterol/phospholipid and sphingomyelin/phosphatidylcholine ratios were reduced or restored to the levels of young animals in cortex membranes of 32 old rats fed the low calorie diet, while the age-related increase in mono- to polyunsaturated fatty acid ratios in phospholipids was further raised. In conclusion we have shown that a diet low in calories and high in fibers affects lipid composition in the rat brain, in a direction opposite to that normally believed to reduce age-related deterioration of brain functions. Toxicol Appl Pharmacol 1993 May;120(1):72-9. Essential fatty acid deficiency in cultured human keratinocytes attenuates toxicity due to lipid peroxidation. Wey HE, Pyron L, Human keratinocytes are commonly grown in culture with a serum-free medium. Under these conditions, keratinocytes become essential fatty acid deficient (EFAD), as determined by gas chromatographic analysis of cell phospholipid fatty acid composition. Exposure of EFAD keratinocytes for 2 hr to concentrations of t-butyl hydroperoxide (tBHP) up to 2 mM did not result in toxicity assessed by lactate dehydrogenase (LDH) release and only a small indication of lipid peroxidation assessed by the release of thiobarbituric acid-reactive substances (TBARS). Addition of 10 microM linoleic acid (LA) to serum-free medium alleviated the EFAD condition by increasing the phospholipid content of LA and its elongation and desaturation products, arachidonic acid and docosatetraenoic acid. Exposure of LA-supplemented keratinocytes to tBHP resulted in significant LDH (at 1 and 2 mM tBHP) and TBARS (tBHP concentration dependent) release. TBARS release was also significantly elevated in unexposed LA-supplemented keratinocytes (basal release). Co-supplementation with the antioxidant, alpha-tocopherol succinate (TS) prevented tBHP (1 mM)-induced LDH release in LA-supplemented cultures. TS supplementation also attenuated the effect of tBHP on TBARS release, but when compared to TS-supplemented EFAD cultures, LA supplementation still led to increased tBHP-induced TBARS release. Keratinocyte cultures are potentially useful as an alternative to animals in toxicology research and testing. It is important, however, that the cell model provide a response to toxic insult similar to that experienced in vivo. Our results suggest that fatty acid and antioxidant nutrition of cultured keratinocytes are important parameters in mediating the toxic effects of lipid peroxidation. Cancer Lett 1997 Jan 1;111(1-2):179-85. Subcutaneous, omentum and tumor fatty acid composition, and serum insulin status in patients with benign or cancerous ovarian or endometrial tumors. Do tumors preferentially utilize polyunsaturated fatty acids? Yam D, Ben-Hur H, Dgani R, Fink A, Shani A, Berry EM. AC Chan, J. of Nutrition, 1998 “The response-to-injury hypothesis explains atherosclerosis as a chronic inflammatory response to injury of the endothelium, which leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components. Inflammatory and other stimuli trigger an overproduction of free radicals, which promote peroxidation of lipids in LDL trapped in the subendothelial space. Products of LDL oxidation are bioactive, and they induce endothelial expression and secretion of cytokines, growth factors and several cell surface adhesion molecules. The last-mentioned are capable of recruiting circulating monocytes and T lymphocytes into the intima where monocytes are differentiated into macrophages, the precursor of foam cells. In response to the growth factors and cytokines, smooth muscle cells proliferate in the intima, resulting in the narrowing of the lumen. Oxidized LDL can also inhibit endothelial production of prostacyclin and nitric oxide, two potent autacoids that are vasodilators and inhibitors of platelet aggregation. Evidence is presented that vitamin E is protective against the development of atherosclerosis. Vitamin E enrichment has been shown to retard LDL oxidation, inhibit the proliferation of smooth muscle cells, inhibit platelet adhesion and aggregation, inhibit the expression and function of adhesion molecules, attenuate the synthesis of leukotrienes and potentiate the release of prostacyclin through up-regulating the expression of cytosolic phospholipase A2 and cyclooxygenase. Collectively, these biological functions of vitamin E may account for its protection against the development of atherosclerosis.” 6: Early Hum Dev 1994 Nov 18;39(3):177-88 Vitamin A and related essential nutrients in cord blood: relationships with anthropometric measurements at birth. Ghebremeskel K, Burns L, Burden TJ, Harbige L, Costeloe K, Powell JJ, Crawford M. Institute of Brain Chemistry and Human Nutrition, Queen Elizabeth Hospital for Children, London, UK. Following the advice given by the Department of Health to women who are, or may become pregnant, not to eat liver and liver products because of the risk of vitamin A toxicity, the concentrations of vitamins A and E, and copper, magnesium and zinc in cord blood were investigated. The study was conducted in Hackney, an inner city area of London. Esters of vitamin A were not detected in any of the samples, indicating that there was no biochemical evidence of a risk of toxicity. Indeed, vitamin A correlated significantly with birthweight, head circumference, length, and gestation period. There was also a significant positive relationship between zinc and birthweight. In contrast, copper showed a negative correlation with birthweight and head circumference. Vitamin E and magnesium were not associated with any of the anthropometric measurements, although magnesium showed an increasing trend with birthweight. The data suggest that most of the mothers of the subjects studied may have been marginal with respect to vitamins A and E and zinc. In those with low birthweight babies. a higher intake would have improved their nutritional status and possibly the outcome of their pregnancy. For these low-income mothers, liver and liver products are the cheapest and the best source of vitamins A and E, haem iron, B vitamins and several other essential nutrients; hence the advice of the Department of Health may have been misplaced. © Ray Peat 2006. All Rights Reserved. www.RayPeat.com </markdown> Edit:2021.08.25 <markdown> </markdown> 讨论列表 AKP讨论 查看原帖及回帖