, ,

2002/07 衰老的眼睛、婴儿的眼睛和易兴奋组织

Aging Eyes, Infant Eyes, and Excitable Tissues

“The attitude of great poets is to cheer up slaves and horrify despots”  Walt Whitman

The eyes and the lungs are sensitive tissues that are easily harmed by inappropriate environmental exposure. They are especially sensitive in infancy and old age. 眼睛和肺是敏感组织,很容易受到不适当环境暴露的伤害。他们在婴儿期和老年期特别敏感。

For 60 years there have been controversies about the cause of retinopathy of prematurity ,which has blinded tens of thousands of people.60年来,关于导致成千上万人失明的早产儿视网膜病变的病因一直存在争议。

Degeneration of the retina is the main cause of blindness in old people. Retinal injury is caused by ordinary light, when the eyes are sensitized by melatonin, prolactin, and polyunsaturated fats. Bright light isn't harmful to the retina, even when it is continuous, if the retina isn't sensitized.视网膜退化是老年人失明的主要原因。视网膜损伤是由普通光引起的,当眼睛被褪黑素、催乳素和多不饱和脂肪致敏时。如果视网膜没有敏化,即使是连续的强光也不会对视网膜有害。

Melatonin and prolactin are induced by stress, and darkness is a stress because it impairs mitochondrial energy production.褪黑素和催乳素是由应激引起的,而黑暗是一种应激,因为它会损害线粒体能量的产生。

The polyunsaturated fats which accumulate in the brain and ,retina damage mitochondria.积聚在大脑和视网膜中的多不饱和脂肪会损伤线粒体。

Iron, which accumulates prenatally, and then again with aging, reacts with unsaturated fats during stress to destroy cells.铁在出生前积累,然后随着年龄的增长,在压力下与不饱和脂肪反应破坏细胞。

The popular supplements melatonin, tryptophan, fish oils, St. John's wort, and the various omega-3 oils, all increase the risk of retinal light damage and macular degeneration. Serotonin uptake inhibiting antidepressants are suspected to be able to cause It.流行的补充物褪黑素、色氨酸、鱼油、圣约翰草和各种欧米茄-3油都会增加视网膜光损伤和黄斑变性的风险。5-羟色胺摄取抑制抗抑郁药被怀疑是导致这种疾病的原因。

Processes similar to those that damage the over-sensitized retina can occur in other cells, as a result of stress. The substances that sensitize the retina to light-damage, can also increase the incidence of new or metastatic cancers.由于压力,类似于损伤过度敏感视网膜的过程也可能发生在其他细胞中。使视网膜对光损伤敏感的物质也会增加新的或转移性癌症的发病率。

Iron supplements and the use of supplemental oxygen, especially with a vitamin E deficiency exacerbated by excessive unsaturated fats in the diet, are still commonly used exactly when they can do the most damage.铁补充剂和补充氧气的使用,尤其是在饮食中过量的不饱和脂肪加剧了维生素E缺乏的情况下,仍然被广泛使用,而这恰恰是它们能造成最大伤害的时候。

One of the recognized achievements of biology has been the demonstration of life's universality, in the sense that organisms of all sorts use the same fundamental genetic code, and that yeasts, lizards, apes, and people have remarkably similar cellular systems, as well as a great amount of genetic similarity.

生物学公认的成就之一是证明了生命的普遍性,即各种生物体使用相同的基本遗传密码,酵母、蜥蜴、猿和人类具有非常相似的细胞系统以及大量的遗传相似性。

There has been another, less well recognized, sort of convergence going on in physiology and pathophysiology. Hans Selye's concept of stress, “the syndrome of being sick,” Otto Warburg's argument that a “respiratory defect” was behind all kinds of cancer, and the idea of free radical damage as a common factor in disease and aging, helped to create a more general way of looking at the nature of disease that superceded medicine's theories of disease pathogens and genetic mutations, which created thousands of “disease entities,” none of which had much to do with the individuality of the patient or his environment.

在生理学和病理生理学方面,还有另一种不太为人所知的趋同。Hans Selye的压力概念,“生病的综合征”,Otto Warburg关于“呼吸缺陷”是各种癌症背后的论点,以及自由基损伤是疾病和衰老的共同因素的观点,有助于创造一种更普遍的看待疾病本质的方式,取代了医学关于疾病病原体和基因突变的理论,从而创造了数千种“疾病实体”,而这些实体都与患者的个性或环境没有太大关系。

The understanding that plants and animal's have much biochemistry in common has gradually changed the assumptions of the science establishment, which until recently insisted that only “ionizing radiation” could affect animals or other organisms that lacked chlorophyll—and insisted that ionizing rays acted only on the DNA. Visible light, the textbooks said, was not “chemically active,” and so couldn't possibly affect animals' cells. In animals, coloration was seen mainly as decoration and disguise, rather than as a functional part of their biochemistry.

植物和动物的生物化学有许多共同点,这一认识逐渐改变了科学机构的假设。直到最近,科学机构一直坚持只有“电离辐射”才能影响缺乏叶绿素的动物或其他生物,并坚持电离射线只作用于DNA。教科书上说,可见光没有“化学活性”,因此不可能影响动物的细胞。在动物身上,着色主要被视为装饰和伪装,而不是其生物化学的功能部分。

(Chemically, the meaning of “a pigment” is that it's a chemical which selectively absorbs radiation. Old observations such as Warburg's, that visible light can restore the activity of the “respiratory pigments,” showed without doubt that visible light is biochemically active. By the 1960s, several studies had been published showing the inhibition of respiratory enzymes by blue light, and their activation by red light. The problem to be explained is why the science culture simply couldn't accept crucial facts of that sort.)

(从化学角度来说,“色素”的含义是它是一种选择性吸收辐射的化学物质。Warburg等以前的观察结果表明,可见光可以恢复“呼吸色素”的活性毫无疑问,可见光具有生物化学活性。到20世纪60年代,已经发表了几项研究,表明蓝光抑制呼吸酶,红光激活呼吸酶。需要解释的问题是,为什么科学文化无法接受这类关键事实。)

The retina, of course, was allowed (in the views of mainline science) to respond to ordinary light, but the few people who studied the biological effects of seasonal or daily cycles of light have until recently stayed very close to the nerve pathways leading from the retina to the pineal gland, because those pathways could be described in terms of an evolutionarily specialized “third eye.” Even with a doctrine of a genetically specialized link between the retina and a little of the animal's physiological chemistry, the great, slowwitted science establishment has done its best to avoid thoughts of any deep interaction between an organism and its environment, by insisting that the organism runs according to a genetically determined “clock” which is located in a few cells in a certain area of the brain, and that nervous impulses from the retina have only the small privilege of “setting the clock.”

当然,视网膜(在主流科学的观点中)可以对普通光做出反应,但研究季节性或日常光循环的生物效应的少数人直到最近都非常接近从视网膜到松果体的神经通路,因为这些途径可以用进化上专门化的“第三只眼”来描述。即使有视网膜和动物生理化学之间基因专门化联系的学说,伟大的,懒散的科学机构尽最大努力避免思考生物体与其环境之间的任何深层次相互作用,坚持生物体按照基因决定的“时钟”运行,该“时钟”位于大脑特定区域的几个细胞中,而来自视网膜的神经冲动只有“设定时钟”的小特权

It didn't matter to the academic and medical worlds that a professor, Frank A. Brown, had long ago disproved the idea of an innate genetic “clock,” because philosophy is much stronger than evidence. Leibniz had said that everything in the world runs on its own inner clock, without needing to perceive its surroundings, and this idea that everything in the world is a “windowless monad” resonated through the world of science, because it justified the pompous authoritarian attitudes of the experts who knew that anything that wasn't already in their heads couldn't be considered knowledge. If an organism's “essence is contained in its genes,” then it clearly doesn't interact in any meaningful way with most of its environment. This is the sort of culture that imbued research on the biology of light cycles.

对于学术界和医学界来说,弗兰克·布朗教授很久以前就反驳了先天基因“时钟”的观点并不重要,因为哲学比证据更有力。莱布尼茨曾说过,世界上的一切都是在自己的内部时钟上运行的,而不需要感知周围的环境。这种认为世界上的一切都是“没有窗户的单子”的想法在科学界引起了共鸣,因为它证明了专家们浮夸的威权态度是正确的,他们知道任何不在他们头脑中的东西都不能被视为知识。如果一个有机体的“本质包含在其基因中”,那么它显然不会以任何有意义的方式与其大部分环境相互作用。这是一种渗透在光周期生物学研究中的文化。

When I moved from Mexico, first to Montana and then to Oregon in 1966, I became very conscious of how light affects the hormones and the health. (For example, in Montana I experienced an interesting springtime shedding of body hair.) Many people who came to cloudy Eugene to study, and who often lived in cheap basement apartments, would develop chronic health problems within a few months. Women who had been healthy when they arrived would often develop premenstrual syndrome or arthritis or colitis during their first winter in Eugene.

当我从墨西哥搬到蒙大拿州,然后在1966年搬到俄勒冈州时,我非常清楚光线是如何影响荷尔蒙和健康的。(例如,在蒙大拿州,我经历了一个有趣的春天,身上的毛发脱落。)许多来到多云尤金学习的人,通常住在廉价的地下室公寓里,会在几个月内患上慢性健康问题。抵达尤金的第一个冬天,那些健康的女性经常会出现经前综合症、关节炎或结肠炎。

The absence of bright light would create a progesterone deficiency, and would leave estrogen and prolactin unopposed. Beginning in 1966, I started calling the syndrome “winter sickness,” but over the next few years, because of the prominence of the premenstrual syndrome and fertility problems in these seasonally exacerbated disorders, I began calling it the pathology of estrogen dominance. In the endocrinology classes I taught at the National College of Naturopathic Medicine, I emphasized the importance of light, and suggested that medicine could be reorganized around these estrogen-related processes. If the sparrows of Times Square mated in the winter because of the bright lights, it seemed clear that bright artificial light would be helpful in regulating human hormones.

如果没有明亮的光线,会导致孕酮缺乏,进而导致雌激素和催乳素无法被阻挠。从1966年开始,我开始将该综合征称为“冬季疾病”,但在接下来的几年里,由于经前综合征和生育问题在这些季节性恶化的疾病中的突出,我开始将其称为雌激素优势的病理学。在我在国家自然疗法医学院教授的内分泌学课程中,我强调了光的重要性,并建议可以围绕这些雌激素相关过程重组医学。如果时代广场的麻雀因为明亮的灯光而在冬季交配,那么明亮的人造光显然有助于调节人体激素。

In our lab at the University of Oregon, our hamsters would try to hibernate, even though they were in temperature-controlled laboratories with regular cycles of artificial light. (The ceiling lights provided only dim illumination inside their cage boxes, so they were probably in a chronic state of light deprivation, which probably increased their sensitivity to the weak environmental cues that Frank Brown had investigated, possibly microwaves that easily penetrated the lab walls.) During the winter, when they were infertile, I found that their thymus glands practically disappeared. The mechanism seemed to include the increase of pineal gland activity (probably increasing melatonin synthesis) in the winter, under the intensified activity of the “sympathetic nervous system” (with increased activity of adrenalin and other catecholamines), and the melatonin was apparently a signal for suppressing fertility during the stressful winter. In some animals (Shvareva and Nevretdinova, 1989), estrogen is increased during hibernation, contributing to the reduction of body temperature.

在我们俄勒冈州大学的实验室里,我们的仓鼠会尝试冬眠,即使它们在有规律的人工光循环的温度控制实验室里。(天花板上的灯在笼子里只能提供微弱的照明,因此它们可能长期处于光照不足的状态,这可能增加了它们对弗兰克·布朗所调查的微弱环境线索的敏感性,可能是容易穿透实验室墙壁的微波。),当他们不育时,我发现他们的胸腺几乎消失了。其机制似乎包括在“交感神经系统”活动增强(肾上腺素和其他儿茶酚胺活动增强)的情况下,松果体活动在冬季增加(可能增加褪黑激素的合成),褪黑素显然是在紧张的冬季抑制生育能力的信号。在一些动物中(Shvareva和Nevrettinova,1989),雌激素在冬眠期间增加,有助于降低体温。

In 1994 A.V. Sirotkin found that melatonin inhibits progesterone production but stimulates estrogen production, and it's widely recognized that melatonin generally inhibits the thyroid hormones, creating an environment in which fertilization, implantation, and development of the embryo are not possible. This combination of high estrogen with low progesterone and low thyroid decreases the resistance of the organism, predisposing it to seizures and excitotoxic damage, and causing the thymus gland to atrophy.

1994年,A.V.Sirotkin发现褪黑素抑制孕酮的产生,但刺激雌激素的产生,人们普遍认为褪黑素通常会抑制甲状腺激素,从而创造一个无法受精、着床和胚胎发育的环境。这种高雌激素、低孕酮和低甲状腺的结合降低了机体的抵抗力,使其易于癫痫发作和兴奋性毒性损伤,并导致胸腺萎缩。

Cyclical exposure to melatonin can have an effect on the reproductive system opposite to that of chronic exposure, and the way exogenous melatonin is delivered to the animal can have unexpected effects on the actual amount of melatonin circulating in the blood (Wright and Alves, 2001). The actual amount of melatonin in the tissues, its relation to the normal cycling of the animal, and the influence of temperature, are often disregarded in melatonin research, making it hard to interpret many of the publications.

周期性接触褪黑素会对生殖系统产生与慢性接触相反的影响,外源性褪黑素传递给动物的方式会对血液中褪黑素的实际循环量产生意想不到的影响(Wright和Alves,2001)。在褪黑素研究中,组织中褪黑素的实际含量、其与动物正常循环的关系以及温度的影响常常被忽视,这使得许多出版物难以解释。

There is a lot of talk about melatonin's function as an antioxidant, but, like so many other “antioxidants,” melatonin can act as a pro-oxidant at physiologically relevant concentrations; some studies have found that it, like estrogen, increases the activity of the pro-oxidative free radical nitric oxide (which acts like melatonin on pigment cells, causing them to lighten). The promoters of estrogen are also making claims that estrogen is a protective antioxidant, though that isn't true of physiological concentrations of the estrogens, which can catalyze intense oxidations. The market culture seems to guide most research in these substances.

有很多关于褪黑素作为抗氧化剂的功能的讨论,但是,像许多其他“抗氧化剂”一样,褪黑素可以在生理相关浓度下作为促氧化剂;一些研究发现,它与雌激素一样,增加了促氧化自由基一氧化氮(其作用类似于褪黑素对色素细胞的作用,使色素细胞变亮)的活性。雌激素的促进者也声称雌激素是一种保护性抗氧化剂,尽管这对于能够催化强烈氧化的雌激素的生理浓度是不正确的。市场文化似乎指导了这些物质的大部分研究。

Almost any kind of stress increases the formation of melatonin. 几乎任何一种压力都会增加褪黑素的形成。

In some animals, melatonin has been shown to be responsible for whitening of the hair during the winter. In some species it acts directly on the pigment cells, but in other species it seems to inhibit the action of the melanocyte stimulating hormone.

在一些动物身上,褪黑素被证明在冬季对头发的漂白有作用。在某些物种中,它直接作用于色素细胞,但在其他物种中,它似乎抑制黑素细胞刺激激素的作用。

In snowy climates, it's “ecologically” rational for animals to turn white in the winter, for camouflage. But tadpoles also turn white in the dark, or under the influence of melatonin, and the biological meaning of that isn't so clear. It's possible that being white would reduce their loss of heat through radiation, but I think it is more likely that it relates to an increased ability of weak radiation to penetrate their tissues, rather than being stopped near the surface by the melanin in the skin. The absence of melanin makes them more sensitive to light. Bright light suppresses their melatonin, and makes them turn dark brown or black, and this protects them from bright sunlight.

在多雪的气候中,动物在冬天变白是为了伪装,这在“生态”上是合理的。但是蝌蚪在黑暗中或在褪黑素的影响下也会变白,其生物学意义尚不清楚。白色有可能会减少他们在辐射中的热量损失,但我认为这更可能与弱辐射穿透他们组织的能力增强有关,而不是被皮肤中的黑色素阻挡在表面附近。黑色素的缺乏使它们对光更敏感。强光会抑制它们的褪黑激素,使它们变成深棕色或黑色,这可以保护它们免受强光照射。

In the retina, melatonin increases the sensitivity of the cells to dim light. It, along with prolactin, another nocturnal hormone, helps to produce dark adaptation of the eyes.

在视网膜中,褪黑素增加了细胞对昏暗光线的敏感性。它与催乳素(另一种夜间激素)一起,有助于眼睛产生暗适应。

Melatonin increases the concentration of free fatty acids during the night (John, et al., 1983; John and George, 1976), so it's interesting that one of the long-chain highly unsaturated fatty acids, DHA (docosahexaenoic acid), also increases the light sensitivity of the retina.

褪黑素会增加夜间游离脂肪酸的浓度(John等人,1983年;John和George,1976年),因此有趣的是,一种长链高度不饱和脂肪酸DHA(二十二碳六烯酸)也会增加视网膜的感光度。

Melatonin lowers body temperature, causes vasoconstriction in the brain, heart, and other organs, and slows reactions. An antagonist to melatonin acts as an antidepressant, reducing “behavioral despair” resulting from stress. (Dubocovich, et al., 1990.) So, in the behavioral sense, melatonin reduces sensitivity, yet it increases the eyes' sensitivity to light, causing them to be injured by light that would otherwise be harmless.

褪黑素降低体温,引起大脑、心脏和其他器官的血管收缩,并减缓反应。褪黑素的拮抗剂起到抗抑郁剂的作用,减少由压力引起的“行为绝望”。(Dubocovich,et al.,1990)因此,在行为意义上,褪黑激素降低了敏感性,但它增加了眼睛对光的敏感性,导致眼睛受到光的伤害,而光本来是无害的。

Since a hibernating animal under the influence of melatonin can become very cold, the light-sensitizing function of melatonin is probably related to the biological need to be roused out of the torpor occasionally. (Hibernators apparently have to warm up occasionally to sleep in the ordinary manner.) Melatonin is said to intensify dreaming, which is part of the process of arousal from sleep.

由于受褪黑素影响的冬眠动物可能会变得非常寒冷,褪黑素的光敏功能可能与偶尔从麻木中唤醒的生物需要有关。(冬眠者显然必须偶尔热身才能以正常的方式入睡。)据说褪黑激素能强化做梦,这是睡眠唤醒过程的一部分。

All of the stress-related hormones increase during the night. One of the ways these hormones of darkness act is to increase the sensitivity to light, in a process that is an important adaptation for organisms in dim light. In the night, our ability to see (and respond to) dim light is increased. But dark-adapted eyes are very sensitive to injury by bright light. Light that ordinarily wouldn't harm the eyes, will do serious damage when the eyes are dark adapted.

所有与压力相关的荷尔蒙在夜间都会增加。这些黑暗激素的作用方式之一是增加对光的敏感性,这是生物体在昏暗光线下的重要适应过程。在夜间,我们看到(和响应)昏暗光线的能力增强。但适应黑暗环境的眼睛对强光的伤害非常敏感。通常不会伤害眼睛的光线,在眼睛适应黑暗时会造成严重伤害。

In thinking about the effects of stress and oxygen deprivation, I read the studies demonstrating that the formation of the oxygen-wasting age pigment, lipofuscin, is increased by estrogen, by oxygen deprivation (in carp living below the ice, or even in fetuses), by metals such as iron, by x-rays, and by highly unsaturated fats.

在思考压力和缺氧的影响时,我阅读了研究表明,雌激素、缺氧(生活在冰下的鲤鱼,甚至胎儿)、铁等金属、x射线和高度不饱和脂肪都会增加耗氧衰老色素脂褐素的形成。

Free fatty acids that are mobilized from storage tissues in the night and in the winter also tend to increase with aging, as the ability to tolerate stress decreases. Poor circulation and lipofuscin tend to be associated, in a vicious cycle. This means that the retina becomes easier to injure by light in old age, for some of the same reasons that the infant's retina is susceptible.

夜间和冬季从储存组织中动员的游离脂肪酸也会随着年龄的增长而增加,因为承受压力的能力会降低。血液循环不良和脂褐素倾向于在恶性循环中相互关联。这意味着老年时视网膜更容易受到光损伤,原因与婴儿视网膜易受伤害的原因相同。

The fetus accumulates' a very large amount of iron, and it absorbs melatonin from the maternal circulation. Prolactin is sometimes elevated in the newborn. Premature babies are often given extra oxygen, which tends to cause vasoconstriction by displacing carbon dioxide. Melatonin's ability to cause vasoconstriction means that stress makes supplemental oxygen more toxic. Synthetic glucocorticoids are often given to premature babies, adding to the risk of retinal damage.

胎儿积累了非常多的铁,并从母体循环中吸收褪黑激素。新生儿的催乳素有时会升高。早产儿经常被给予额外的氧气,这往往会通过置换二氧化碳而引起血管收缩。褪黑激素引起血管收缩的能力意味着压力使补充的氧气更具毒性。人工合成的糖皮质激素经常被给予早产儿,增加了视网膜损伤的风险。

When the mother has been given iron supplements during pregnancy, along with unsaturated oils in the diet, the baby is likely to be born with a vitamin E deficiency and suppressed thyroid function, increasing the probability that it will be jaundiced, leading to treatment of the jaundice with exposure to very bright light.

当母亲在怀孕期间服用了铁质补充剂,同时在饮食中加入不饱和油,婴儿出生时很可能缺乏维生素E和抑制甲状腺功能,增加了出现黄疸的概率,导致用暴露在非常明亮的光线下治疗黄疸的情况。

Although Yandell Henderson had already, in 1928, explained the need for carbon dioxide to be used with oxygen for resuscitating infants or adults, medical researchers and hospital workers could never accept the idea, probably because of a fundamental misunderstanding of the Henderson-Hasselbalch equation. Animal experiments show that supplemental oxygen, without carbon dioxide, causes vasoconstriction, reducing the tissues' supply of glucose as well as oxygen. In combination with too much light, especially blue light, it damages the retina. At hyperbaric pressure, oxygen causes seizures, as well as damage to the lungs and other tissues.

尽管Yandell Henderson在1928年已经解释了二氧化碳需要和氧气一起用于复苏婴儿或成人,但医学研究人员和医院工作人员始终无法接受这个想法,可能是因为对Henderson-Hasselbalch方程的根本误解。动物实验表明,在没有二氧化碳的情况下,补充氧气会导致血管收缩,减少组织的葡萄糖以及氧气的供应。与太多的光,特别是蓝光结合在一起,会损害视网膜。在高压下,氧气会导致癫痫发作,以及对肺部和其他组织的损害。

The contribution of bright light to retinal damage in babies has been denied in several recent publications, and these articles undoubtedly provide useful material for defense lawyers to use when hospitals are sued for causing blindness. One publication based on experiments with kittens concludes that bright light does not harm the newborn's retina, but the comparison is between continuous light and intermittent light, rather than between bright light and dim light. Twelve hours of total darkness, rather than sparing the eye by reducing its exposure to light, would sensitize the eye. The only reason such appalling things can be published is that their conclusions protect the hospitals.

在最近的一些出版物中,强光对婴儿视网膜损伤的作用被否认,这些文章无疑为辩护律师在医院因致盲而被起诉时提供了有用的材料。一份基于小猫实验的出版物得出结论,明亮的光线不会伤害新生儿的视网膜,但比较的是连续光线和间歇光线,而不是明亮光线和暗淡光线。12小时的完全黑暗,而不是通过减少眼睛暴露在光线下来保护眼睛,会使眼睛敏感。这些骇人听闻的事情能够公布的唯一原因是他们的结论保护了医院。

A few good studies of the effect of bright light on the retina, and the fact that dark-skinned people with more protective pigment in their eyes have a lower incidence of retinopathy of prematurity, make it clear that the ordinary laws of physics and chemistry actually do apply to the infant eye.

关于强光对视网膜影响的一些好的研究,以及眼睛中含有更多保护性色素的深色皮肤的人早产视网膜病变的发病率较低的事实,表明普通的物理和化学定律实际上适用于婴儿的眼睛。

Light and stress, especially with excess iron, damage the retina when the cells contain too much PUFA, since these fats react with light and free radicals. The nocturnal/stress hormones, especially prolactin and melatonin, make the retina more sensitive to light, and more easily damaged. (It's too much darkness that sets up the problem, since the eyes will adapt to excess light, but darkness increases their sensitivity.)

光线和压力,特别是过量的铁,当细胞含有过多的多不饱和脂肪酸时,会损害视网膜,因为这些脂肪会与光线和自由基发生反应。夜间活动/应激激素,特别是催乳素和褪黑素,使视网膜对光更敏感,更容易受损。(太多的黑暗会造成问题,因为眼睛会适应过多的光线,但黑暗会增加他们的敏感性。)

The use of lasers to operate on eyes produces intense inflammation of the eye, but even at low dose the diffusing light causes retinal/macular damage.

使用激光对眼睛进行手术会产生强烈的眼部炎症,但即使在低剂量下,漫射光也会导致视网膜/黄斑损伤。

Cytochrome oxidase is one of the enzymes damaged by stress and by blue light, and activated or restored by red light, thyroid, and progesterone. It's a copper enzyme, so it's likely to be damaged by excess iron. It is most active when it is associated with a mitochondrial lipid, cardiolipin, that contains saturated palmitic acid; the substitution of polyunsaturated fats lowers its activity. Mitochondrial function in general is poisoned by the unsaturated fats, especially arachidonic acid and DHA.

细胞色素氧化酶是一种被应激和蓝光破坏的酶,被红光、甲状腺和孕酮激活或恢复。它是一种铜酶,所以它很可能被过量的铁所破坏。当它与含有饱和棕榈酸的线粒体脂质心磷脂结合时,它最为活跃;多不饱和脂肪的替代降低了它的活性。不饱和脂肪酸,特别是花生四烯酸和DHA,通常会损害线粒体的功能。

Creating a “deficiency” of DHA, even when an oil of known toxicity is used to replace the omega-3 oils, prevents retinal damage from light. Despite evidence of this sort, Mead Johnson is going ahead with the marketing of its baby formula containing added DHA which is industrially extracted from algae. (Although the researchers who claim that DHA is beneficial haven't answered my letters, a representative of the company that manufactures it did answer my question about the actual composition of the oil, and acknowledged that they don't have any idea what the minor ingredients might be.)

造成DHA的“缺乏”,即使使用具有已知毒性的油来替代欧米茄-3油,也可以防止光对视网膜的损害。尽管有这方面的证据,美赞臣仍在继续销售其添加DHA的婴儿配方奶粉,DHA是从海藻中工业提取的。(尽管声称DHA有益的研究人员没有回答我的信,但生产DHA的公司的一位代表确实回答了我关于油的实际成分的问题,并承认他们不知道其中的次要成分可能是什么。)

When animals are made “deficient” in all the exogenous polyunsaturated fatty acids, linoleic and arachidonic acid as well as linolenic and DHA, they become remarkably resistant to all sorts of stress and toxins.

当动物缺乏所有的外源性多不饱和脂肪酸、亚油酸和花生四烯酸以及亚麻酸和DHA时,它们就会对各种压力和毒素产生显著的抵抗力。

The polyunsaturated fats make the lungs more sensitive to excess oxygen or hyperventilation, they make the eyes more sensitive to light, and they make the brain more sensitive to fatigue.

多不饱和脂肪使肺部对过量氧气或过度通气更敏感,使眼睛对光线更敏感,使大脑对疲劳更敏感。

The use of synthetic glucocorticoid hormone is standard in treating very premature babies, although it is known to contribute to eye damage. This is because it is considered necessary to improve the lung function of premature babies with respiratory distress. But there is no clear evidence that it is beneficial for lung function in the long run, and very clear evidence that it damages the brain and other organs. There is widespread agreement regarding the use of the glucocorticoids prenatally to accelerate lung development in women who seem likely to deliver prematurely. Natural cortisol is a factor that promotes lung development prenatally. But cortisol is also a signal produced by a stressed fetus, that triggers the birth process. Cortisol, or the synthetic glucocorticoid, inhibits progesterone production, and stimulates estrogen production, activating uterine contractions and other processes that terminate the pregnancy.

使用合成糖皮质激素是治疗非常早产婴儿的标准方法,尽管已知会导致眼睛损伤。这是因为有必要改善患有呼吸窘迫的早产儿的肺功能。但是没有明确的证据表明从长远来看它对肺功能有益,也没有非常明确的证据表明它会损害大脑和其他器官。关于产前使用糖皮质激素加速早产妇女肺部发育的问题,已经达成广泛共识。天然皮质醇是一种促进胎儿肺发育的因子。但是皮质醇也是一种由压力过大的胎儿产生的信号,它会触发分娩过程。皮质醇,或合成糖皮质激素,抑制孕酮的产生,刺激雌激素的产生,激活子宫收缩和其他终止妊娠的过程。

Apparently, it doesn't occur to many people that administering the glucocorticoid triggers premature birth, creating the problem they are intending to treat.

显然,许多人没有想到服用糖皮质激素会引发早产,从而产生他们想要治疗的问题。

Recognizing causal connections between premature birth and respiratory distress and retinopathy of prematurity, it would be obvious that the greatest effort should be made to prevent the problems by improving the health of pregnant women. Hospitals, however, are invested in high technology systems for treating these problems, and even though their results are dismal, they can't make money by getting pregnant women to eat enough protein to prevent preeclampsia, which is a major cause of premature birth, or by treating the problems with salt, magnesium, progesterone, thyroid, and aspirin when the women haven't had a good diet.

认识到早产与呼吸窘迫和早产儿视网膜病变之间的因果关系,显然应尽最大努力通过改善孕妇健康来预防这些问题。然而,医院投资于治疗这些问题的高科技系统,尽管其结果令人沮丧,但他们无法通过让孕妇摄入足够的蛋白质来预防先兆子痫(早产的主要原因),当女性没有良好饮食时可以通过盐、镁、黄体酮、甲状腺、阿司匹林来解决问题。

Historically, preeclampsia has been blamed on the mother's or fetus's' “bad genes,” and that cultural bias was the setting in which these high technology prenatal and neonatal systems developed. High technology “neonatology” derives from the same ideology that motivated Josef Mengele's genetic research in Auschwitz. The idea of genetic determination is still motivating resistance to reasonable preventive approaches.

从历史上看,先兆子痫被归咎于母亲或胎儿的“坏基因”,而这种文化偏见是这些高科技产前和新生儿系统发展的背景。高科技“新生儿学”源自于推动约瑟夫·门格尔在奥斯威辛进行基因研究的同一种意识形态。基因决定的想法仍在激发对合理预防方法的抵制。

Thyroid, i.e., T3, is very effective in accelerating lung development in the fetus, and it doesn't have any of the harmful effects of the synthetic glucocorticoids. It normalizes the hormones, increasing progesterone and decreasing estrogen, which are needed for full-term gestation, the opposite of the glucocorticoids' effects. While the cortisol-like drugs damage the brain and other organs, thyroid and progesterone protect them.

甲状腺,即T3,在加速胎儿肺发育方面非常有效,并且它没有任何合成糖皮质激素的有害影响。它使足月妊娠所需的激素正常化,增加孕酮和减少雌激素,与糖皮质激素的作用相反。当皮质醇类药物损害大脑和其他器官时,甲状腺和黄体酮保护它们。

*Old organisms, like newborns, are easily injured by all sorts of inappropriate excitation. As in premature babies, the aged eyes, lungs, and brain are especially sensitive to damage by stress. But all organs are subject to the same kinds of damage. *Medical treatments for respiratory distress and macular degeneration in old people are often the same as those used so inappropriately for babies. The good health practices that can prevent the inflammatory and degenerative diseases can often make it possible for damaged tissues to recover, even in old age.

*像新生儿这样的老生物体很容易受到各种不适当的刺激的伤害。与早产儿一样,老年人的眼睛、肺和大脑对压力的损害特别敏感。*但是所有的器官都会受到同样的伤害。老年人呼吸窘迫和黄斑变性的医疗方法通常与婴儿不适当使用的方法相同。预防炎症和退行性疾病的良好健康实践通常可以使受损组织恢复,甚至在老年。

The pituitary hormones, especially prolactin and TSH, are pro-inflammatory, and darkness increases TSH along with prolactin, so to compensate for a light deficiency, the pituitary should be well-suppressed by adequate thyroid. Armour thyroid or Thyrolar or Cynoplus, Cytomel, would probably be helpful. (Eye-drops containing T3 might be a way to restore metabolic activity more quickly.) Limiting water intake (or using salt generously) helps to inhibit prolactin secretion. The saturated fats protect against the body's stored PUFA, and keeping the blood sugar up keeps the stored fats from being mobilized. Aspirin (or indomethacin) is generally protective to the retina, analogously to its protection against sunburn. Adequate vitamin E is extremely important. There are several prescription drugs that protect against serotonin excess, but thyroid and gelatin (or glycine, as in magnesium glycinate) are protective against the serotonin and melatonin toxicities. Copper and magnesium deficiencies predispose to retinal damage. Red light is protective, blue light (or u.v.) is harmful, so wearing orange lenses would be helpful. Progesterone and pregnenolone, by reducing the stress reactions, should be helpful–in the eye diseases of infancy and old age, as they are in the respiratory distress syndromes.

垂体激素,特别是催乳素和TSH,具有促炎症作用,黑暗会增加TSH和催乳素,因此,为了补偿光线不足,应通过适当的甲状腺充分抑制垂体。甲状腺炎、甲状腺炎或小天鹅、细胞分裂素可能会有所帮助。(含有T3的滴眼液可能是更快恢复代谢活动的一种方法。)限制水的摄入(或大量使用盐)有助于抑制催乳素的分泌。饱和脂肪可以防止身体储存的PUFA,保持血糖水平可以防止储存的脂肪被调动。阿司匹林(或吲哚美辛)通常对视网膜有保护作用,类似于它对晒伤的保护作用。充足的维生素E是极其重要的。有几种处方药可以防止血清素过量,但甲状腺和明胶(或甘氨酸,如甘氨酸镁)可以防止血清素和褪黑素的毒性。铜和镁缺乏易导致视网膜损伤。红光是保护性的,蓝光(或紫外线)是有害的,所以戴橙色镜片会有帮助。孕酮和孕烯醇酮,通过减少应激反应,应该对婴儿和老年的眼病有帮助,因为它们是在呼吸窘迫综合征中。


REFERENCES

Eksp Klin Farmakol 1999 Mar-Apr; 62(2):58-60. **Melatonin lowers the threshold of light sensitivity of the human retina**] ; Arushanian EB, Ovanesov KB. Department of Pharmacology, Stavropol State Medical Academy, Russia. After chronic use of melatonin (3 mg before night-time for 14 days) campimetry showed a significant decrease of the threshold of brilliance sensitiveness of the retina in the absence of authentic changes of the sensorimotor response latency in individuals of the older age group. A connection between the eye light sensitivity and the direct effect of the hormone on the photoreceptors is suggested.

Cochrane Database Syst Rev 2001;4:CDOOI077. **Restricted versus liberal oxygen exposure for preventing morbidity and mortality in preterm or low birth weight infants** (Cochrane Review).  Askie LM, Henderson-Smart DJ.

Prog Clin Bioi Res 1989;312:95-112. **The metabolism of omega-3 polyunsaturated fatty acids in the eye: the possible role of docosahexaenoic acid and docosanoids in retinal physiology and ocular pathology**. Bazan NG.

Biull Eksp BioI Med 1976 Oct;82(10):1181-3. **Role of the biological activity of serotonin in the production of the "shock lung" syndrome.**] ; Bazarevich GI, Deviataev AM, Likhtenshtein AO, Natsvlishvili BP, Sadeko MK.

Invest Ophthalmol Vis Sci 1993 Sep;34(10):2878-80. **An elevated hematogenous photosensitizer in the preterm neonate.** Bynoe LA, Gottsch JD, Sadda SR, Panton RW, Haller EM, Gleason CA.

Eur 1 Endocrinol 1995 Dec;133(6):691-5. **Melatonin enhances cortisol levels in aged but not young women.** Cagnacci A, Soldani R, Yen SS

Am 1 Psychiatry 1976 Oct; 133(10): 1181-6. [Negative effects of melatonin' on depression.]( Negative effects of melatonin' on depression. ) Carman lS, Post RM, Buswell R, Goodwin FK. In order to test the efficacy of the pineal neurohumor melatonin on depression, the hormone was administered in varying doses to six moderately to severely depressed patients and two patients with Huntington's chorea in double-blind crossover study. Melatonin exacerbated symptoms of dysphoria in these patients, as well as causing a loss of sleep and weight and a drop in oral temperature. Melatonin increased cerebrospinal fluid 5-hydroxyindoleacetic acid and calcium in three of four patients studied. The authors discuss the implications of this finding.

Neuro endocrinol Lett 2001 Dec;22(6):432-4.** Melatonin shortens the survival rate of Ehrlich ascites-inoculated mice.**

J Neurochem 1988 Apr;50(4):1185-93. **Induction of intra cellular superoxide radical formation by arachidonic acid and by polyunsaturated fatty acids in primary astrocytic cultures**. Chan PH, Chen SF, Yu AC.

Graefes Arch Clin Exp Ophthalmol 1993 lul;23 1(7):416-23. **Inhibition of cytochrome oxidase and blue-light damage in rat retina.** Chen E. St. Erik's Eye Hospital, Karolinska Institute, Stockholm, Sweden. The activity of cytochrome oxidase, outer nuclear layer thickness, and edema were quantitatively evaluated in the blue-light exposed rat retina.

Acta Ophthalmol Suppl 1993;(208):1-50. **Inhibition of enzymes by short-wave optical radiation and its effect on the retina**. Chen E. Eye Laboratory, St. Erik's Eye Hospital, Stock holm, Sweden. “Exposure to short-wave optical radiation is a potential hazard for vision. In the present study, blue-light damage is studied in rat retina.” “Blue light inhibited cytochrome oxidase at a retinal dose of about 110 kJ/m2. This inhibition was reversible, and is probably related to the light regulation of retinal metabolism. At a retinal dose of about 380 kllm2, the inhibition of cytochrome oxidase was followed consecutively by a probable redistribution of chlorine and potassium in the inner and outer segments, damage to the mitochondria in the inner segments, edema in the inner and outer segments, and progressive degeneration of photoreceptor cells. Dark adaptation did not increase the blue-light retinal injury. These findings support the hypothesis that inhibition of cytochrome oxidase is one of the causes of blue-light retinal damage.

Aust NZ1 Ophthalmol 1997 May;25 Suppl I:S73-5. **Retinal control of scleral precursor synthesis**. Devadas M,Morgan

Eur 1 Pharmacol 1990 lui 3;182(2):313-25. **Antidepressant-like activity of the melatonin receptor antagonist, luzindole (N-0774), in the mouse behavioral despair test. **Dubocovich ML, Mogilnicka E, Areso PM.

J Pharmacol Exp Ther 1988 Sep;246(3):902-10. [Luzindole (N-0774): a novel melatonin receptor antagonist](Luzindole (N-0774): a novel melatonin receptor antagonist). Dubocovich ML.

Exp Eye Res 1985 Oct;41(4):497-507. [The diurnal susceptibility of rat retinal photoreceptors to light-induced damage](The diurnal susceptibility of rat retinal photoreceptors to light-induced damage).

Nature 1983 Dec 22-1984 Jan 4;306(5945):782-4. Melatonin is a potent modulator of dopamine release in the retina. Dubocovich ML.

Semin Perinatol 2000 Aug;24(4):291-8. Environmental light and the preterm infant.

Pediatrics 1992 Apr;89(4 Pt 1):648-53. Light and retinopathy of prematurity: does retinal location offer a clue?

N Engl J Med 1985 Aug 15;313(7):401-4. Effect of bright light in the hospital nursery on the incidence of retinopathy of prematurity. Glass P, Avery GB, Subramanian KN, Keys MP, Sostek AM, Friendly OS.

Doc Ophthalmol 1990 Mar;74(3):195-203. Light and the developing retina. Glass P. George Washington University School of Medicine & Health Sciences, Washington, DC. “Retinopathy of prematurity (ROP) has increased in the United States in the past decade.”

Pediatr Res 1987 Oct;22(4):414-6. Calcemic responses to photic and pharmacologic manipulation of serum melatonin. Hakanson DO, Penny R, Bergstrom WH.

Pediatr Res 1990 Jun;27(6):571-3. Pineal and adrenal effects on calcium homeostasis in the rat. Hakanson DO, Bergstrom WH.

Science 1981 Nov 13;214(4522):807-9. Phototherapyinduced hypocalcemia in newborn rats: prevention by melatonin. Hakanson DO, Bergstrom WH.

Doc Ophthalmol 1992;79(2):141-50. Diurnal variations in the electroretinographic c-wave and retinal melatonin content in rats with inherited retinal dystrophy. Hawlina M, Jenkins HG, IkedaH.

J.A.M.A. 90:353 (Feb. 25) 1928. The Prevention and Treatment of Asphyxia in the New-Born, Henderson, Yandell.

Neuroendocrinology 2001 Feb;73(2):111-22. Estrogen modulates alpha(I)/beta-adrenoceptor- induced signaling and melatonin production in female rat pinealocytes. HemandezDiaz FJ, Sanchez JJ, Abreu P, Lopez-Coviella I, Tabares L, Prieto L, Alonso R.

J Neurosci Res 1989 Oct;24(2):247-50. Brain mitochondrial swelling induced by arachidonic acid and other long chain free fatty acids. Hillered L, Chan PH.

J Neurosci Res 1988;19(1):94-100. Effects of arachidonic acid on respiratory activities in isolated brain mitochondria. Hillered L, Chan PH.

J Neurosci Res 1988 Aug;20(4):451-6. Role of arachidonic acid and other free fatty acids in mitochondrial dysfunction in brain ischemia. Hillered L, Chan PH.

J Neurosci Res 1989 Oct;24(2):247-50. Brain mitochondrial swelling induced by arachidonic acid and other long chain free fatty acids. Hillered L, Chan PH.

J Clin Epidemiol 1992 Nov;45(11):1265-87. Oxygen as a cause of blindness in premature infants: “autopsy” of a decade of errors in clinical epidemiologic research.

Curr Eye Res 2001 Jul;23(1):11-9. Rod outer segments mediate mitochondrial DNA damage and apoptosis in human retinal pigment epithelium. Jin GF, Hurst JS, Godley BF.

Endocrinol Exp 1976 Jun;10(2):131-7. Diurnal variation in the effect of melatonin on plasma and muscle free fatty acid levels in the pigeon.

Arch Int Physiol Biochim 1983 Jul;91(2): 115-20. Diurnal impact of locomotory activity and melatonin and N-acetylserotonin treatment on blood metabolite levels in the rainbow trout.

J Neural Transm 1977;40(2):87-97. The adrenal medulla may mediate the increase in pineal melatonin synthesis induced by stress, but not that caused by exposure to darkness. Lynch HJ, Ho M, Wurtman RJ.

Bull Acad Natl Med 2000;184(2):415-28; discussion 428-30.[Pulmonary toxicity of oxygen] [Article in French] Mantz lM, Stoeckel ME.

Br J Pharmacol 1977 Dec;61(4):607-14. The action of melatonin on single amphibian pigment cells in tissue culture. Messenger EA, Warner AE.

Oftalmol Zh 1989;(8):469-73. [The early diagnosis, evaluation of treatment results and modelling of certain aspects of the pathogenesis of retinal dystrophy] ;

J Clin Endocrinol Metab 1977 Oct;45(4):768-74. The effects of oral melatonin on skin color and on the release of pituitary hormones.

Invest Ophthalmol 1976 Oct; 15(1 0):869-72. Hormonal influences on photoreceptor damage: the pituitary gland and ovaries.

Invest Ophthalmol Vis Sci 1996 Oct;37(11):2243-57. Retinal light damage in rats with altered levels of rod outer segment docosahexaenoate. Organisciak DT, Darrow RM, Jiang YL, Blanks JC.

Exp Neurol 1970 May;27(2):194-205. Retinal and optic nerve serotonin and retinal degeneration as influenced by photoperiod. G'Steen WK.

Invest Ophthalmol Vis Sci 1982 Jan;22(1):1-7. Antagonistic effects of adrenalectomy and ether/surgical stress on light-induced photoreceptor damage.

Brain Res 1990 Nov 26;534(1-2):99-105. Water deprivation protects photoreceptors against light damage.

Brain Res 1985 Oct 7;344(2):231-9. Neuronal damage in the rat retina after chronic stress.

Invest Ophthalmol Vis Sci 1977 Oct;I6(10):940-6. Effects of hypophysectomy, pituitary gland homogenates and trans plants, and prolactin on photoreceptor destruction. O'Steen WK, Kraeer SL.

Life Sci 1985 Nov 4;37(18): 1743-6. Stress-induced synthesis of melatonin: possible involvement of the endogenous monoamine oxidase inhibitor (tribulin). Oxenkrug GF, Mcintyre 1M.

Mech Ageing Dev 2000 Jan 10;112(3):169-83. Double bond content of phospholipids and lipid peroxidation negatively correlate with maximum longevity in the heart of mammals. Pamplona R, Portero-Otin M, Ruiz C, Gredilla R, Herrero A, Barja G.

Prostaglandins Leukot Essent Fatty Acids 200 I Feb;64(2):75-80. Comparative studies on lipid peroxidation of microsomes and mitochondria obtained from different rat tissues: effect of retinyl palmitate. Piergiacomi VA, Palacios A, Catala A.

Curr Eye Res 1992 Oct; 11(10):939-53. Oxygen-induced retinopathy in the rat: hemorrhages and dysplasias may lead to retinal detachment. Penn JS, Tolman BL, Lowery LA, Koutz CA.

Vision Res 1995 May;35(9):1247-64. Studies on the role of the retinal dopamine/melatonin system in experimental refractive errors in chickens. Schaeffel F, Bartmann M, Hagel G. Zrenner E.

Exp Clin Endocrinol Diabetes 1997;105(2): 109-12.Melatonin and serotonin regulate the release of insulin-like growth factor-I, oxytocin and progesterone by cultured human granulosa cells. Schaeffer HJ, Sirotkin AV.

Zh Evol Biokhim Fiziol 1989 Jan-Feb;25(l):52-9. [Seasonal characteristics of the functioning of the hypophysis-gonad system in the suslik Citellus parryi] Shvareva NV, Nevretdinova ZG. “In females, FSH was found in the blood in October, being absent from November to January; beginning from February, it may be found both in sleeping and active animals.” “Estradiol secretion was noted in hibernating females, whereas progesterone was found in the blood only in May.”

J Pineal Res 1985;2(1):39-49. Melatonin and N-acetylserotonin stress responses: effects of type ofstimulation and housing conditions. Seggie J, Campbell L, Brown GM, Grota LJ.

Acta Ophthalmol Scand 2001 Aug;79(4):428-30. Presumed sertraline maculopathy. Sener EC, Kiratli H.

Paediatr Perinat Epidemiol 1999 Apr; 13(2):128-30. Effects of premature exposure to light: a credibility struggle. Silverman WA.

J Pineal Res 1994 Oct; 17(3): i 12-7. Direct influence of melatonin on steroid, nonapeptide hormones, and cyclic nucleotide secretion by granulosa cells isolated from porcine ovaries. Sirotkin AV. “It was found that melatonin is able to inhibit progesterone and stinluiatc estradiol H111e PiCS'-:llt observations suggest a direct effect of melatonin on the steroid, nonapeptide hormone, and cyclic nucleotide release from porcine ovarian cells.”

J Pineal Res 1994 Oct;17(3):112-7. Direct influence of melatonin on steroid, nonapeptide hormones, and cyclic nucleotide secretion by granulosa cells isolated from porcine ovaries.Sirotkin AV.

Prog Clin Bioi Res 1989;312:229-49. Inbibitors of the arachidonic acid cascade in the management of ocular inflammation. Srinivasan BD, Kulkarni PS.

J Nutr 2000 Dec;130(12):3028-33. Polyunsaturated (n-3) fatty acids susceptible to peroxidation are increased in plasma and tissue lipids of rats fed docosahexaenoic acid-containing oils. Song JH, Fujimoto K, Miyazawa T. “Thus, high incorporation of (n-3) fatty acids (mainly DHA) into plasma and tissue lipids due to DHA-containing oil ingestion may undesirably affect tissues by enhancing susceptibility of membranes to lipid peroxidation and by disrupting the antioxidant system.”

Acta Ophthalmol (Copenh) 1992 Feb;70(1):115-22. Effects of steady electric fields on human retinal pigment epithelial cell orientation and migration in culture. Sulik GL, Soong HK, Chang PC, Parkinson WC, Elner SG, Elner VM

Ned Tijdschr Geneeskd 2001 Dec 29; 145(52):2521-5.[Administration of glucocorticosteroids to premature infants: increasing evidence of adverse effects] [Article in Dutch] van Bel F. “Neonatal glucocorticosteroid therapy is increasingly being used for the prevention of chronic lung disease in very premature infants. In the short term this therapy is usually successful. There is, however, increasing evidence for long-term adverse effects. In particular there seems to be an increased chance of abnormal brain development, which later results in locomotory dysfunction, developmental delay and cerebral palsy.”

Brain Res 1984 Feb 27;294( I): 166-8. Pineal methoxyindoles depress calcium uptake by rat brain synaptosomes. Vacas Ml, Keller Sarmiento MI, Cardinali DP.

Ann N Y Acad Sci 1994 Nov 17;738:408-18. Serotonin bmding proteins: an in vitro model system for monoamine. related neurotoxicity. Vauquelin G, Del Rio MJ, Pardo CV.

J Hypertens Suppl 1985 Dec;3 Suppl 3:SI07-9. Seasonal variation in the development of stress-induced systolic hypertension in the rat.

Invest Ophthalmol Vis Sci 1992 May;33(6): 1894-902.Melatonin increases photoreceptor susceptibility to lightinduced damage. Wiechmann AF, O'Steen WK. “Pinealectomy has been shown to protect photoreceptors from light-induced damage, and melatonin treatment has been reported to increase the degree of photoreceptor damage in albino rats.”

J Neurochem 1986 Oct;47(4):1181-9. Effects of arachidonic acid on glutamate and gamma-aminobutyric acid uptake in primary cultures of rat cerebral cortical astrocytes and neurons. Yu AC, Chan PH, Fishman RA.

讨论列表 查看原帖及回帖