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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The glutathione content of retinal Muller (glial) cells: effect of pathological conditions.
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The glutathione content of retinal Muller (glial) cells: effect of pathological conditions.

机译：视网膜穆勒（胶质）细胞的谷胱甘肽含量：病理条件的影响。

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Maintenance of isolated retinal Muller (glial) cells in glutamate-free solutions over 7 h causes a significant loss of their initial glutathione content; this loss is largely prevented by the blockade of glutamine synthesis using methionine sulfoximine (5 mM). Anoxia does not reduce the glutathione content of Muller cells when glucose (11 mM), glutamate and cystine (0.1 mM each) are present. In contrast, simulation of total ischemia (i.e., anoxia plus removal of glucose) decreases the glutathione levels dramatically, even in the presence of glutamate and cystine. Less severe effects are caused by high extracellular K+ (40 mM). Reactive oxygen species are generated in the retina under various conditions, such as anoxia, ischemia, and reperfusion. One of the crucial substances protecting the retina against reactive oxygen species is glutathione, a tripeptide constituted of glutamate, cysteine and glycine. It was recently shown that glutathione can be synthesized in retinal Muller glial cells and that glutamate is the rate-limiting substance. In this study, glutathione levels were determined in acutely isolated guinea-pig Muller cells using the glutathione-sensitive fluorescent dye monochlorobimane. The purpose was to find out how the glial glutathione content is affected by anoxia/ischemia and accompanying pathophysiological events such as depolarization of the cell membrane. Our results further strengthen the view that glutamate is rate-limiting for the glutathione synthesis in glial cells. During glutamate deficiency, as caused by e.g., impaired glutamate uptake, this amino acid is preferentially delivered to the glutamate-glutamine pathway, at the expense of glutathione. This mechanism may contribute to the finding that total ischemia (but not anoxia) causes a depletion of glial glutathione. In situ depletion may be accelerated by the ischemia-induced increase of extracellular K+, decreasing the driving force for glutamate uptake. The ischemia-induced lack of glutathione is particularly fatal considering the increased production of reactive oxygen species under this condition. Therefore the therapeutic application of exogenous free radical scavengers is greatly recommended.
机译：在无谷氨酸溶液中维持分离的视网膜Muller（神经胶质）细胞超过7小时，会导致其初始谷胱甘肽含量显着下降;使用甲硫氨酸亚砜亚胺（5 mM）阻止谷氨酰胺合成可大大防止这种损失。当存在葡萄糖（11 mM），谷氨酸和胱氨酸（每个0.1 mM）时，缺氧不会降低穆勒细胞的谷胱甘肽含量。相反，即使在存在谷氨酸和胱氨酸的情况下，模拟总缺血（即缺氧加葡萄糖去除）也可显着降低谷胱甘肽水平。较高的细胞外K +（40 mM）引起的影响较小。在各种条件下，例如缺氧，局部缺血和再灌注，在视网膜中产生活性氧。保护视网膜免受活性氧影响的关键物质之一是谷胱甘肽，它是由谷氨酸，半胱氨酸和甘氨酸组成的三肽。最近显示谷胱甘肽可以在视网膜Muller神经胶质细胞中合成，而谷氨酸是限速物质。在这项研究中，使用谷胱甘肽敏感的荧光染料一氯bimane确定了急性分离的豚鼠穆勒细胞中的谷胱甘肽水平。目的是找出神经胶质谷胱甘肽含量如何受到缺氧/缺血以及伴随的病理生理事件（例如细胞膜去极化）的影响。我们的结果进一步证实了谷氨酸对神经胶质细胞中谷胱甘肽合成的速率限制。在例如由谷氨酸摄取受损引起的谷氨酸缺乏期间，该氨基酸优先以谷胱甘肽为代价被递送至谷氨酸-谷氨酰胺途径。该机制可能有助于发现总缺血（但不是缺氧）导致神经胶质谷胱甘肽耗竭。缺血诱导的细胞外K +的增加可促进原位耗竭，从而降低谷氨酸摄取的驱动力。考虑到在这种条件下增加的活性氧的产生，缺血诱导的谷胱甘肽的缺乏特别致命。因此，强烈推荐外源性自由基清除剂的治疗应用。

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