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眼部的超氧化物歧化酶:超氧化物歧化酶和过氧化氢酶在保护晶状体免受氧化损伤方面的相对功能。

Superoxide dismutase of the eye: relative functions of superoxide dismutase and catalase in protecting the ocular lens from oxidative damage.

作者信息

Bhuyan K C, Bhuyan D K

出版信息

Biochim Biophys Acta. 1978 Aug 3;542(1):28-38. doi: 10.1016/0304-4165(78)90229-5.

Abstract
  1. Activities of superoxide dismutase (superoxide: superoxide oxidoreductase, EC 1.15.1.1) have been estimated in eye tissues. In rabbit eye, superoxide dismutase is present in corneal epithelium, corneal endothelium, lens, iris, ciliary body and retina. In lens the activity is in capsule epithelium. 2. Copper chelator diethyldithiocarbamate inhibited lens superoxide dismutase in vitro and in vivo in rabbit. 3. H2O2 caused inhibition of superoxide dismutase activity of lens extract, and this inhibition was potentiated by the catalase inhibitor 3-amino-1H-1,2,4-triazole (3-aminotriazole) or NaN3. 3-Aminotriazole or NaN3 had no effect on lens superoxide dismutase. Thus endogenous catalase of lens affords protection to the lens superoxide dismutase from inactivation by H2O2. 4. In rabbit having early cataract (vacuolar stage) induced by feeding-3-aminotriazole, there was a decrease in superoxide dismutase of lens, a fall in ascorbic acid of ocular humors and lens, and a 2--3-Fold increase in H2O2 of aqueous humor and vitreous humor. We conclude that catalase of eye affords protection to the lens from H2O2 and it also protects superoxide dismutase of lens from inactivation by H2O2. Superoxide dismutase, in turn, protects the lens from the superoxide radical, O2.-. It is likely that inhibition of these enzymes may lead to production of the highly reactive oxidant, the hydroxyl radical, under pathological conditions when H2O2 concentration in vivo exceeds physiological limits as in cataract induced by 3-aminotriazole. A scheme of reaction mechanism has been proposed to explain the relative functions of ocular catalase and superoxide dismutase. Such a mechanism may be involved in cataractogenic process in the human.
摘要
  1. 已对眼组织中的超氧化物歧化酶(超氧化物:超氧化物氧化还原酶,EC 1.15.1.1)活性进行了评估。在兔眼中,超氧化物歧化酶存在于角膜上皮、角膜内皮、晶状体、虹膜、睫状体和视网膜中。在晶状体中,活性存在于囊膜上皮。2. 铜螯合剂二乙基二硫代氨基甲酸盐在体外和兔体内均抑制晶状体超氧化物歧化酶。3. H₂O₂ 导致晶状体提取物的超氧化物歧化酶活性受到抑制,而过氧化氢酶抑制剂 3 - 氨基 - 1H - 1,2,4 - 三唑(3 - 氨基三唑)或NaN₃ 可增强这种抑制作用。3 - 氨基三唑或NaN₃ 对晶状体超氧化物歧化酶无影响。因此,晶状体的内源性过氧化氢酶可保护晶状体超氧化物歧化酶不被H₂O₂ 灭活。4. 在经喂食 3 - 氨基三唑诱导出现早期白内障(空泡期)的兔中,晶状体的超氧化物歧化酶减少,眼房水和晶状体中的抗坏血酸含量下降,房水和玻璃体液中的H₂O₂ 增加2 - 3倍。我们得出结论,眼内的过氧化氢酶可保护晶状体免受H₂O₂ 损伤,并且还可保护晶状体的超氧化物歧化酶不被H₂O₂ 灭活。反过来,超氧化物歧化酶可保护晶状体免受超氧阴离子自由基O₂⁻的损伤。在病理条件下,当体内H₂O₂ 浓度超过生理限度时,如在3 - 氨基三唑诱导的白内障中,这些酶的抑制可能会导致高活性氧化剂羟基自由基的产生。已提出一种反应机制方案来解释眼内过氧化氢酶和超氧化物歧化酶的相关功能。这种机制可能参与了人类的白内障形成过程。

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