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糖尿病或实验性半乳糖血症中视网膜代谢异常。III. 抗氧化剂的作用。

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. III. Effects of antioxidants.

作者信息

Kowluru R A, Kern T S, Engerman R L, Armstrong D

机构信息

Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison 53706-1532, USA.

出版信息

Diabetes. 1996 Sep;45(9):1233-7. doi: 10.2337/diab.45.9.1233.

Abstract

Effects of antioxidants on hyperglycemia-induced alterations of retinal metabolism were evaluated in rats diabetic or experimentally galactosemic for 2 months. Oxidative stress was estimated by measuring lipid peroxides (measured as thiobarbituric acid reactive substances [TBARS]) in retina and plasma. Erythrocyte osmotic fragility, another measure of oxidative stress, also was determined in the same groups of rats. In diabetic rats, TBARS were elevated by 74% in retina and 87% in plasma. In galactose-fed rats, TBARS were significantly elevated in retina (P < 0.05), but were normal in plasma. The administration of supplemental dietary ascorbic acid and alpha-tocopherol acetate for 2 months prevented the elevation of retinal TBARS and the decrease of Na(+)-K(+)-ATPase and calcium ATPase activities in retinas of diabetic animals without having any beneficial effect on plasma TBARS. In galactosemic rats, these antioxidants had a partial beneficial effect on the activity of retinal Na(+)-K(+)-ATPase, but failed to have any effect on calcium ATPase. The beneficial effects of antioxidants in diabetes and experimental galactosemia were not caused by the amelioration of hyperglycemia or retinal polyol accumulation. Erythrocyte osmotic fragility was increased by more than twofold in diabetes, but was normal in experimental galactosemia, and antioxidants prevented diabetes-induced increases in erythrocyte osmotic fragility-Diabetes-induced increased oxidative stress and subnormal ATPase activities in the retina can be inhibited by dietary supplementation with antioxidants.

摘要

在糖尿病或实验性半乳糖血症大鼠中评估了抗氧化剂对高血糖诱导的视网膜代谢改变的影响,这些大鼠为期2个月。通过测量视网膜和血浆中的脂质过氧化物(以硫代巴比妥酸反应性物质[TBARS]衡量)来估计氧化应激。在同一组大鼠中还测定了红细胞渗透脆性,这是氧化应激的另一种衡量指标。在糖尿病大鼠中,视网膜中的TBARS升高了74%,血浆中升高了87%。在喂饲半乳糖的大鼠中,视网膜中的TBARS显著升高(P<0.05),但血浆中正常。补充膳食抗坏血酸和α-生育酚醋酸酯2个月可防止糖尿病动物视网膜中TBARS的升高以及视网膜中Na(+)-K(+)-ATP酶和钙ATP酶活性的降低,而对血浆TBARS没有任何有益作用。在半乳糖血症大鼠中,这些抗氧化剂对视网膜Na(+)-K(+)-ATP酶的活性有部分有益作用,但对钙ATP酶没有任何作用。抗氧化剂在糖尿病和实验性半乳糖血症中的有益作用不是由高血糖或视网膜多元醇积累的改善引起的。糖尿病时红细胞渗透脆性增加了两倍多,但实验性半乳糖血症时正常,抗氧化剂可防止糖尿病引起的红细胞渗透脆性增加——糖尿病诱导的视网膜氧化应激增加和ATP酶活性低于正常水平可通过膳食补充抗氧化剂来抑制。

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