Kowluru R A, Kern T S, Engerman R L
Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison 53706-1532, USA.
Free Radic Biol Med. 1997;22(4):587-92. doi: 10.1016/s0891-5849(96)00347-4.
Activities of enzymes that protect the retina from reactive oxygen species were investigated in experimentally diabetic rats and experimentally galactosemic rats, two animal models known to develop vascular lesions consistent with diabetic retinopathy. Diabetes or experimental galactosemia of 2 months duration significantly decreased the activities of glutathione reductase and glutathione peroxidase in the retina while having no effect on the glutathione synthesizing enzymes glutathione synthetase and gamma-glutamyl cysteine synthetase. Activities of two other important antioxidant defense enzymes-superoxide dismutase (SOD) and catalase-also were decreased (by more than 25%) in retinas of diabetic rats and galactosemic rats. Administration of supplemental antioxidants, vitamins C and E, for the 2 months prevented the diabetes-induced impairment of antioxidant defense system in the retina. In experimentally galactosemic rats, the supplemental antioxidants were not as effective: SOD activity was normalized, but the enzymes of the glutathione redox cycle were only partly restored, and the subnormal catalase activity was unaffected. Diabetes or experimental galactosemia results in significant impairment of the antioxidant defense system in the retina, and exogenous antioxidant supplementation can help alleviate the subnormal activities of antioxidant defense enzymes.
在实验性糖尿病大鼠和实验性半乳糖血症大鼠中，研究了保护视网膜免受活性氧损伤的酶的活性。这两种动物模型已知会发生与糖尿病视网膜病变一致的血管病变。持续2个月的糖尿病或实验性半乳糖血症显著降低了视网膜中谷胱甘肽还原酶和谷胱甘肽过氧化物酶的活性，而对谷胱甘肽合成酶谷胱甘肽合成酶和γ-谷氨酰半胱氨酸合成酶没有影响。另外两种重要的抗氧化防御酶超氧化物歧化酶（SOD）和过氧化氢酶的活性在糖尿病大鼠和半乳糖血症大鼠的视网膜中也降低了（超过25%）。在2个月内给予补充抗氧化剂维生素C和E可预防糖尿病诱导的视网膜抗氧化防御系统损伤。在实验性半乳糖血症大鼠中，补充抗氧化剂的效果不佳：SOD活性恢复正常，但谷胱甘肽氧化还原循环的酶仅部分恢复，而过低的过氧化氢酶活性未受影响。糖尿病或实验性半乳糖血症会导致视网膜抗氧化防御系统显著受损，外源性补充抗氧化剂有助于缓解抗氧化防御酶的异常活性。
