Vural H, Sabuncu T, Arslan S O, Aksoy N
Department of Biochemistry, Faculty of Medicine, University of Harran, 63100 Sanliurfa, Turkey.
J Pineal Res. 2001 Oct;31(3):193-8. doi: 10.1034/j.1600-079x.2001.310301.x.
Although melatonin has been established as a free radical scavenger and antioxidant, its effects in diabetes have not been thoroughly investigated. The purpose of this study, therefore, was to investigate the effects of melatonin administration on lipid peroxidation and antioxidant status in streptozotocin (STZ)-induced diabetes in rats. Concentrations of malondialdehyde (MDA) and reduced glutathione (GSH) in erythrocytes and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were compared in 3 groups of 10 rats each [control non-diabetic rats (group I), untreated diabetic rats (group II) and diabetic rats treated with melatonin (group III)]. In the study groups, diabetes developed 3 days after intraperitoneal (i.p.) administration of a single 60-mg/kg dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10-mg/kg i.p. dose of melatonin per day. After 6 wk, the rats in groups II and III had significantly lower body weights and significantly higher blood glucose levels than the rats of group I (P<0.001 and P<0.001, respectively). There were no significant differences in body weight or blood glucose levels between groups II and III. MDA levels in untreated diabetic rats were higher than those in control group rats and in diabetic rats treated with melatonin (P<0.01 and P<0.05, respectively). However, MDA levels in diabetic rats treated with melatonin were not different from those of the control group. The GSH, GSH-Px and SOD levels of untreated diabetic rats were significantly lower than those of the control group (P<0.02, P<0.002 and P<0.05, respectively). In group III, however, melatonin prevented decreases in the thiol antioxidant and the associated enzymes, and so these levels were not significantly different from those in the control group. These results confirm the presence of oxidative stress in STZ-induced experimental diabetes and indicate the beneficial free radical-scavenging and antioxidant properties of melatonin.
尽管褪黑素已被确认为一种自由基清除剂和抗氧化剂，但其在糖尿病方面的作用尚未得到充分研究。因此，本研究的目的是探讨给予褪黑素对链脲佐菌素（STZ）诱导的糖尿病大鼠脂质过氧化和抗氧化状态的影响。将每组10只大鼠分为3组，比较红细胞中丙二醛（MDA）浓度、还原型谷胱甘肽（GSH）浓度以及超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性[对照非糖尿病大鼠（I组）、未治疗的糖尿病大鼠（II组）和用褪黑素治疗的糖尿病大鼠（III组）]。在研究组中，腹腔注射（i.p.）单次60mg/kg剂量的STZ后3天发生糖尿病。此后，II组大鼠未接受治疗，而III组大鼠开始每天接受10mg/kg i.p.剂量的褪黑素。6周后，II组和III组大鼠的体重显著低于I组大鼠，血糖水平显著高于I组大鼠（分别为P<0.001和P<0.001）。II组和III组之间的体重或血糖水平无显著差异。未治疗的糖尿病大鼠的MDA水平高于对照组大鼠和用褪黑素治疗的糖尿病大鼠（分别为P<0.01和P<0.05）。然而，用褪黑素治疗的糖尿病大鼠的MDA水平与对照组无差异。未治疗的糖尿病大鼠的GSH、GSH-Px和SOD水平显著低于对照组（分别为P<0.02、P<0.002和P<0.05）。然而，在III组中，褪黑素可防止硫醇抗氧化剂和相关酶的减少，因此这些水平与对照组无显著差异。这些结果证实了STZ诱导的实验性糖尿病中存在氧化应激，并表明褪黑素具有有益的自由基清除和抗氧化特性。
