首页> 外文期刊>Archives of Environmental Contamination and Toxicology >The effect of sulfur dioxide inhalation on visual evoked potentials, antioxidant status, and lipid peroxidation in alloxan-induced diabetic rats.
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The effect of sulfur dioxide inhalation on visual evoked potentials, antioxidant status, and lipid peroxidation in alloxan-induced diabetic rats.

机译:吸入二氧化硫对四氧嘧啶诱发的糖尿病大鼠的视觉诱发电位,抗氧化剂状态和脂质过氧化的影响。

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The aim of the study was to investigate the effect of 10 ppm sulfur dioxide (SO(2)) exposure on visual evoked potentials (VEPs), thiobarbituric acid reactive substances (TBARS), and the activities of Cu,Zn superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in diabetes mellitus. Forty healthy male albino rats, aged 3 months, were divided into four equal groups: control (C), sulfur dioxide + control (CSO(2)), diabetic (D), and sulfur dioxide + diabetic (DSO(2)) groups. Experimental diabetes mellitus was induced by IV injection of alloxane monohydrate in a dose of 50 mg/kg body weight. Ten ppm sulfur dioxide was administered to the animals of sulfur dioxide-exposed groups in an exposure chamber for 1 h/day x 7 days/week x 6 weeks while control and diabetic groups were exposed to filtered air in the same condition. SO(2) exposure, though markedly decreasing retina CAT and GSH-Px activities, significantly increased retina Cu,Zn-SOD activity in the diabetic and nondiabetic groups. In contrast to SO(2)-related increase in the activity of Cu,Zn-SOD, decrease in GSH-Px activity was observed in the brain of those groups. Brain CAT activity was unaltered. SO(2) exposure caused the significant elevation in brain TBARS levels of CSO(2) and DSO(2) groups, whereas only in the retina TBARS level of the CSO(2) group. SO(2) exposure caused the significant prolongations of P(1), N(1), P(2), and P(3) components of VEPs in the nondiabetic and all components of VEPs in the diabetic groups. SO(2) exposure also resulted in significant amplitude reductions in both experimental groups.
机译:该研究的目的是研究10 ppm二氧化硫(SO(2))暴露对视觉诱发电位(VEP),硫代巴比妥酸反应性物质(TBARS)以及Cu,Zn超氧化物歧化酶(SOD)活性的影响,谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)在糖尿病中的作用。将40只3个月大的健康白化雄性大鼠分为四个相等的组:对照组(C),二氧化硫+对照(CSO(2)),糖尿病(D)和二氧化硫+糖尿病(DSO(2))组。通过静脉内注射50mg / kg体重剂量的四水合四氧六环乙烷诱导实验性糖尿病。在暴露室内向暴露于二氧化硫的组的动物施用10 ppm二氧化硫,持续时间为1 h /天x 7天/周x 6周,而对照组和糖尿病组则在相同条件下暴露于过滤后的空气中。 SO(2)暴露,虽然显着降低视网膜CAT和GSH-Px活性,但显着增加了糖尿病和非糖尿病组的视网膜Cu,Zn-SOD活性。与SO(2)相关的Cu,Zn-SOD活性增加相反,在这些组的大脑中观察到GSH-Px活性降低。脑CAT活​​性未改变。 SO(2)暴露导致CSO(2)和DSO(2)组的大脑TBARS水平显着升高,而仅CSO(2)组的视网膜TBARS水平升高。 SO(2)暴露导致糖尿病患者中VEP的P(1),N(1),P(2)和P(3)组分显着延长,而VEP的所有组分均显着延长。 SO(2)暴露还导致两个实验组的幅度明显降低。

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