In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats
In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats
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DOI：
10.1007/s002040100219
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发表时间：
2001-04-01
影响因子：
6.1
通讯作者：
Kilinc, I
中科院分区：
文献类型：
--
作者：
Gultekin, F;Delibas, N;Kilinc, I
活性氧（ROS）可能参与了毒死蜱乙基酯（CE）[O，O-二乙基-O-（3，5，6-三氯-2-吡啶基）硫代磷酸酯]的毒性作用。我们拥有：因此，研究了CE对大鼠红细胞抗氧化系统的体内作用，并评价了褪黑素和维生素E和维生素C的组合对CE诱导的氧化损伤的改善作用。实验组为：（1）对照组，（2）CE治疗组（CE），（3）维生素E+维生素C治疗组（Vit），（4）褪黑素治疗组（Mel），（5）维生素E+维生素C + CE治疗组（Vit + CE），（6）褪黑素+CE治疗组（Mel + CE）。维生素E和维生素L分别以150和200 mg/kg的剂量每天肌肉注射一次，连续6天。在Mel和Mel + CE组中，以10mg/kg宠物日肌内施用褪黑激素，连续6天。第五天结束时，CE大鼠。维生素+CE组和Mel a CE组口服41 mg/kg CE，21 h后口服第二次剂量。首次CE给药后24 h采集血样。测定红细胞硫代巴比妥酸反应物质（TBARS）、抗氧化防御能力（AOP）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）活性。与对照组相比，口服CE显著（P <0.05）刺激TEARS活性，显著（P <0.05）抑制AOP和SOD、CAT活性。褪黑素和维生素E + C可显著降低CE引起的TEARS增加（P <0.05），并可克服CE对SOD和CA-P的抑制作用，但对AOP的抑制作用不明显。褪黑激素处理仅显著提高GSH-Px活性（P <0.05），与CE的作用无关。这些结果表明，CE治疗增加体内脂质过氧化，并通过增加大鼠红细胞中的氧化应激降低抗氧化防御，褪黑激素和维生素和维生素C的组合可以减少这种脂质过氧化作用。
Reactive oxygen species (ROS) may he involved in the toxicity of chlorpyrifos-ethyl (CE) [O, O-diethyl-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate]. We have: therefore, examined the in vivo effects of CE on the rat erythrocyte antioxidant system and evaluated the ameliorating effects of melatonin and a combination of vitamin E and vitamin C on the oxidative damage induced by CE. The experimental groups were: (1) control group, (2) CE-treated group (CE); (3) vitamin E plus vitamin C treatment group (Vit) (4) melatonin-treated group (Mel), (5) vitamin E plus; vitamin C: plus CE treatment group (Vit + CE), and (6) melatonin plus CE treatment group (Mel + CE). Vitamin E and vitamin L were administered intramuscularly once a day for 6 consecutive days at 150 and 200 mg/kg, respectively, in the Vit and Vit + CE groups. Melatonin was administered intramuscularly at 10 mg/kg pet day for 6 consecutive days in the Mel and Mel + CE groups. At the end of the fifth day, the rats of CE. Vit + CE and Mel a CE groups were treated orally with the first of two equal doses of 41 mg/kg CE, the second oral dose being given 21 h later. Blood samples were taken 24 h after the first CE administration. Levels of thiobarbituric acid reactive substance (TBARS), antioxidant defence potential (AOP), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were determined in erythrocytes. In comparison with the control group, oral administration of CE significantly (P < 0.05) stimulated TEARS activity while significantly (P < 0.05) inhibiting AOP and the activities of SOD and CAT. However. GSH-Ps activity remained unchanged by CE treatment, Treatment with melatonin and vitamins E plus C significantly (P < 0.05) reduced the CE-induced increase of TEARS, and overcame the inhibitory effect of CE on SOD and CA-P, but not on AOP. Melatonin treatment significantly (P < 0.05) increased only GSH-Px activity, il respective of the effect of CE. These results suggest that CE treatment increases in vivo lipid peroxidation and decreases antioxidant defence by increasing oxidative stress in erythrocytes of rats, and melatonin and a combination of vitamin and vitamin C can reduce this lipooperoxidative effect.