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

Abstract

Reactive oxygen species (ROS) may be 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 C 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 per 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 + 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 TBARS activity while significantly (P < 0.05) inhibiting AOP and the activities of SOD and CAT. However, GSH-Px activity remained unchanged by CE treatment. Treatment with melatonin and vitamins E plus C significantly (P < 0.05) reduced the CE-induced increase of TBARS, and overcame the inhibitory effect of CE on SOD and CAT, but not on AOP. Melatonin treatment significantly (P < 0.05) increased only GSH-Px activity, irrespective 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 E and vitamin C can reduce this lipoperoxidative effect.

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

“…In the present study, malathion caused a significant decrease in activities of SOD, GSH and GPx in rat liver confirming the increased production of free radicals caused by administration of malathion. These findings are in accordance with those of Gultekin et al (2001) who reported that SOD activities decreased with increasing malathion concentration and incubation period. Also Rezg et al (2008) reported that sub chronic treatment with malathion, gradually decreased the activities of SOD in rat liver.…”

“…This protection may be attributed to phosphorylation and activation of endothelial nitric oxide syntheses in endothelial cells through modulation of protein kinase C. A signaling pathways by green tea resulting in endothelial dependant vasorelaxtion (Lorenz et al, 2004). So in our present study demonstrate that, the activity of the MDA in malathion exposed group increased 2 fold compared with that of the control one, these finding is in accordance with Gultekin et al (2001) who reported that MDA values increased with increasing organophosphorous compounds concentration and incubation period (Ranjbar et al, 2005), may be due to Lipid peroxidation was seen in erythrocytes and liver of rats when exposed to malathion orally for 4 weeks at dose of 5,25 and 75 mg/Kg, respectively (Abdollahi et al, 2004) While in groups treated by malathion plus vitamine c or malathion plus green tea there were a significant decrease in MDA values in comparison with malathion group may be due to The protective effect of vitamin c over malathion toxicity is likely to be mediated via the inhibition of free radical generation and enhancement of free radical scavenging activity (Suna et al, 2010) and Green tea prevents the loss of lipophilic antioxidant α-tocopherol by repairing tocopheryl radicals and protection of the hydrophilic antioxidant ascorbate (Skryzdlewska et al, 2002). Therefore, it may decrease the concentration of lipid free radicals and terminate initiation and propagation of lipid peroxidation (Guo et al, 1999).…”

Effects of Lycopene Alone or Combined with Melatonin on Methotrexate-Induced Nephrotoxicity in Rats

“…A number of studies have shown that Mel is significantly better than the classic antioxidants in resisting free radical-induced molecular destruction (Gultekin et al, 2001;Baydas et al, 2002). Beneficial antioxidant effects of Mel have been recently shown in clinical settings for several chronic diseases, including patients with rheumatoid arthritis (Forrest et al, 2007), elderly patients with primary essential hypertension (KedzioraKornatowska, 2008), and females with infertility.…”

Protective Role of Daidzein Against Cyclophosphamide Induced Nephrotoxicity in Experimental Rats

“…The depletion of catalase in turn also prevents the SOD action. The decline in these antioxidant enzymes is mainly due to more ROS and lipid peroxidation [22]. The pretreatment with daidzein significantly increases the level SOD and catalase after CPA treatment.…”