Lambda-cyhalothrin-induced changes in oxidative stress biomarkers in rabbit erythrocytes and alleviation effect of some antioxidants.
Erythrocytes are a convenient model to understand the membrane oxidative damage induced by various xenobiotic-prooxidants. This study was designed to investigate (1) the possibility of lambda-cyhalothrin (LC), a type II pyrethroid, to induce oxidative stress response in rabbit erythrocytes in vitro and its effect on selected antioxidant enzymes and (2) the role of vitamin C (VC; 20mM) and vitamin E (VE; 2mM) in alleviating the cytotoxic effects of LC. Erythrocytes were divided into three groups. The first group, previously prepared erythrocytes was incubated for 4h at 37 degrees C with different concentrations (0, 0.1, 0.5, 1, 2.5, 5mM) of LC. The second and third groups were preincubated with VC or VE, respectively for 20 min and followed by LC incubation for 4h. Following in vitro exposure, LC caused a significant induction of oxidative damage in erythrocytes at different concentrations as evidenced by increased thiobarbituric acid reactive substances (TBARS) levels. However, a significant decrease in the content of sulfhydryl groups (SH-groups), and the activities of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) were observed. The response was concentration dependent. VC or VE pretreated erythrocytes showed a significant protection against the cytotoxic effects induced by LC on the studied parameters. In conclusion, antioxidant vitamins especially VE could be able to ameliorate LC-induced oxidative stress by decreasing lipid peroxidation and altering antioxidant defense system in erythrocytes.
El-Demerdash
Fatma M
FM
Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, 163, Horreya Avenue, PO Box. 832, Alexandria 21526, Egypt. feldemerdash@yahoo.com
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D015415:Biomarkers / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004336:Drug Antagonism; D004912:Erythrocytes / Q000187:drug effects* / Q000378:metabolism; D016166:Free Radical Scavengers / Q000378:metabolism*; D005982:Glutathione Transferase / Q000378:metabolism; D007306:Insecticides / Q000633:toxicity*; D008297:Male; D009570:Nitriles / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D011722:Pyrethrins / Q000633:toxicity*; D011817:Rabbits; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology
D000975:Antioxidants; D015415:Biomarkers; D016166:Free Radical Scavengers; D007306:Insecticides; D009570:Nitriles; D011722:Pyrethrins; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D002374:Catalase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D000110:Acetylcholinesterase; D001205:Ascorbic Acid; C037304:cyhalothrin