Protective effect of green tea on lead-induced oxidative damage in rat's blood and brain tissue homogenates.
Recent studies have shown that lead (Pb) could disrupt tissue prooxidant/antioxidant balance which lead to physiological dysfunction. Natural antioxidants are particularly useful in such situation. Current study was designed to investigate efficacy of green tea extract (GTE), on oxidative status in brain tissue and blood caused by chronic oral Pb administration in rats. Four groups of adult male rats (each 15 rats) were utilized: control group; GTE-group (oral 1.5% w/v GTE for 6 weeks); Pb-group (oral 0.4% lead acetate for 6 weeks), and Pb+GTE-group (1.5% GTE and 0.4% lead acetate for 6 weeks). Levels of prooxidant/antioxidant parameters [lipid peroxides (LPO), nitric oxides (NO), total antioxidant capacity (TAC), glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD)] in plasma, erythrocytes, and brain tissue homogenate were measured using colorimetric methods. Pb concentrations in whole blood and brain tissue homogenate were measured by atomic absorption. In Pb-group, levels of LPO were higher while NO and GSH were lower in plasma, erythrocytes, and brain tissue than controls. TAC in plasma, SOD in erythrocytes, and GST in brain tissue homogenate were lower in Pb-group versus control. GTE co-administrated with Pb-reduced Pb contents, increased antioxidant status than Pb-group. In erythrocytes, Pb correlated positively with LPO and negatively with NO, GSH, SOD, and Hb. In brain tissue homogenate, Pb correlated positively with LPO and negatively with GSH. This study suggests that lead induce toxicity by interfering balance between prooxidant/antioxidant. Treatment of rats with GTE combined with Pb enhances antioxidant/ detoxification system which reduced oxidative stress. These observations suggest that GTE is a potential complementary agent in treatment of chronic lead intoxication.
Department of Physiology, Assiut University, P.O. Box: 71526, Assiut, Egypt. eah3a2003@yahoo.com
Enas A
EA
Hamed
Abdel-Raheim M A
AR
Meki
Nashwa A
NA
Abd El-Mottaleb
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001923:Brain Chemistry / Q000187:drug effects*; D004912:Erythrocytes / Q000737:chemistry / Q000187:drug effects; D005982:Glutathione Transferase / Q000097:blood; D007854:Lead / Q000633:toxicity*; D007855:Lead Poisoning / Q000188:drug therapy; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D010936:Plant Extracts / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000097:blood; D013662:Tea
D000975:Antioxidants; D008054:Lipid Peroxides; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D013662:Tea; D007854:Lead; D013482:Superoxide Dismutase; D005982:Glutathione Transferase