title: Effects of Epigallocatechin-3-gallate on lead-induced oxidative damage.
abstract: Recent studies have shown that lead (Pb) could disrupt the prooxidant/antioxidant balance of tissue which leads to biochemical and physiological dysfunction. Epigallocatechin-3-gallate (EGCG), a catechin polyphenols component, is found to be an effective antioxidant. The present study investigated whether EGCG administration could reverse the changes on redox states in rat hippocampus caused by lead exposure. The association between redox status changes and long-term potentiation (LTP) in CA1 area of hippocampus were also examined. Wistar rats exposed to lead from postnatal day 1 were followed by 10 days of EGCG (10, 25 and 50 mg/kg) administration through intraperitoneally (ip), and the rats were sacrificed for experiments at the age of 21-23 days. The experimental results showed that glutathione (GSH) and superoxide dismutase (SOD) activity decreased accompanied with LTP amplitude decrease in CA1 area of hippocampus in the lead-exposed group. EGCG supplementation following lead intoxication resulted in increases in the GSH and SOD levels and increases in the LTP amplitude. Malondialdehyde (MDA) levels, a major lipid peroxidation byproduct, increased following lead exposure and decreased following EGCG treatment. In hippocampal neuron culture model, lead exposure (20 microM) significantly inhibited the viability of neurons which was followed by an accumulation of ROS and a decrease of mitochondrial membrane potential (delta Psi m). Treatment by EGCG (10-50 microM) effectively increased cell viability, decreased ROS formation and improved delta Psi m in hippocampal neurons exposed to lead. These observations suggest that EGCG is a potential complementary agent in the treatment of chronic lead intoxication through its antioxidative character.
authors.affiliation: School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, PR China.
authors.forename: Shu-Ting
authors.initials: ST
authors.lastname: Yin
authors.forename: Ming-Liang
authors.initials: ML
authors.lastname: Tang
authors.forename: Li
authors.initials: L
authors.lastname: Su
authors.forename: Liang
authors.initials: L
authors.lastname: Chen
authors.forename: Pu
authors.initials: P
authors.lastname: Hu
authors.forename: Hui-Li
authors.initials: HL
authors.lastname: Wang
authors.forename: Ming
authors.initials: M
authors.lastname: Wang
authors.forename: Di-Yun
authors.initials: DY
authors.lastname: Ruan
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004336:Drug Antagonism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D007274:Injections, Intraperitoneal; D007774:Lactation; D015227:Lipid Peroxidation / Q000187:drug effects; D017774:Long-Term Potentiation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D018811:Maternal Exposure; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009942:Organometallic Compounds / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009942:Organometallic Compounds; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D002392:Catechin; C045651:epigallocatechin gallate; D013482:Superoxide Dismutase; D005978:Glutathione; C008261:lead acetate