title: Opposite effects of alpha-lipoic acid on antioxidation and long-term potentiation in control and chronically lead-exposed rats.
abstract: Among the developmental changes identified in rats exposed to lead are impairments in long-term potentiation (LTP) in the hippocampus and changes in the levels of reactive oxygen species (ROS) in cells and some soft tissues. alpha-Lipoic acid (LA) has been reported to be highly effective in improving the thiol capacity of the cells and in reducing lead-induced oxidative stress. To explore the effects of LA on LTP in chronically lead-exposed rats and the relationship between ROS and LTP in both control and lead-exposed rats, we have compared LTP and oxidative stress parameters in groups of lead-exposed and control rats with or without LA treatment (10, 25, 50, and 100 mg/kg through intraperitoneal injection). The capacity of LA to decrease hippocampal lead levels in lead-exposed rats was examined. We found that LA had no effects in decreasing the level of lead in the hippocampus, but it did appear to have both antioxidant properties and a reparatory effect on LTP amplitude in rats developmentally exposed to lead for 2 weeks following birth. Interestingly, bell-shaped dose-response curves emerged. In the lower LA dosage groups (10, 25 mg/kg LA), there was an increasing LTP amplitude. The strongest protective effect in terms of the induction and amplitude of LTP in the lead-exposed group with at 25 mg/kg LA; when higher dosages were applied (50, 100 mg/kg LA), the LTP amplitude decreased as compared to the 25 mg/kg LA treatment group. The administration of LA to control animals resulted in a significant impairment of LTP amplitude, with the 100 mg/kg LA treatment having harmful effects on the oxidative parameters. These differential effects of LA on LTP in control and lead-exposed rats may be due to the different redox status of the control and lead-exposed rats.
authors.affiliation: Department of Neurobiology and Biophysics, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, People's Republic of China.
authors.forename: Hui-Li
authors.initials: HL
authors.lastname: Wang
authors.forename: Xiang-Tao
authors.initials: XT
authors.lastname: Chen
authors.forename: Shu-Ting
authors.initials: ST
authors.lastname: Yin
authors.forename: Jin
authors.initials: J
authors.lastname: Liu
authors.forename: Ming-Liang
authors.initials: ML
authors.lastname: Tang
authors.forename: Chuan-Yun
authors.initials: CY
authors.lastname: Wu
authors.forename: Di-Yun
authors.initials: DY
authors.lastname: Ruan
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D004594:Electrophysiology; D005978:Glutathione / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007854:Lead / Q000378:metabolism; D020263:Lead Poisoning, Nervous System / Q000378:metabolism* / Q000503:physiopathology*; D017774:Long-Term Potentiation / Q000187:drug effects*; D008315:Malondialdehyde / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D008063:Thioctic Acid / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D007854:Lead; D008315:Malondialdehyde; D008063:Thioctic Acid; D013482:Superoxide Dismutase; D005978:Glutathione