title: The effects of meso-2,3-dimercaptosuccinic acid and oligomeric procyanidins on acute lead neurotoxicity in rat hippocampus.
abstract: Oxidative stress is considered to be a mechanism involved in lead neurotoxicity. Apoptosis is also thought to relate to lead neurotoxicity. The present study, focused on the hippocampus, was designed to investigate the two possible mechanisms involved in lead neurotoxicity and the potential protective effects of 2,3-dimercaptosuccinic acid (DMSA) and oligomeric procyanidins (OPC). It was proved that reactive oxygen species and oxidative damage were implicated in the induction of apoptosis induced by lead in the hippocampus. Administration of DMSA attenuated the oxidative stress and apoptosis in addition to having strong chelating and lead-removing capacity. OPC alone had antioxidant protective effects in the hippocampus but no removing capacity for lead in vivo despite showing higher affinity and stronger chelating ability for Pb(2+) than DMSA in vitro. It is suggested that OPC chelates Pb(2+) but does not discharge it from the body and even accumulates Pb(2+) in some organs. At the same time, a reasonable deduction can also be made that the complex of OPC-Pb(2+) prevents or at least weakens the neurotoxicity of Pb(2+). Whether this complex displays toxicity over a long time span should be studied further.
authors.affiliation: Laboratory of Visual Information Processing, Center for Brain and Cognitive Sciences, Institute of Biophysics, Academia Sinica, Beijing 100101 China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.forename: Xue-Fei
authors.initials: XF
authors.lastname: Wang
authors.forename: Zhong-Bing
authors.initials: ZB
authors.lastname: Lu
authors.forename: Nian-Qing
authors.initials: NQ
authors.lastname: Liu
authors.forename: Bao-Lu
authors.initials: BL
authors.lastname: Zhao
mesh_terms: D000818:Animals; D000872:Anthocyanins / Q000737:chemistry* / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002614:Chelating Agents / Q000494:pharmacology; D016166:Free Radical Scavengers / Q000494:pharmacology; D005609:Free Radicals / Q000378:metabolism; D005978:Glutathione / Q000737:chemistry / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D007854:Lead / Q000633:toxicity*; D007855:Lead Poisoning / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D004113:Succimer / Q000494:pharmacology*; D013997:Time Factors; D051028:bcl-2-Associated X Protein
chemical_list: D000872:Anthocyanins; D002614:Chelating Agents; D016166:Free Radical Scavengers; D005609:Free Radicals; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D007854:Lead; C017154:cyanidin; D004113:Succimer; D005980:Glutathione Reductase; D005978:Glutathione