Molecular mechanisms of metal neurotoxicity.
Recent epidemiological and experimental research indicates that toxic and carcinogenic effects of certain trace elements including metals may occur at levels compatible with exposure in the general environment. Despite a large number of studies describing metal cytotoxicity, the molecular mechanisms involved are still poorly understood. However, it now appears clear that several metals can interact with proteins involved in signal transduction, including Ca2+ channels and pumps. The resulting impairment of the ability of cells to respond adequately to the stimulation by hormones and growth factors results in the loss of important cell functions and can ultimately compromise cell survival.
Department of Toxicology and Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
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D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D008627:Mercuric Chloride / Q000633:toxicity*; D008670:Metals / Q000633:toxicity*; D009414:Nerve Growth Factors / Q000494:pharmacology; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D016716:PC12 Cells; D015398:Signal Transduction / Q000187:drug effects
D015220:Calcium Channels; D008670:Metals; D009414:Nerve Growth Factors; D008627:Mercuric Chloride; D002118:Calcium