Arsenic neurotoxicity — A review
Tóm tắt
Arsenic (As) is one of the oldest poisons known to men. Its applications throughout history are wide and varied: murder, make-up, paint and even as a pesticide. Chronic As toxicity is a global environmental health problem, affecting millions of people in the USA and Germany to Bangladesh and Taiwan. Worldwide, As is released into the environment by smelting of various metals, combustion of fossil fuels, as herbicides and fungicides in agricultural products. The drinking water in many countries, which is tapped from natural geological resources, is also contaminated as a result of the high level of As in groundwater. The environmental fate of As is contamination of surface and groundwater with a contaminant level higher than 10 particle per billion (ppb) as set by World Health Organization (WHO). Arsenic exists in both organic and inorganic species and either form can also exist in a trivalent or pentavalent oxidation state. Long-term health effects of exposure to these As metabolites are severe and highly variable: skin and lung cancer, neurological effects, hypertension and cardiovascular diseases. Neurological effects of As may develop within a few hours after ingestion, but usually are seen in 2—8 weeks after exposure. It is usually a symmetrical sensorimotor neuropathy, often resembling the Guillain—Barré syndrome. The predominant clinical features of neuropathy are paresthesias, numbness and pain, particularly in the soles of the feet. Electrophysiological studies performed on patients with As neuropathy have revealed a reduced nerve conduction velocity, typical of those seen in axonal degeneration. Most of the adverse effects of As, are caused by inactivated enzymes in the cellular energy pathway, whereby As reacts with the thiol groups of proteins and enzymes and inhibits their catalytic activity. Furthermore, As-induced neurotoxicity, like many other neurodegenerative diseases, causes changes in cytoskeletal protein composition and hyperphosphorylation. These changes may lead to disorganization of the cytoskeletal framework, which is a potential mechanism of As-induced neurotoxicity. Human & Experimental Toxicology (2007) 26, 823— 832
Từ khóa
Tài liệu tham khảo
Steingass A., 1947, A comprehensive persian english dictionary
Marsh J., 1836, Eddinburgh New Philosophical J, 21, 229
Wikipedia. Arsenic. Wikipedia . 2007. Ref Type: Electronic Citation.
De Wolff FA, Edelbroek PM Neurotoxicity of arsenic and its compounds. In Vinken & Bruyn's, ed. Handbook of clinical neurology . Elsevier Science BV 1994 : 283—91.
Lynch E., 2005, Drug Saf, 4, 769
Miller Jr WH, 2002, Cancer Res, 62, 3893
Pullen-James S., 2006, J Natl Med Assoc, 98, 1998
Kelynack Tnv., 1900, The Lancet, 1600
Mayans MV, 2000, Bull World Health Organ, 78, 1167
Mukherjee A., 2006, J Health Popul Nutr, 24, 142
Mees RA, 1919, Ned Tijdsch Geneeskd, 1, 391
Tseng HP, 2006, J Health Popul Nutr, 24, 182
Hilmy AM, 1991, Comp Biochem Physiol, 99
Shirachi DY, 1981, Proc West Pharmacol Soc, 24, 159
Yamamoto S., 1995, Cancer Res, 55, 1271
Bolla-Wilson K, Bleecker, 1987, J Occup Med, 29, 500
Mazumder DN, 1992, Bull World Health Organ, 70, 481
Shin RW, 1995, Histol Histopathol, 10, 969