Arsenic neurotoxicity — A review

Human and Experimental Toxicology - Tập 26 Số 10 - Trang 823-832 - 2007
A. Vahidnia1, Gijsbert B. van der Voet2, F.A. de Wolff3
1Department of Clinical Pharmacy and Toxicology, Leiden University Medical Center, Leiden, The Netherlands
2Department of Environmental and Toxicological Pathology, Armed Forces Institute of Pathology, Washington, USA
3Chair of Clinical and Forensic Toxicology, Leiden University Medical Center, Leiden, The Netherlands,

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

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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.

10.1007/BF00302528

10.1038/299627a0

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.

10.1023/A:1018413522959

10.1182/blood-2001-12-0325

10.1056/NEJM199509213331217

10.1093/jaoac/82.4.963

10.1001/jama.292.23.2868

Lynch E., 2005, Drug Saf, 4, 769

10.1182/blood.V97.1.264

10.1038/sj.leu.2402106

Miller Jr WH, 2002, Cancer Res, 62, 3893

10.1016/j.beha.2006.11.002

10.1016/0303-8467(92)90179-7

10.1159/000204205

10.1136/bmj.3.5983.559

Pullen-James S., 2006, J Natl Med Assoc, 98, 1998

10.1002/(SICI)1097-4598(199612)19:12<1611::AID-MUS13>3.0.CO;2-U

10.1016/0022-510X(77)90025-9

10.1579/0044-7447(2007)36[78:GIOGAA]2.0.CO;2

Kelynack Tnv., 1900, The Lancet, 1600

10.1016/S0140-6736(01)81230-7

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

10.1016/j.taap.2006.12.032

10.1289/ehp.00108393

10.1289/ehp.02110s5883

10.1097/01.jom.0000169089.54549.db

10.1081/CLT-200035344

Tseng HP, 2006, J Health Popul Nutr, 24, 182

10.1016/S0035-3787(06)75025-1

10.1081/CLT-100108509

10.1080/15563650701232489

Hilmy AM, 1991, Comp Biochem Physiol, 99

10.1016/S0378-4274(01)00534-3

10.1093/oxfordjournals.aje.a114631

10.5271/sjweh.1480

10.1016/j.taap.2003.10.030

10.1007/s002040000134

10.1007/BF00343122

10.1016/0006-2952(88)90313-9

10.1146/annurev.pharmtox.37.1.397

Shirachi DY, 1981, Proc West Pharmacol Soc, 24, 159

10.1002/elps.200500614

Yamamoto S., 1995, Cancer Res, 55, 1271

10.1093/carcin/17.11.2435

10.1093/mutage/gem010

10.1016/S1532-0456(02)00018-2

10.1034/j.1600-0773.2001.d01-128.x

10.1016/j.taap.2003.10.027

10.1289/ehp.9008

10.1021/tx050106d

10.4161/cc.3.3.657

10.1080/10643389991259227

10.1016/S0378-4274(02)00084-X

10.1021/tx025615j

10.1007/BF00293690

10.1021/tx00026a012

10.1073/pnas.98.4.1643

Bolla-Wilson K, Bleecker, 1987, J Occup Med, 29, 500

Mazumder DN, 1992, Bull World Health Organ, 70, 481

10.1177/0960327107070561

10.1515/REVEH.2006.21.2.105

10.1016/S0079-6336(11)80190-7

Shin RW, 1995, Histol Histopathol, 10, 969

10.1016/j.tox.2005.09.015

10.1097/00001648-200205000-00012

10.1159/000089625

10.1097/00019052-200008000-00006

10.1136/oem.2006.028761

10.3233/JAD-2006-102-309

10.1002/bies.10251

10.1017/S0317167100030614

10.1177/0960327106070671

Carpenter DA, 1996, J Cell Sci, 109, 2493, 10.1242/jcs.109.10.2493

10.1016/j.tiv.2007.04.007

10.1016/j.taap.2007.01.022

10.1016/S0006-8993(99)02148-4

10.1016/j.pain.2004.04.031

10.1111/j.1460-9568.2006.04793.x

10.1021/bi026813c

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Human and Experimental Toxicology

Tập 26 Số 10

823-832

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