Arsenical neuropathy

Chhuttani, P. N.; Chawla, L. S.; Sharma, T. D.

doi:10.1212/wnl.17.3.269

Cited by 59 publications

(17 citation statements)

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“…In addition, As can also have detrimental effects on the peripheral nervous system [1][2][3][4][5][6][7] and central nervous system (CNS) [8][9][10][11][12][13]. Epidemiological studies have shown that As causes impairment in hearing, learning, memory, and concentration [12][13][14][15][16] and pattern memory and switching attention were affected by long-term accumulative exposure to As.…”

Section: Introductionmentioning

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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To better understand the effect of arsenic on central nervous system by prenatal and early life exposure, the oxidative stress and neurotransmitter metabolic enzymes were determined in offspring rats' brain cortex and hippocampus. Forty-eight pregnant rats were randomly divided into four groups, each group was given free access to drinking water that contained 0, 10, 50, and 100 mg/L NaAsO(2) from gestation day 6 (GD 6) until postnatal day 42 (PND 42). Once pups were weaned, they started to drink the same arsenic (As)-containing water as the dams. The level of malondialdehyde in 100 mg/L As-exposed pup's brain on PND 0 and cortex on PND 28 and 42 were significantly higher than in the control group (p < 0.05). Reduced glutathione (GSH) levels showed a clear decreasing trend in pup's cortex and hippocampus on PND 42. Activity of acetylcholinesterase was significantly higher in 100 mg/L As-exposed pup's hippocampus than in control group on PND 28 and 42. mRNA expression of glutamate decarboxylase (GAD(65) and GAD(67)) in 100 mg/L As-exposed pup's cortex or hippocampus on PND 28 and 42 were significantly higher than in control (p < 0.05). These alterations in the neurotransmitters and reduced antioxidant defence may lead to neurobehavioral and learning and memory changes in offspring rats.

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Section: Introductionmentioning

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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“…The extrahepatic manifestations of chronic arsenic ingestion are well known. Peripheral neuropathy is an important clinical syndrome (Chhuttani et al, 1967) and the finding of nerve conduction defects and the reduction of deep reflexes are suggestive of the demyelination seen in patients showing high levels of hepatic arsenic and may be further proof of arsenic poisoning.…”

Section: Discussionmentioning

confidence: 99%

Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India.

Datta¹,

Mitra²,

Chhuttani³

et al. 1979

Gut

103

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SUMMARY Estimates were made of the arsenic concentration in liver specimens from nine patients having idiopathic portal hypertension (IP), and in four livers these were found to be significantly higher than those in patients with cirrhosis and in control subjects. The splenovenogram revealed extensive portosystemic collateral circulation. Corrected sinusoidal pressure and blood flow studies showed higher levels in four patients than in normal subjects. Microscopic examination of liver tissues revealed periportal fibrosis. The higher hepatic arsenic levels that were found were due to the inadvertent drinking of water contaminated with arsenic, adulterated opium, and indigenous medicines. A history of opium intake was not forthcoming but two patients had drunk water contaminated with arsenic and two others had taken bhasams (Ayurvedic medicines prepared by repeated oxidation of ores). Though the aetiology of idiopathic portal hypertension is not known, it is possible that arsenic intake may be one of the factors.Idiopathic portal hypertension (IP) has recently been recognised as a new entity (Ramalingaswami et al., 1962;Boyer et al., 1967;Basu Mallik et al., 1967;Sama et al., 1971;Datta, 1975;Datta, 1976a). In this condition haematemesis and splenic enlargement are common features, and solenovenographic studies reveal collaterals in 80% of cases. The aetiology of the syndrome is unknown and it has been suggested that there may be several causes (Datta, 1975;Mahajan and Datta, 1976 Received for publication 27 February 1979 Methods SUBJECTSThe livers of nine patients with idiopathic portal hypertension (IP) and seven with cirrhosis were investigated for their content of arsenic. A piece of liver (about 2 g) was obtained by wedge biopsy at laparotomy in six patients and the same quantity from necropsy in three patients. The gross and microscopic examination of 18 patients who showed no evidence of hepatic disease and who died from non-hepatic causes served as controls in our studies.Nine liver tissues were obtained from newborn infants. In addition, 105 livers were obtained through

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“…Arsenic reacts with an essential thiol, inactivating one component of the pyruvate and alpha-glutarate oxidase systems of enzymes. The site of toxicity is intracellular, causing axonal changes [24,25], and fragmentation of myelin occurs after axonal degeneration takes place [26]. Sensory fibers are affected before motor fibers, and distal fibers are attacked before proximal portions [27].…”

Section: Disturbance Of Memory and Behaviormentioning

confidence: 99%

Occupational Neurology

Feldman¹

2015

Handbook of Clinical Neurology

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Arsenical neuropathy

Cited by 59 publications

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Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India.

Occupational Neurology

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