Mercury adverse renal effects

Analysis of the tubular enzyme N-acetyl-p-D-glu-cosaminidase appears to be particularly effective in detecting early evidence of adverse renal effects from mercury [119,120]. In an extensive cross sectional examination of chloralkah workers exposed to mercirry at air concentrations around 25 pg/m , Langworth et al. [121] noted a significant correlation and dose-response relationship between urinary excretion of mercury and... 

Biochemical indicators of possible renal dysfunction (increased urinary NAG levels, and elevated porphyrins) have been associated with increased urinary levels of mercury (Rosenman et al. 1986 Wada et al. 1969 Woods 1996). Functional indicators of adverse neurological effects (reduced nerve conduction velocity, prolonged nerve latency, increased tremor frequency, increased reaction time, reduced hand-eye coordination, and performance on memory and verbal intelligence tests) have also been correlated with increased urinary levels of mercury (Levine et al. 1982 Piikivi et al. 1984 Smith et al. 1970, 1983 Verberk et al. 1986 Vroom and Greer 1972 Williamson et al. 1982). Decreased nerve conduction velocity has been correlated with increased tissue levels of mercury (Shapiro et al. 1982). These biomarkers are not specific for mercury and may be induced by exposure to other metals and... 

Studies from New Zealand and the Faroe Island indicate that adverse effects in children can be correlated with maternal hair levels as low as 10-20 pg/g [44]. Mercury analyses conducted on a single human hair can be used to monitor daily variations in methyl mercury exposure among fish eaters [45,46], and have been utilized to track maternal fish consumption and risk of preterm delivery [47]. Other investigators [48] have utilized measurements of total mercury in hair, toenails and urine to assess exposures in a group of non-occupationally exposed women in relation to renal tubular effects. 

Chronic-Duration Exposure and Cancer. Occupational exposure to metallic mercury vapors has been reported to result in adverse cardiovascular, gastrointestinal, renal, ocular, immunological, and reproductive health effects (Barregard et al. 1988, 1990 Bencko et al. 1990 Bidstrup et al. 1951 Buchet et al. 1980 Cardenas et al. 1993 Cordier et al. 1991 Danziger and Possick 1973 Ehrenberg et al. 1991 ... 

D-penicillamine is so named because it was first isolated as an amine, from the degradation products of penicillin by Abraham et al [87]. Later studies showed the characteristic chemical behavior of D-penicillamine which involve three types of reactions, formation of disulphide links, formation of thiazolidine rings, and formation of metal complexes and chelates [67]. It was first used in 1956 in the treatment of Wilson s disease [88]. D-penicillamine has since been used in the treatment of many diseases, such as cystinuria [89], rheumatoid arthritis [90-92], systemic sclerosis [93], primary bdiary cirrhosis [94], heavy metal poisoning due to lead [95], cadmium [%], and mercury [97], and hyperviscosity syndrome [99]. In rheumatoid arthritis, D-peni-cdlamine has been widely accepted as an effective second line treatment. Despite of its effectiveness, it causes many adverse effects, such as skin rashes [99,100], taste abnormalities [100,101], hepatic dysfunction [102-104], gastrointestinal toxiciiy [99,105], proteinuria [100,106], hematuria [107, 108], thrombocytopenia [92, 109], aplastic anemia [110], lupus-like syndrome [111, 112], Goodpasture s-tike pulmonary renal syndrome [113-115], vasculitis [116,117], myasthenia gravis [118-122], polymyositis [123, 124], and dermatomyositis [125]. 

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