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Mercury urinary biomarkers

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... [Pg.557]

Woods JS, Bowers MA, Davis HA. 1991. Urinary porphyrin profiles as biomarkers of trace-metal exposure and toxicity Studies on urinary porphyrin excretion patterns in rats during prolonged exposure to methyl mercury. Toxicol Appl Pharmacol 110(3) 464-476. [Pg.656]

Woods JS, Martin MD, Naleway CA, Echeverria D. Urinary porphyrin profiles as a biomarker of mercury exposure Studies on dentists with occupational exposure to mercury vapour. J Toxicol Environ Health 1993 40 235-46. [Pg.1235]

Urinary pesticide concentrations (glyphosate, 2,4-D, and chlorpyifos) Organic and inorganic mercury used as biomarker for methylmercury exposure... [Pg.746]

Roels et al. [38] points out that the analytical techniques identified in Table 1 are not easily available and are not well-suited for routine biomonitoring of occupational or environmental exposures. Instead, indirect biomarkers such as urinary enzymes are often used with success to evaluate mercury exposure and injury. Zalups [35] identifies numerous methods used to detect renal tubular injury induced by mercury. These methods monitor the urinary excretion of enzymes that leak from injured and necrotic proximal tubules, including lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and N-acetyl-P-D-glucosaminidase (NAG). Although advocated by Zalups (35) to detect renal tubular injury, Mason et al. (48) questions the practical utility of such biomarkers in occupational surveillance. According to Mason et al., small increases in NAG, leucine... [Pg.535]

The distinctive porphyrin patterns associated with exposure of animals to lead, mercury, and arsenic, compared with the normal profile, are depicted in Fig. 8. Changes in urinary porphyrin patterns associated with these and other metals offer promise as biomarkers of metal exposures and potential toxicity in humans from several perspectives. As biological responses to metal effects in target tissues, changes in porphyrin patterns are indicative of the internal concentration of metals in target tissues, and clear dose-response and time-related effects of metals with respect to development of porphyrin profile changes have been demonstrated in animal studies. These findings... [Pg.43]

The efficacy of urinary porphyrin profiles as a biomarker of exposures to metals other than lead in human populations is less well established. Studies on dentists with occupational mercury exposure have provided preliminary evidence of the potential utility of urinary porphyrin changes as a biomarker of low-level mercury exposure in human subjects (Woods et al. 1993), and further studies have demonstrated their efficacy as a measure of cumulative effects of mercury on specific tests of neurobehavioral function (Echeverria... [Pg.45]

Woods JS, Martin MD, Naleway GA, Echeverria D (1993) Urinary porphyrin profiles as a biomarker of mercury exposure studies in dentists with occupational exposure to mercury vapor. J Toxicol Environ Health 40 239-250 Yamanaka K, Hoshino M, Okamoto M, Sawamura R, Hasegawa A, Okada S (1990) Induction of DNA damage by dimethylarsine, a metabolite of inorganic arsenics, is for the major part likely due to its peroxyl radical. Biochem Biophys Res Gommun 168 58-64... [Pg.52]

Since mercuric mercury mainly accumulates in the kidney, Hg causes severe nephrophathy, characterized by extensive loss of proximal tubule function and viability (Ganote et al. 1975). The renal toxicity of Hg " can be estimated by increases in urinary levels of biomarker enzymes, such as lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, and y-glutamyltranspeptidase. Among these marker enzymes, alkaline phosphatase and aspartate aminotransferase are the most sensitive indicators, and lactate dehydrogenase is the most responsive marker to renal mercury toxicity (Dieter et al. 1992). [Pg.172]


See other pages where Mercury urinary biomarkers is mentioned: [Pg.816]    [Pg.342]    [Pg.352]    [Pg.353]    [Pg.194]    [Pg.35]    [Pg.36]    [Pg.46]   
See also in sourсe #XX -- [ Pg.624 ]




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