Mercury renal toxicity

Talmage, S.S. and B.T. Walton. 1993. Food chain transfer and potential renal toxicity of mercury to small mammals at a contaminated terrestrial field site. Ecotoxicology 2 243-256. 

Several adulterants added to nonherbal supplements, vitamins, and herbal medicine preparations can cause renal dysfunction and renal failure. Aristolochic acid is used as a herbal remedy for weight loss and has been reported to cause Chinese herb nephropathy characterized by extensive interstitial fibrosis with tubular atrophy and loss. Herbal medicine preparations produced in South Asia contain potentially harmful levels of lead, mercury, and/or arsenic which can lead to renal toxicity. 

Although there is experimental evidence of nephrotoxicity from methyl mercury in animals, no reports of human renal toxicity from methyl mercury exposure have been identified [14]. 

The results from a number of studies show renal toxicity in workers chronically exposed to mercury vapor (Barregard et al. 1988 Bernard et al. 1987 Buchet et al. 1980 Cardenas et al. 1993 Danziger and Possick 1973 Ehrenberg et al. 1991 Kazantzis et al. 1962 Langworth et al. 1992b Piikivi and Ruokonen 1989 Roels et al. 1982 Stewart et al. 1977 Stonard et al. 1983 Sunderman 1978 Tubbs et al. 

Several investigators have suggested that the renal toxicity exhibited after administration of organic forms of mercury (e.g., methylmercury) may actually result from the in vivo metabolism of this form to... 

The data indicate that zinc-induced metallothionein binds mercury in the renal cortex and shifts the distribution of mercury from its site of toxicity at the epithelial cells of the proximal tubules. Thus, the renal content of mercury is increased, yet less is available to cause toxicity. In contrast, the renal toxicity of mercuric chloride is exacerbated in zinc-deficient animals (Fukino et al. 1992). In the zinc-deficient state, less mercury accumulates in the kidneys, but the toxicity is greater. The mechanism of the protection appears to involve more than simply a redistribution of renal mercury, because in the absence of mercury exposure, zinc deficiency increases renal oxidative stress (increased lipid peroxidation, decreased reduced ascorbate). When mercury exposure occurs, the oxidative stress is compounded (increased lipid peroxidation and decreased glutathione and glutathione peroxidase). Thus, zinc appears to affect the biochemical protective mechanisms in the kidneys as well. 

Chan HM, Satoh M, Zalups RK, et al. 1992. Exogenous metallothionein and renal toxicity of cadmium and mercury in rats. Toxicology 76(1) 15-26. 

Zalups RK, Cherian MG. 1992. Renal metallothionein metabolism after a reduction of renal mass II. Effects of zinc pretreatment on the renal toxicity and intrarenal accumulation of inorganic mercury. Toxicology 71(1-2) 103-117. 

Additional studies or pertinent information that lend support to this MRL Renal toxicity has been observed in other intermediate-duration oral studies on rats and mice exposed to inorganic mercury (Carmignani et al. 1992 Jonker et al. 1993a NTP 1993), as well as case reports on humans ingesting inorganic mercury for acute and chronic durations (Afonso and deAlvarez 1960 Davis et al. 1974 Kang-Yum and Oransky 1992 Nielsen et al. 1991 Pesce et al. 1977). 

Treatment of mercury poisoning requires removal from the exposure followed by chelation. New chelation methods that use Ai-acetylpenicillamine, 2,3,-dimercaptopropane-l-sulfonate, or di-mercaptosuccinic acid replaced early uses of British Anti-Lewisite and D-penicillamine (Marsh 1985). British Anti-Lewisite (2,3-di-mercaptopropanol) increases cerebral organic mercury in some cases (Goetz 1985). Ethylenediaminetetraacetic acid does not displace mercury and worsens the renal toxicity of mercury (Goetz 1985). 

Endo et al. (2003) investigated the renal toxicity in rats caused by a single oral administration of mercury-contaminated boiled whale livers that contained both the inorganic mercury and dimethylmercury. The concentration of mercury in the rat kidney increased markedly after the dose, so also the urinary excretion of A-acetyl-beta-D-glucosanidase, albumin, and sodium. Also, the concentrations of creatinine, potassium, and phosphorus in the serum and the lactate dehydrogenase activity increased. The study showed that the renal toxicity was caused by inorganic mercury and that the human consumption of boiled whale liver could cause acute intoxication from contaminated inorganic mercury. 

Endo, T., K. Haraguchi, and M. Sakata. 2003. Renal toxicity in rats after oral administration of mercury — contaminated boiled whale livers marketed for human consumption. Arch. Environ. Contam. Toxicol 44(3) 412-16. 

Kojima, S., H. Shimada and M. Kiyozumi. 1989. Comparative effects of chelating agents on distribution, excretion and renal toxicity of inorganic mercury in rats. Res. Commun. Ghent. Pathol Pharmacol 64(3) 471-84. 

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). 

Dieter MP, Boorman GA, Jameson CW, Eustis SL, Uraih LC (1992) Development of renal toxicity in F344 rats gavaged with mercuric chloride for 2 weeks, or 2,4,6,15, and 24 months. J Toxicol Environ Health 36 319-340 Druet P (1991) Effect of inorganic mercury on the immune system. In Suzuki T, Imura N, Clarkson TW (eds) Advances in mercury toxicology. Plenum, New York, pp 395-409... 

The most common toxic metals in industrial use are cadmium, chromium, lead, silver, and mercury less commonly used are arsenic, selenium (both metalloids), and barium. Cadmium, a metal commonly used in alloys and myriads of other industrial uses, is fairly mobile in the environment and is responsible for many maladies including renal failure and a degenerative bone disease called "ITA ITA" disease. Chromium, most often found in plating wastes, is also environmentally mobile and is most toxic in the Cr valence state. Lead has been historically used as a component of an antiknock compound in gasoline and, along with chromium (as lead chromate), in paint and pigments. 

Concentrations of V, Mn, Fe, Cr, Co, Cu, Zn, As, Se, Mo, Ag, Cd, Tl, Hg, Pb, and organic mercury (Org-Hg) were determined in liver, kidney, and muscle of healthy Caspian seals (Phoca caspica) collected in 1998. These concentrations were compared with those of seals infected with canine distemper virus (CDV) found stranded along the coastal areas in 2000 (Table 1). Concentrations of toxic elements (As, Ag, Cd, Tl, Hg, Pb, and Org-Hg) in Caspian seals stranded in 2000 were comparable or lower than those of samples collected in 1998 and in other pinnipeds. Thus it may be inferred that these elements were not the causative agents in the deaths of the seals. In contrast, concentrations of Zn and Fe were much higher in diseased Caspian seals than those in other pinnipeds. Zinc concentrations in all tissues of Caspian seals also increased during 1993-2000. Furthermore, negative correlations were found between blubber thickness and hepatic and renal Zn concentrations. These results imply the disturbance... 

Information concerning the effects of selenium in man is lacking and it is doubtful whether administration of selenium in man has any effect on the toxicity of mercuric mercury. However, mercury and selenium were found in the cellular lysozomes in renal tubular cells in two patients with inorganic mercury poisoning [143]. 

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