A histochemical study on some enzyme changes in the kidney, liver and brain after chronic mercury intoxication in the rat

Modulating effects of dietary fats on methylmercury toxicity and distribution in rats

“…To our knowledge, this is the first report on the effects of different types of dietary fats on target tissue retention and toxicity of MeHg in rats, although studies of acute and chronic toxicity of MeHg in rats have been well documented (Klein et al, 1972;Chang Verschuuren et al, 1976a,b,c;Planas-Bohne, 1978;Bogden et al, 1979;Munro et al, 1980;Kabuto, 1986;Vachhrajani and Chowdhury, 1990;Lin et al, 1996;Eto et al, 1997).…”

Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection

“…Exposure to mercurial compounds induces hepatotoxicity associated with oxidative stress [182][183][184][185], generating hepatocellular defects like hepatomegaly, centrilobular hepatic steatosis [186,187], decrease in the synthesis of hepatic coagulation factors [188][189][190][191][192] and diminution in the activity of metabolic enzymes [193]. EA reduces mercuric chloride damage, avoiding the generation of oxidative stress and diminishing the possibility of damage to liver cells [194,195].…”

Dietary fats altered nephrotoxicity profile of methylmercury in rats

“…In the rodent kidney, MeHg produced ultrastructural changes in pars recta epithelia of proximal tubules, consisting of occupational epithelial exfoliation, a modest increase in cellular cytoplasmic density, floccular degeneration of mitochondrial matrix material, and the loss of cristae and disruption of inner limiting membrane (Ware et al, 1975). Along with the ultrastructural damage, MeHg also inhibited a number of renal enzymes such as γ-glutamyl transpeptidase, glucose-6 phosphatase, alkaline phosphatase, ATPase, succinic dehydrogenase, δ-aminolevulinic acid synthetase and monoamine oxidase in exposed rodents (Chang et al, 1973;Fowler and Woods, 1977). The inhibition of renal δ-aminolevulinic acid synthetase, a rate-limiting enzyme in the heme biosynthetic pathway, occurred even prior to the onset of clinical changes in blood urea nitrogen, serum creatinine and overt neurological symptoms (Fowler and Woods, 1977).…”

“…In addition to the central and peripheral nervous system, the kidney is also a known target organ of mercury accumulation and toxicity in both animals (Folsom and Fishbein, 1972;Ohi et al, 1976;Yasutake et al, 1997;Zalups, 2000) and humans (Jalili and Abbasi, 1961;Kevorkian et al, 1972;Himeno et al, 1986;Barregard et al, 1988;Ohno et al, 2007;Johansen et al, 2007). The ultrastructural, histological, clinical, and biochemical changes associated with renal toxicity of MeHg have been well described (Chang et al, 1973;Ware et al, 1975;Fowler and Woods, 1977;Fair et al, 1985;WHO, 2000). In the rodent kidney, MeHg produced ultrastructural changes in pars recta epithelia of proximal tubules, consisting of occupational epithelial exfoliation, a modest increase in cellular cytoplasmic density, floccular degeneration of mitochondrial matrix material, and the loss of cristae and disruption of inner limiting membrane (Ware et al, 1975).…”