We examined the effect of mercury (Hg) associated with dental amalgam fillings on biomarkers of renal and oxidative stress in children between the ages of 5–15.5 years. Our data provide evidence that low exposure to Hg from dental amalgam fillings exerts an effect on kidney tubular functions in children. Oxidative stress may have played a role in this mechanism. The results of this study would also suggest that urinary NAG is the most sensitive of all the investigated renal biomarkers.
This review describes the current understanding and the mechanisms involved by different forms of mercury in eliciting their toxicity in kidney along with the knowledge of major intracellular reductant that plays important role in the mitigation of mercury toxicity for the maintenance of homeostasis within the body of living organisms. Mercury toxicity has the ability to produce a variety of deleterious health effects, ranging from single to multiple target effects inside the body of living organisms.
Heavy metals are known to induce functional alterations in kidney mitochondria, this damage plays a central role in the mercury-induced acute renal failure. In fact, mercury causes rapid and dramatic changes in the membrane's ionic permeability in such a way that a supra load of mitochondrial Ca(2+) occurs. As a consequence, the phenomenon of permeability transition takes place.
A close link between stress protein up-regulation and oxidative damage may counteract nephrotoxicity induced by toxic metals. As biochemical indicators of oxidative stress we detected reactive oxygen species ROS and nitrogen species RNS. Our results clearly demonstrated that mercury increases ROS and RNS levels. These findings are corroborated by evident mitochondrial damage, apoptosis or necrosis.
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