Are Developmental Changes in Methylmercury Metabolism and Excretion Mediated by the Intestinal Microflora?

Abstract

Methylmercury, unlike mercuric mercury, is rapidly and almost completely absorbed from the mammalian gut, hence the body burden of mercury after exposure to methylmercury is related to the rate of mercury excretion. By comparison to adult mice, sucking mice excrete very little mercury after methylmercury exposure until the 16th-18th postnatal days, when there is an abrupt increase in fecal mercury excretion coinciding with the time of weaning. Several explanations of this developmental change in mercury elimination can be proposed, including an increase in biliary secretion of mercury compounds at weaning, changes in binding of mercury to gut contents or ohanges in the rate of demethylation of methylmercury by the intestinal microflora. It is probable that more than one of these factors are responsible but evidence is presented here to support the view that bacterial demethylation plays an important role. It is known that the majority of mercury in feces, after methylmercury exposure of adult animals, is in the mercuric form and that there is an increase in the amount of mercuric mercury in young mice at weaning when the rate of mercury elimination increases. The major changes in intestinal flora which occur during weaning are reflected in an increase in the ability of the gut contents of weaned mice to demethylate methylmercury in vitro. Similarly, feces from neonatal and preweaned human infants show negligible rates of methylmercury demethylation in vitro by comparison to weaned infants and adults. Further evidence for the implication of the gut flora in determining rates of mercury excretion has been obtained by modification of the gut flora by diet and antibiotics. We conclude that the conversion of methylmercury to the poorly absorbed mercuric mercury by the intestinal flora is a major factor determining excretion rate and therefore body burden of mercury after methylmercury exposure.