Revision of reciprocal action of mercury and selenium.

Diverse forms of mercury (Hg) have various effects on animals and humans because of a variety of routes of administration. Inorganic mercury (iHg) binds to thiol groups of proteins and enzymes in one's body or is methylated by microorganisms. Organic form of Hg, contrary to the iHg, is more stable but may be demethylated to Hg2+ in the tissue of intestinal flora. Selenium (Se) also occurs in a variety of chemical forms in one's body but both of these elements behave very differently from one another. Mercury binding to selenide or Se-containing ligands is a primary molecular mechanism that reduces toxicity of Hg. Complexes formed in such a way are irreversible, and thus, biologically inactive. Se deficiency in a human body may impair normal synthesis of selenoproteins and its expression because expression of mRNA may be potentially regulated by the Se status. This paper provides a comprehensive review concerning Hg-Se reciprocal action as a potential mechanism of protective action of Se against Hg toxicity as well as a potential detoxification mechanism. Although interactions between Hg-Se have been presented in numerous studies concerning animals and humans, we have focused mainly on animal models so as to understand molecular mechanisms responsible for antagonism better. The review also investigates what conclusions have been drawn by researchers with respect to the chemical species of Se and Hg (and their relationship) in biological systems as well as genetic variations and expression and/or activity of selenoproteins related to the thioredoxin (thioredoxin Trx/TrxR) system and glutathione metabolism. Int J Occup Med Environ Health 2018;31(5):575-592.

An acute mercuric mercury poisoning: chemical speciation of hair mercury shows a peak of inorganic mercury value.

A woman ingested a dose of sublimate (approximately 0.9 g) in an attempted suicide. She survived and recovered in response to a combination of therapies including chelate (BAL) therapy, plasma exchange, haemodialysis and peritoneal dialysis. Serum inorganic mercury concentration, urinary inorganic mercury excretion and hair inorganic and organic mercury and selenium concentrations, along the length from the scalp to the distal part, were measured. Longitudinal analysis of hair, revealed a peak in inorganic mercury corresponding to the time of mercury ingestion. Organic mercury and selenium in the hair had different patterns of longitudinal variation from that of inorganic mercury. The biological half-life (23.5 d) of serum inorganic mercury levels was in good agreement with values previously reported in the literature.

Synergism of methylmercury and selenium producing enhanced antibody formation in mice.

Mice fed 1, 5, and 10 ppm methylmercury plus 6 ppm selenium for 10 wk had a significant increase in antibody synthesis. Since methylmercury singly depresses antibody synthesis and the response was greater than that produced by selenium alone, synergism between methylmercury and selenium occurred. In this case, the synergism is considered to be advantageous to a host, while exposure by other combinations of environmental contaminants may be detrimental. Mercury concentrations in the kidney were markedly elevated when methylmercury and selenium were administered simultaneously compared to when methylmercury was given without selenium supplement. These results indicate that data collected from individual pollutants may not be of value in predicting responses to multiple exposure.

The influence of selenium on the level of mercury and metallothionein in rat kidneys in prolonged exposure to different mercury compounds.

Mercuric chloride, phenylmercuric chloride, ethylmercuric chloride /0,23 mg Hg/kg/ and methylmercurycyan guanidine /0,46 mg Hg/kg/ were orally administered to rats every second day for 14 weeks. The same doses of the above mentioned mercury compounds were administered alternately with sodium selenite /0,18 mg Se/kg/ to parallel groups of rats at the same time. The level of total and inorganic mercury and of metallothionein was determined. All mercury compounds increased the level of metallothionein in rat kidneys. In rats which received only selenium the level of metallothionein was twice lower in the kidneys in relation to the physiological level of this protein. Selenium eliminated the stimulation of biosynthesis of metallothionein by mercury.

The effect of selenium on the brain uptake of methylmercury.

Twenty-four h after the subcutaneous administration of 0.5 mumoles selenite labelled with 75Se to rats of 200 g body weight, the retention of selenium at the injection site was significantly increased by the presence of equimolar amounts of methylmercury in the injection solution. The retention of Me203HgCl was not affected by the presence of selenite. The most significant shift caused by interaction was a decrease in the blood content and an increase in the brain content of 203Hg. The brain content of 75Se was also increased to a lesser extent. The shift in the distribution--which was the same whether the two metals were injected at the same site or separately--continuously decreased from 6-48 h. The same interaction pattern was observed when methylmercury and selenite were administered by gastric gavage and differences in distribution increased when the dose was increased from 1.25 mumoles/kg to 2.5 mumoles/kg. The increase in the brain content of mercury caused by selenite was not restricted to simultaneous administration and occurred when selenite was given 2-7 days after methylmercury.

Factors involved in heavy metal poisoning.

The heavy metals include at least 40 elements but cadmium, lead, and mercury have been most extensively studied. The biological properties of heavy metals are discussed in terms of three important characteristics: the ability to form, irreversibly, complexes and chelates with organic ligands; the properties to form organic-metallic bonds; and the potential to undergo oxidation-reduction reactions. The formation of complexes and chelates within the body is shown to influence greatly the dynamics of transport, distribution, and excretion of several important metal cations. The excretion of uranium is influenced by acid-base balance in the body because uranium forms complexes with bicarbonate anions that are filtered by the kidneys. The biliary excretion of methylmercury depends on the formation of small molecular weight complexes with sulfur-containing amiono acids and the peptides in the liver. The degree of enterohepatic recirculation of a variety of heavy metals appears to depend on the chemical nature of the bilary complexes. The oxidation of elemental to divalent ionic mercury is the crurial step in the retention and tissue deposition of inhaled mercury vapor. That the oxidation process is, at least in part, catalyzed by the enzyme, catalase, explains the effects of ethanol, aminotriazole and the state of acatalasemia on the metabolism of inhaled vapor in man and animals. The formation of covalent bonds between metal cations and the carbon atom usually greatly modifies the biological properties of the metal. Methylarsenic and methylmercury compounds both differ from the inorganic forms in accumulation in animals.