Hemolytic effects of sodium selenite and mercuric chloride in human blood.

Many works have reported the interaction between selenium and mercury in the mammalian body and that chalcogen seems to have a protective effect against mercury toxicity. The aim of this study was to investigate the hemolytic effects of sodium selenite and/or mercuric chloride in human blood under in vitro conditions. For this, total venous blood from healthy subjects (males and females) was heparinized and incubated at 37 degrees C for 90 min with different concentrations of sodium selenite and/or mercuric chloride. The hemolytic effects of compounds were evaluated by measuring plasma hemoglobin concentration after centrifugation. In addition, 2-thiobarbituric acid reactive substances (TBARS) from plasma and erythrocytes, as well as erythrocyte nonprotein thiols (NPSH), were also evaluated in order to investigate molecular mechanisms related to selenite- or mercury-induced hemolysis. Mercuric chloride and sodium selenite, alone (400 microM), promoted a small in vitro hemolytic effect in human erythrocytes. However, when blood was exposed to both compounds (200 microM of each), there was an extremely high synergistic hemolytic effect. The exposure of blood to sodium selenite (400 microM), mercuric chloride (400 microM), and both compounds (200 microM each) did not alter erythrocyte TBARS levels. Sodium selenite presented a high oxidant effect toward erythrocyte NPSH; however, this effect was inhibited by mercuric chloride. The current results point to a synergistic hemolytic effect of sodium selenite and mercuric chloride in human blood, suggesting new understanding on the selenium-mercury antagonism. Moreover, this observed hemolysis seems to be not related to lipoperoxidation or thiol depletion.

Profile of nonprotein thiols, lipid peroxidation and delta-aminolevulinate dehydratase activity in mouse kidney and liver in response to acute exposure to mercuric chloride and sodium selenite.

The effects of mercury (Hg(2+)) and selenite (Se(4+)) on delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, 2-thiobarbituric acid reactive substances (TBARS) and nonprotein sulfhydryl content (NPSH) in mouse kidney and liver were investigated. Male mice were given a single i.p. injection of Hg(2+) and/or Se(4+) (25 micromol/kg) and were killed at 6, 12, 24 and 48 h after treatment. Hg(2+) inhibited renal delta-ALA-D at 6 and 12 h after treatment. Se(4+) abolished the inhibitory effect of mercury on renal delta-ALA-D at 12 h after treatment. Renal and hepatic NPSH content decreased after Hg(2+) exposure and selenite inhibited, at least in part, the Hg-induced oxidation of renal and hepatic NPSH. Se(4+) and Hg(2+), when injected alone, did not alter hepatic or renal TBARS levels; however, simultaneous exposure to these compounds increased hepatic and renal TBARS levels at 12 and 48 h after treatment, respectively. Present results suggest that selenium abolishes the interaction of Hg(2+) with sulfhydryl groups of protein and nonprotein sources.