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

Toxicology. 2003 Mar 3;184(2-3):179-87. doi: 10.1016/s0300-483x(02)00576-0.

Abstract

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.

MeSH terms

  • Animals
  • Kidney / drug effects
  • Kidney / enzymology
  • Kidney / metabolism*
  • Lipid Peroxidation / drug effects*
  • Liver / drug effects
  • Liver / enzymology
  • Liver / metabolism*
  • Male
  • Mercuric Chloride / antagonists & inhibitors*
  • Mercuric Chloride / pharmacology*
  • Mercuric Chloride / toxicity
  • Mice
  • Porphobilinogen Synthase / metabolism*
  • Sodium Selenite / pharmacology*
  • Sulfhydryl Compounds / metabolism*
  • Thiobarbituric Acid Reactive Substances / metabolism

Substances

  • Sulfhydryl Compounds
  • Thiobarbituric Acid Reactive Substances
  • Mercuric Chloride
  • Porphobilinogen Synthase
  • Sodium Selenite