Effects of Dietary α‐Tocopherol and β‐Carotene on Lipid Peroxidation Induced by Methyl Mercuric Chloride in Mice

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Abstract
Exposure of male CBA mice to methyl mercuric chloride, CH3HgCl, (10–40 mg/1 in drinking water) for 2 weeks resulted in dose-related Hg deposition and enhanced lipid peroxidation in liver, kidney and brain. Mice were fed well-defined semisynthetic diets containing different levels of α-tocopherol (10, 100 or 1000 mg/kg) or β-carotene (1000, 10000 or 100000 IU/kg) for four weeks, two groups on each diet. The concentrations of α-tocopherol and β-carotene used corresponded to deficient, normal and high levels. During the last two weeks, one group on each diet was given 40 mg CH3HgCl/1 of drinking water. High dietary α-tocopherol protected against CH3HgCl induced hepatic lipid peroxidation, whereas the α-tocopherol deficient diet further enhanced CH3HgCl induced hepatic lipid peroxidation. Similar, though statistically non-significant effects occured in the kidneys, α-Tocopherol did not protect against CH3HgCl induced lipid peroxidation in the brain. Excess dietary β-carotene further enhanced CH3HgCl induced lipid peroxidation in liver, kidney and brain. CH3HgCl significantly decreased the activity of total glutathione peroxidase (T-GSH-Px) and Se-dependent glutathione peroxidase (Se-GSH-Px) in the kidneys in all dietary groups. High dietary α-tocopherol enhanced the activity of Se-GSH-Px in liver and kidney compared to the activity in mice fed the normal level of α-tocopherol. This occured in mice exposed to CH3-HgCl as well as in unexposed mice, and the difference between CH3HgCl exposed and unexposed mice was not diminished. High dietary α-tocopherol increased the activity of both Se-GSH-Px and T-GSH-Px in the brain of CH3HgCl-exposed mice. The dietary level of β-carotene did not affect the activity of the two enzymes in the organs investigated.