In vitro effects of selenite and mercuric chloride on liver thiobarbituric acid–reactive substances and non-protein thiols from rats: Influences of dietary cholesterol and polyunsaturated and saturated fatty acids

Abstract

Objective We measured the in vitro effects of mercuric chloride (Hg 2+) and selenite (Se 4+) on hepatic 2-thiobarbituric acid–reactive substances (TBARS) and non-protein sulfhydryl (NPSH) levels of rats fed diets enriched with polyunsaturated or saturated fatty acids with and without cholesterol. Methods Male Wistar rats (21 d old) were assigned to one of four groups and fed diets containing 20% soybean oil, 20% soybean oil plus 1% cholesterol, 20% coconut oil, or coconut oil plus 1% cholesterol. After the feeding period (6 wk), body weight gain was equal in all groups. TBARS levels and NPSH content were measured after in vitro exposure to mercuric chloride (100 μM) and sodium selenite (25 μM) for 1 h. Results The lipid peroxidation, measured as TBARS levels in the control group, were statistically higher in hepatic homogenates of rats fed diets containing soybean oil than in groups fed coconut oil ( P = 0.009). However, cholesterol supplementation did not change TBARS levels. Selenite alone did not modify TBARS production, whereas mercury alone significantly increased TBARS levels. Moreover, Se 4+ protected against mercury-induced lipid peroxidation only in rats fed diets containing coconut oil. In the control group, dietary fat acids did not change NPSH levels. Selenite produced higher oxidative effects toward NPSH content, whereas Hg 2+ decreased NPSH levels only in liver from rats fed diets containing soybean oil. NPSH levels were higher after concomitant exposure to Se 4+ and Hg 2+ chloride that after exposure to Se 4+ alone, suggesting an interaction between Hg 2+ and Se 4+. Catalase activity was higher in animals fed diets containing soybean oil. Dietary cholesterol decreased glutathione peroxidase activity. Conclusion Together these results indicated that the protective effect of Se 4+ against mercury-induced lipid peroxidation depends on dietary fat saturation.