Lipid peroxidation and urinary excretion of vitamin E in rats submitted to an immunological inflammatory process

Inflammation is a protective physiologic response, generally controlled by the organism at the injury site. Vitamin E is the most important antioxidant in the lipid phase present in nature and acts by interrupting the chain reaction produced by free radicals. The objective of this study was to evaluate the effect of inflammation on vitamin E levels and lipid peroxidation in rats. Forty Wistar rats (four groups of 10 rats each) were studied over a period of 15 days. Two substances inducing the inflammatory process were parenterally administered, anti-rat basement membrane serum (ABMG) and Freund's complete adjuvant (FAG). Lipid peroxidation levels in hepatic and renal tissue and in plasma and urine were analyzed and compared with the control (CG). Vitamin E was determined by HPLC and lipid peroxidation by quantification of thiobarbituric acid reactive substances (TBARS). ABMG produced more (p < 0.05) TBARS in renal and hepatic tissues (0.7 +/- 0.11 and 1.28 +/- 0.27 nmol/g protein, respectively) compared to CG (0.65 +/- 0.81 and 0.69 +/- 0.13 nmol/g protein). Analysis of TBARS in urine did not show statistically significant differences between the experimental groups and the control. Vitamin E levels in the hepatic tissue of ABMG and FAG (40.7 +/- 10.04 and 44.26 +/- 20.24 micrograms/g tissue) were higher than in CG (22.37 +/- 8.20 micrograms/g tissue) while in kidney tissue and plasma these values were lower (P < 0.05). Renal excretion was increased (P < 0.05) in the group that received anti-rat basement membrane serum (22.39 +/- 0.11 mmol/mL) compared to CG (0.56 +/- 0.056 mmol/mL). We conclude that the acute inflammatory process causes important alterations in the metabolism of vitamin E and lipid peroxidation leading to a significantly increased excretion of this vitamin in the urine.