Background And Objectives: Sevoflurane is a fluorinated ether with low blood solubility and biotransformed by an oxidative enzymatic liver system involving cytochrome P450 2E1. Lipid peroxidation occurs during ethers biotransformation process under action of cytochrome P450, a possible mechanism for liver and kidney toxicity promoted by such compounds. This study aimed at determining the levels of substances reactive to thiobarbituric acid (TBARS), as an index for lipid peroxidation in sevoflurane-treated rats, previously treated or not with isoniazid, enzymatic inducer of cytochrome P450 2E1.
Methods: Forty two male Wistar rats were randomly distributed in 4 groups receiving respectively: G1 - 1 L.min-1/60 minutes of 100% oxygen for 5 consecutive days; G2 - 4% sevoflurane in 1 L.min-1/60 minutes of 100% oxygen for 5 consecutive days; G3 - intraperitoneal isoniazid (50 mg.kg-1/day) for 4 consecutive days and then treated as G1; G4 - intraperitoneal isoniazid (50 mg.kg-1/day) for 4 consecutive days and then treated as G2. Animals were sacrificed 12 hours after the last treatment, plasma was collected for TBARS analysis and the liver left lobe and both kidneys were removed for histological evaluation.
Results: Results have shown increased TBARS levels in G3 and G4, with mild increase in G2. Histological evaluation has revealed focal liver necrosis in rats pretreated with isoniazid (G3).
Conclusion: Sevoflurane has promoted lipid peroxidation only when associated to isoniazid.
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