Abstract

Puromycin-treated apolipoprotein E (ApoE)-deficient mice were used to study lipid peroxidation (LPO) in the cochlea. Puromycin causes accelerated peroxidation of lipids and induces both inner ear and renal lesions in experimental animals presenting with abnormally high serum cholesterol. To prevent LPO, we used probucol, an effective inhibitor of LPO, and, simultaneously, also a lipid-lowering drug. The mice were given a single injection of the aminonucleoside of puromycin (25 mg/100 g). Polyclonal malondialdehyde and 4-hydroxynonenal antibodies were used to localize the LPO products. LPO products were mainly found in the stria vascularis of puromycin-treated mice. No LPO products were observed in the hair cells. LPO product immunoreactivity was clearly diminished in the animal group treated with both puromycin and probucol. In the cochlea of the ApoE-deficient mouse, puromycin affects mainly the stria vascularis due to the accelerated peroxidation of structural lipids. Probucol treatment prevented the formation of LPO products.

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