Abstract

Studies ranging from epidemiological to molecular suggest that dietary antioxidants protect against chronic diseases. The hypothesis was investigated that hamster kidney homogenates are better protected against induced oxidative damage after animals were fed a purified vitamin E deficient diet supplemented with 30 international units (IU) vitamin E/kg (30 IU diet) than fed the minimum required 3 IU vitamin E/kg (3 IU diet). The addition of 200 mg (+)-catechin to the 3 IU diet may offer protection. The effects of dietary (+)-catechin and α-tocopherol on tissue oxidizability were investigated by measuring (i) fluorescent products in lipid extracts, (ii) heme protein oxidation and (iii) heme destruction. A rapid initial increase of oxidation markers was measured over the 4 h incubation period for iron + ascorbate induced oxidation and a constant increase for lipoxygenase catalyzed products. Analysis of covariance over time and comparison at specific incubation times showed that iron + ascorbate induced homogenates from hamsters fed the 30 IU diet generated less fluorescent products and oxidized heme proteins than homogenates from the 3 IU or the 3 IU plus (+)-catechin fed animals. Incubation with lipoxygenase produced more lipid fluorescent products and heme protein oxidation in the 3 IU than in the 30 IU vitamin E group. In conclusion, supplementary dietary vitamin E but not supplementary (+)-catechin in a diet containing the minimum requirement of vitamin E for the species enhances oxidative resistance of kidney tissue.

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