Vitamin E deficiency and photosensitization of electron‐transport carriers in microsomes

introduction Materials and methodsCellular and membrane damage mediated by endogenous chromophores, in the presence of visible light and oxygen has been reported in [l-6].In particular, the aerobic illumination of rat liver microsomes with heterochromatic light (X > 400 nm) showed a preferential inactivation of NADPH-cytochrome P450-reductase and cytochrome P45O [5] with a strong correlation between cytochrome P4SO destruction and lipid peroxidation.Here, we used microsomal membranes isolated from both control and vitamin Edeflcient animals to determine how the lack of vitamin E in these membranes would affect the sensitivity of hemo-and flavoproteins and lipids to photodamage.Male Long-Evans rats (-100 g body wt) were purchased from Simonsen Labs.(Gilroy CA).Two different diets were from BioServ Inc. (Frenchtown NJ): Bio-Mix 1331 contained <l IU vitamin E/100 g; Bio-Mix 1332 had 21 IU vitamin E/100 g.Over 3 months a group of 8 rats (controls) were fed BioMix 1332 and another group of 8 rats (vitamin E-deficient animals) were fed BioMix 133 1.The vitamin E deficiency was estimated by red blood cell hemolysis [7]: vitamin E-deficient animals exhibited 93 f 3% hemolysis, compared to 10 f 3% hemolysis for controls.