IMPACT OF VITAMIN-E SUPPLEMENT IN STANDARD LABORATORY-ANIMAL DIET ON MICROVASCULAR MANIFESTATION OF ISCHEMIA-REPERFUSION INJURY

Aimed at improving animal fertility and health, diets for farm and lab oratory animals have over the last few years been supplemented with in creasing amounts of the antioxidant vitamin E. We now demonstrate by i ntravital microscopy that feeding hamsters with a vitamin E-supplement ed ''standard'' rodent diet (60 ppm vitamin E) significantly reduces t he microvascular manifestations of ischemia/reperfusion injury when co mpared to animals fed a nonsupplemented diet. Postischemic leukocyte a dhesion to venular endothelium was reduced from 770 +/- 204 cells/mm(2 ) at 24 h after reperfusion in control animals on the nonsupplemented diet to 403 +/- 105 cells/mm(2) in animals on the ''standard'' rodent diet (means +/- SD, n = 7 animals per group, p < 0.01). Animals on the nonsupplemented diet showed a dramatic loss of capillary perfusion de nsity until 7 days after reperfusion (to 21 +/- 13% of preischemic bas eline values), whereas this loss was significantly attenuated (to 71 /- 12% of preischemic values, p < 0.01) in animals on the ''standard'' rodent diet. No difference in the extent of reperfusion injury was se en between animals on the ''standard'' rodent diet and animals on diet s with substantially higher vitamin E supplements (300 ppm-30.000 ppm) . Besides underscoring the benefit of vitamin E in reducing the extent of ischemia/reperfusion injury, this study raises the concern that vi tamin E supplements in ''standard'' laboratory animal diets may have a far-reaching impact on biomedical research by jeopardizing establishe d animal models of disease.