Vitamin E as an index of tissue peroxidation: The effect of vitamin C deficiency and ischemia/reperfusion.

Abstract

Levels and turnover of vitamin E ($\alpha$-T) were studied in guinea pigs placed for three weeks on a diet containing a scorbutic level of vitamin C and either a low level (LE group) or a high level (HE group) of hexadeuterium-labelled vitamin E (d$\sb6$-RRR-$\alpha$-T acetate). The levels of vitamin C in the ten tissues analyzed declined very rapidly at rates that were the same in both the LE and HE groups, indicating that the level of dietary vitamin E had no effect upon tissue vitamin C levels. On the vitamin C deficient diet, the total $\alpha$-T (d$\sb0$- + d$\sb6$-$\alpha$-T) declined significantly over 21 days in the HE group in two tissues with high P-450 enzyme activity and in one tissue with a high partial pressure of oxygen, whereas on a vitamin C-sufficient diet with the same concentration of vitamin E the levels of total $\alpha$-T remained steady in the same tissues. In the LE "scorbutic" group, the total $\alpha$-T declined only in heart and kidney, whereas in the vitamin C-sufficient LE group there was a decline of total $\alpha$-T in all tissues analyzed except brain. The results show that in guinea pigs, at least, vitamin C is indispensable for proper uptake of vitamin E from the gut and absorption into tissues. Changes of vitamin E levels also were studied in six anatomical regions of the brain of rats subjected to controlled ischemia/reperfusion. Analysis showed that ischemia/reperfusion caused statistically significant losses of vitamin E in all regions, except the pons-medulla, and the extent of loss correlated well with the previously determined deterioration of the blood-brain barrier in the corresponding regions. (Abstract shortened by UMI.)