Twelve weanling male rats averaging 50 g were used in this study. One half of them were fed a vitamin E-deficient (E-def) diet and the remainder a vitamin E-sufficient (E-suff) diet. All animals were killed after a 4-week feeding period, and their liver mitochondria isolated. State 4 and state 3 oxidative metabolism of E-def and E-suff rat liver mitochondria using three substrate conditions: endogenous, pyruvate plus malate, and α-ketoglutarate, were measured by oxygen electrode analysis. Statistically significant differences were seen among state 4 respiration with α-ketoglutarate, state 4 respiration(combined data with endogenous, pyruvate plus malate and α-ketoglutarate), state 3 endogenous respiration, and state 3 respiration (combined data with endogenous, pyruvate plus malate, and α-ketoglutarate) of E-def and E-suff rat liver mitochondria.

In vitro vitamin E addition studies were carried out to measure any toxic or beneficial effects of the vitamin on liver mitochondrial respiration from both groups. No significant effect of in vitro additions of vitamin E on liver mitochondrial respiration was found.

Liver mitochondria from E-def rats generally had faster respiration rates than those from E-suff animals. It is possible that the effect of vitamin E deficiency on the membranes of the mitochondria accounted for these results.

If so, then those mitochondria deficient in the vitamin could become swollen and broken allowing substrates to enter the mitochondria at a faster rate and thus be utilized faster. It is postulated that vitamin E may play an important role in the body by maintaining proper liver mitochondrial respiration through the vitamin's beneficial influence on mitochondrial membranes.