Malondialdehyde formation in liver mitochondrial and microsomal fractions of vitamin E- and selenium-deficient rats as a function of alpha-tocopherol level: the effect of treatment in vitro with iron.

Weanling rats were given diets with adequate vitamin E and selenium or deprived of one or the other or both, nutrients. After 28 days, liver mitochondrial and microsomal fractions were prepared and alpha-tocopherol (alpha-T) and selenium measured. alpha-Tocopherol fell by eight-fold in the doubly deficient rats and selenium fell three-fold. Malondialdehyde (MDA) was found to be undetectable by a sensitive HPLC method. The fractions were subjected to peroxidative stress in in vitro using 0.5 mM Fe2+/10 mM ADP, and MDA and alpha-T were measured at intervals during 30 min. The results showed that in the mitochondrial fractions there was a lag time of at least 2 min before peroxidation became significant, during which time most of the alpha-T was consumed. In the microsomal fraction the lag phase was very short prior to the establishment of a linear rate of peroxidation, although little alpha-T was used up. It was concluded that the mitochondrial fraction withstood the peroxidative challenge better than the microsomal fraction even though the initial level of alpha-T in the microsomal fraction was about double that in the mitochondrial fraction. Selenium deficiency had no effect on the length of the lag phase of the fractions which therefore appears to be a characteristic of mitochondrial or microsomal fractions.