Vitamin E and age alter liver mitochondrial morphometry

Oxidative damage to mitochondrial. membranes caused by free radical production during respiration plays a major role in tissue dysfunction. It has been hypothesized that aging is associated with mitochondrial enlargement and elongation. These changes may be enhanced by deficiencies in vitamin E and selenium. Vitamin E supplementation minimizes the age-related mitochondrial enlargement and elongation in the mouse liver. This study investigated the effects of vitamin E supplementation (500 IU/kg) on "old" (760 days) and "older" (827 days) C57BL/6 mice liver mitochondrial. (Mt morphometry. Fixed mitochondria from homogenized liver samples taken from control and vitamin E-supplemented mice were examined by transmission electron microscopy and measured by image analysis. Morphometric measurements included Mt area, short and long axis, and size distributions. "Old" vitamin E-supplemented mice had significantly smaller (p < 0.0001) liver mitochondria than age-matched controls. While age had no significant effect on Mt area and short axis in the vitamin E-supplemented mice, it had a significant effect (p < 0.002) on the long axis. Analysis of the long axis to short axis ratio indicated that age had a significant effect of mitochondrial elongation in the vitamin E fed mice. Vitamin E supplementation results in smaller mouse liver mitochondria as compared to age-matched cohorts and aging results in elongation but does not alter the size of liver mitochondria in mice supplemented with vitamin E. These results suggest that vitamin E provides a protective effect against age-related mitochondrial enlargement.