Date of Award

1999

Degree Type

Thesis

Degree Name

Master of Science in Kinesiology

Department

Kinesiology

First Advisor

Thomas Manfredi

Abstract

Cell oxidative damage caused by free radical production during respiration plays a major role in tissue dysfunction. Mitochondria are subcellular sites for oxidative phosphorylation and are the major source of free radicals. Their high oxidative activity makes them susceptible to oxidative damage. Antioxidants protect the cell against oxidative damage, but when defenses are not adequate cells are subjected to oxidative stress. A lack of vitamin E, and selenium results in enlargement ofliver mitochondria, suggesting mitochondrial fusion, and an inability to divide. Recent studies suggest that aging is associated with mitochondrial enlargement and elongation, and that these mitochondria are less oxidatively efficient, and less resistant to oxidative damage. Vitamin E supplementation may protect against these age-related effects. The purpose of this study was to assess the effects of vitamin E supplementation (500 IU/kg diet) on "old" (760 days) and "older" (827 days) C57BL/6 mice liver mitochondrial (Mt) morphometry. Measurements of Mt area, short and long axis, and size distributions were taken from control and vitamin E supplemented mice. Transmission electron microscopy and image analysis were used to measure fixed mitochondria from liver homogenized samples. We hypothesized that vitamin E supplementation will result in smaller, more round liver mitochondria. The "old" vitamin E supplemented mice had significantly smaller (p

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