The male reproductive tract of the Brown Norway rat is profoundly affected by aging. In the epididymis, the site of sperm maturation and storage, aging results in histological and biochemical changes that are suggestive of oxidative stress.
Vitamin E is a potent
lipid-soluble
antioxidant that ameliorates the oxidative stress load associated with some
chronic disease conditions. To determine the effects of long-term (18-mo)
vitamin E deficiency and supplementation on aging in the epididymis, we assessed gene expression changes using
cDNA microarrays and lipid peroxidation using immunohistochemical detection of
4-hydroxynonenal (4-HNE) in 24-mo-old rats. Plasma
vitamin E levels were significantly lower in
vitamin E-deficient animals and higher in
vitamin E-supplemented animals compared with age-matched controls.
Vitamin E deficiency resulted in increased expression of oxidative stress-related transcripts along the epididymis. This effect was most marked in the corpus epididymidis, where expression of
glutathione S-
transferases pi, 8, and mu, as well as
superoxide dismutase, increased by over 50%. The effect of
vitamin E supplementation on the expression of oxidative stress-related transcripts was primarily decreased expression; however, the magnitude of the gene expression changes was smaller than that observed for
vitamin E deficiency. 4-HNE immunostaining was present throughout the epididymis in control animals.
Vitamin E deficiency both increased the intensity and altered the distribution of 4-HNE staining, while
vitamin E supplementation had no observable effect. In summary, we found that long-term
vitamin E treatment alters the expression of oxidative stress-related transcripts. Moreover, long-term
vitamin E deficiency exacerbates the effects of age on the accumulation of oxidative stress damage in the epididymis.