Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The eye lens is subjected to many risk factors over time, which contribute to changes in its transparency, finally leading in combination to cataract development. Ultra violet (UV) radiation is regarded as one of the widespread risk factors contributing to cataract formation, for example in combination with nutritional deficiencies. Both factors possibly contribute to the high number of cataracts in the sunbelt region of the world. In this study, two essential nutritional factors were investigated in Brown Norway rats, zinc and vitamin E deficiencies, alone and in combination with UV-A and UV-B irradiation. Young female Brown Norway rats were put on a special diet for 10 weeks, either highly deficient in Zinc or in vitamin E. The diet was otherwise identical to the control diet. Two weeks after putting the animals on the diet, UV irradiation was started in some of the groups with mydriatic pupils with 3 irradiation sessions per week (UV-A 1 J/cm2; UV-B 0.2 J/cm2). Irradiation was continued until the end of the diet treatment period. Body weight and food consumption were established at weekly intervals, as well as slitlamp microscopy to monitor changes in anterior eye segment morphology. In addition changes in transparency of the cornea and lens have been monitored and evaluated with a Scheimpflug camera (Topcon SL-45) at baseline, and after 4 and 8 weeks of irradiation. After sacrifice of the animals, the lens wet weight as well as the activity of superoxide dismutase (SOD) were determined. Zinc deficiency alone led to an almost complete arrest of body weight increase. In the cornea, UV-A in combination with zinc or vitamin E deficiency did not have any interactive effects. The combination of UV-B and zinc deficiency showed subtractive instead of additive effects on corneal transparency and neovascularization. In the lens both deficiencies positively interacted with UV-A and UV-B by increasing the density of the capsular and cortical layers. The lens fresh weight was significantly lower in zinc-deficient animals additionally irradiated with UV-A or UV-B. The activity of SOD was significantly lower in the lenses of zinc- or vitamin E-deficient animals additionally irradiated with UV-B. The experiments presented clearly demonstrate that dietary zinc and vitamin E deficiencies do interact with UV radiation damage in the cornea and lens of Brown Norway rats.
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PMID:Experimental evidence for interactive effects of chronic UV irradiation and nutritional deficiencies in the lens. 1206 Dec 68

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.
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PMID:The effects of long-term vitamin E treatment on gene expression and oxidative stress damage in the aging Brown Norway rat epididymis. 1517 34