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Query: UMLS:C0155339 (Brown)
12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anti-phlogistic effect of dietary vitamin E supplementation on the acute inflammation observed in experimental lens-induced uveitis in Brown Norway rats was studied. The effects of vitamin E were examined using histopathologic parameters as well as by measuring the levels of arachidonic acid metabolites. Histologic examination of the eyes revealed that the vitamin E-deficient animals had the most severe destruction of the retina, while those animals receiving the vitamin E-supplemented diet exhibited the best preservation of the retinal architecture. Levels of arachidonic acid metabolites, as determined by radioimmunoassay, were significantly higher in vitamin E deficient rats as compared with rats on a normal diet.
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PMID:Anti-inflammatory effects of vitamin E on experimental lens-induced uveitis. 153 46

The systemic vasculitides are characterized by necrotizing inflammation of blood vessels. Neutrophils are implicated in tissue damage by their presence at the site of injury. They can mediate injury by release of cellular contents including proteinases, cytokines and reactive oxygen species. Antioxidants such as vitamin E and N-acetyl cysteine (NAC) may therefore be predicted to ameliorate oxidative damage in vivo and could be a cheap and non-toxic form of therapy. We examined this hypothesis in an experimental model of vasculitis which has some similarities to human disease, and in which depletion of neutrophils ameliorates tissue injury. Mercuric chloride (HgCl2) treatment induces an autoimmune syndrome and necrotizing leucocytoclastic vasculitis in the Brown Norway (BN) rat; anti-myeloperoxidase (MPO) and anti-glomerular basement (GBM) antibodies are present, and vasculitis is reduced by antimicrobials. Methyl prednisolone given intravenously was effective in reducing tissue injury, demonstrating that the model was responsive to a treatment used in man. Vitamin E and NAC were given as daily injections intraperitoneally to BN rats either before, during or after HgCl2 administration. Serial blood samples were taken for anti-MPO and IgE antibodies, which were assayed by ELISA. Necropsies were performed on animals killed at peak disease. At doses of 50-200 mg/kg per day vitamin E had no beneficial effect on tissue injury, regardless of timing of treatment. NAC at 100 or 200 mg/kg also had no significant protective effect on vasculitis. Autoantibody and IgE levels were not affected by either methyl prednisolone or the antioxidants. The lack of benefit of vitamin E and NAC suggests that oxidative damage, whether generated by neutrophils or other cells, does not play a major role in the pathogenesis of vasculitis, and that antioxidant therapy is unlikely to be of benefit in systemic vasculitis in man.
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PMID:Use of methyl prednisolone and antioxidants in mercuric chloride-induced experimental vasculitis. 792 87

The Brown Bowel Syndrome is characterised by degeneration and pigmentation of large bowel mucosa. We present a report of this unusual syndrome in which, for the first time, a functional deficit, reflected in a reduced internal and sphincter tone, is documented. This abnormality was reversed following sub-total colectomy and vitamin E therapy.
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PMID:Anorectal functional deficit in the Brown Bowel syndrome. 798 64

In this review, the involvement of vitamin E in free radical physiology and antioxidant mechanisms is discussed. Moreover, structure-activity relationship (SAR) studies on vitamin E analogues are presented. A molecular explanation for the antioxidant activity often is based on molecular parameters, such as Hammett sigma and Brown sigma +. These parameters correlate with the activity. Using semiempirical calculations, we have found other molecular parameters related to electron distribution and structure (such as the difference in heat of formation between the compound and its radical or the energy of the highest occupied molecular orbital, HOMO) which correlate with the antioxidant action of vitamin E and its derivatives.
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PMID:Molecular pharmacology of vitamin E: structural aspects of antioxidant activity. 840 31

Trial 1 tested the effects of ground vs whole flaxseed at dietary levels of 5, 10, or 15% compared to a corn-soybean or fish oil control on egg production of Leghorn hens over a period of 8 wk. Dietary flaxseed decreased feed consumption, weight gain, and egg weights compared to the control diets; however, flaxseed and fish oil significantly improved egg production (88.9 and 93.0%, respectively) compared to the control (83.1%). Incorporation of linolenic acid (C18:3n-3) into the egg increased linearly as the level of dietary flaxseed increased (2.31, 4.18, or 6.83% of the yolk fatty acids for 5, 10, and 15% flaxseed diets, respectively). In Trial 1, flaxseed and fish oil significantly increased percentage white and decreased percentage yolk compared to the control treatment but had no effects on egg cholesterol. Trial 2 was a factorial design of varieties of flaxseed (brown vs golden), types (ground vs whole), levels of dietary vitamin E (27 vs 50 IU/kg), and feed storage temperatures (4 vs 21 C) fed to hens for 6 wk. Brown flaxseed significantly increased egg weight and egg production compared to the golden variety. There was no difference in whole vs ground flaxseed for measured production variables. Vitamin E (50 IU) significantly improved egg production (96.1 vs 94.3%) compared to 27 IU. Storage temperature of flaxseed did not significantly affect any production variables. In conclusion, dietary flaxseed can be safely added whole to layer diets up to 15% without any detrimental effects on hen-day egg production. Levels of 10 to 15% flaxseed yield eggs with 4 to 7% yolk n-3 fatty acids, respectively, making these eggs rich sources of n-3 fatty acids.
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PMID:The combined influence of dietary flaxseed variety, level, form, and storage conditions on egg production and composition among vitamin E-supplemented hens. 889 98

Because of the proposed cardioprotective benefits of n-3 fatty acids and vitamin E, a trial was carried out to investigate the possibility of enriching eggs with n-3 fatty acid and vitamin E added to the hen's diet. One hundred ninety-two Hy-Line Brown hens, 39-wk-old, were divided into eight groups: four groups received the basal diet supplemented with 3% lard and four doses of dl-alpha-tocopheryl acetate (0, 50, 100, and 200 ppm), whereas the diets of the other groups were supplemented with 3% of fish oil and the same doses of vitamin E. The performances of the hens and egg weights were not affected either by the type of lipid supplement or by the vitamin level. The treatment with fish oil caused a dramatic increase (P < 0.01) of all n-3 fatty acids of the yolk, particularly EPA (19.53 vs. 0.74 mg/egg) and DHA (143.70 vs. 43.66 mg/egg), and an appreciable decrease of arachidonic acid (25.54 vs. 67.72 mg/egg). The different levels of dietary vitamin E slightly affected the fatty acid composition of the yolk. Yolk alpha-tocopherol increased linearly as dietary dl-alpha-tocopheryl acetate increased (P < 0.01) from the control level of 90.93 microg/g of yolk to 313.84 microg/g of yolk when 200 ppm were added to the hen diets. Twenty-eight days of storage at room temperature (20 to 25 C) did not alter the yolk fatty acid profile, and, moreover, the levels of vitamin E remained still very close to those observed in fresh egg.
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PMID:Effects of dietary vitamin E on the quality of table eggs enriched with n-3 long-chain fatty acids. 1078 Jun 51

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

This study evaluated the effects of two dietary doses of vitamins E and C supplemented separately and together, on the content of vitamin E in the yolk, on the lipid stability of fresh and stored eggs, and on their sensory and functional properties. Hy-Line Brown hens (n = 216) received a basal diet for 8 wk supplemented with 100 or 200 mg DL-alpha-tocopheryl acetate (E100 or E200, respectively)/kg, 500 or 1,000 mg ascorbic acid (C500 and C1000, respectively)/kg, or 100 mg DL-alpha-tocopheryl acetate plus 500 mg ascorbic acid (E100+C500)/kg, whereas the control group received no supplementation. Fresh eggs and eggs stored 30,60, and 90 d at 4 C or stored 28 d at room temperature were analyzed for vitamin E content and TBA-reactive substances (TBARS). We also evaluated functional properties of fresh and cooked eggs and sensory properties of boiled and scrambled eggs. The yolk content of vitamin E depended on the level of dietary addition and decreased after 90 d of storage at 4 C or after 28 d at 25 C. Vitamin supplementation had no effect on fresh or refrigerated eggs, whereas 4 wk of storage at room temperature increased TBARS in the control and the group supplemented with the highest doses of vitamins. Ascorbic acid improved Haugh units and elasticity of albumen gels, whereas cohesiveness and hardness of yolk, albumen and whole-egg gels were not affected by dietary treatment. Panelists were not able to distinguish treated eggs from control eggs.
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PMID:Oxidative stability and sensory and functional properties of eggs from laying hens fed supranutritional doses of vitamins E and C. 1245 4

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

Previous studies have suggested that oxidant-induced damage may play a role in the reduced ability of aged Brown Norway rat Leydig cells to produce testosterone. We reasoned that if this was the case, antioxidants such as vitamin E (VE) would be expected to have protective effects on steroidogenesis. To test this hypothesis, the effects of VE on Leydig cell steroidogenesis were examined both in vitro and in vivo. In vitro studies were conducted using Leydig cells isolated from the testes of young adult Brown Norway rats. In one experiment, isolated cells were incubated with luteinizing hormone (LH) alone or with LH plus VE (1.3-40 microg/ml). At each of 3, 5 and 7 days thereafter, the ability of the cells to produce testosterone was greater in the presence of VE than in its absence, and depended upon VE dose. Culturing the Leydig cells with the antioxidants melatonin or N-tert-butyl-alpha-phenylnitrone also protected Leydig cell steroidogenic function. Additionally, VE was found to suppress Fe2+/sodium ascorbate-induced lipid peroxidation in Leydig cells. These studies strongly supported the contention that VE has a protective effect on Leydig cell steroidogenesis. These in vitro results prompted us to ask whether, in vivo, VE also would affect steroidogenesis as Leydig cells age. To this end, rats were provided one of three diets, begun when the rats were 6 months of age and carried out through age 25 months: VE-deficient, VE-control, or VE-supplemented. The VE-deficient diet had no effect on the age-related reductions in Leydig cell testosterone production observed in VE-control rats. The VE-supplemented diet did not prevent age-related reductions in steroidogenesis, but the reductions at ages 23 and 25 months were significantly less than those seen in Leydig cells from VE-control or VE-deficient rats. Taken together, the results of the in vitro and in vivo studies reported herein are consistent with the conclusion that vitamin E exerts a protective effect on Leydig cell steroidogenesis.
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PMID:Vitamin E, aging and Leydig cell steroidogenesis. 1605 18


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