Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol valerate (EV) treatment has been shown to result in the destruction of 60% of beta-endorphin neurons in the hypothalamic arcuate nucleus. Evidence suggests that the mechanism of EV-induced neurotoxicity involves the conversion of estradiol to catechol estrogen and subsequent oxidation to free radicals in local peroxidase-positive astrocytes. In this study, we examined whether treatment with the antioxidant, vitamin E, protects beta-endorphin neurons from the neurotoxic action of estradiol. Our results demonstrate that chronic vitamin E treatment prevents the decrement in hypothalamic beta-endorphin concentrations resulting from arcuate beta-endorphin cell loss, suggesting that the latter is mediated by free radicals. Vitamin E treatment also prevented the onset of persistent vaginal cornification and polycystic ovarian condition which have been shown to result from the EV-induced hypothalamic pathology.
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PMID:Vitamin E protects hypothalamic beta-endorphin neurons from estradiol neurotoxicity. 142 46

Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present study, the effect on MDA excretion of several additional dietary and endogenous factors was evaluated. The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed n-3 fatty acids (20:5 and 22:6) from CLO, intermediate for those fed n-6 (18:2) acids from corn oil (CO) and lowest for those fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected by the level of CO in the diet (5, 10 or 15%), indicating that feeding n-6 acids does not increase lipid peroxidation in vivo. Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E + BHT + vitamin C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl4 administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo. 282 43

D-alpha tocopheryl succinate (vitamin E succinate), which is known to induce differentiation and growth inhibition in murine B-16 melanoma cells, reduced basal and melanocyte-stimulating hormone (MSH)-stimulated adenylate cyclase (AC) activity in vitro. Vitamin E succinate treatment also reduced sodium fluoride- and forskoline-stimulated AC activity of melanoma cells in vitro. Treatment of cells with vitamin E succinate (6 micrograms/ml] for a period of 24 hours was sufficient to reduce MSH-stimulated AC activity. Other forms of vitamin E, such as d1-alpha tocopheryl nicotinate, d1-alpha tocopheryl acetate, and d1-alpha tocopherol, which did not affect growth or morphology of melanoma cells, were relatively less effective in altering basal and MSH-stimulated AC activity. Retinoic acid, which inhibited the growth of B-16 melanoma cells, also reduced basal and MSH-, NaF-, and forskolin-stimulated AC activity in vitro. Prostaglandin A2, which inhibited growth and altered morphology, did not change basal or MSH-stimulated AC activity. These results show that one of the mechanisms of action of vitamin E succinate and retinoic acid on melanoma cells may involve reduction of basal and MSH-sensitive AC activity, and this vitamin effect is not necessarily related to growth inhibition.
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PMID:Alpha tocopheryl succinate inhibits melanocyte-stimulating hormone (MSH)-sensitive adenylate cyclase activity in melanoma cells. 369 13

Chronic adrenocorticotropin (ACTH) treatment in rats leads to a fall in aldosterone secretion (aldosterone turn-off or "aldosterone escape" phenomenon) with a concomitant rise in corticosterone. To elucidate whether ACTH-induced aldosterone suppression is mediated by steroid type II receptor or related to a free-radical effect by over-synthesized corticosterone, we examined the effects of a glucocorticoid antagonist, RU486, and antioxidants dimethyl sulfoxide (DMSO) and vitamin E, on the aldosterone turn-off phenomenon in rats. Each rat received daily for 5 days a different dose of ACTH-Z (5, 10, 20 or 40 micrograms/100 g body weight) 1 mg RU486/100 g body weight, 100 microliters (1.3 mmol) DMSO/100 g body weight or 2 mg vitamin E/100 g body weight with subcutaneous injection. Plasma steroid levels and in vitro release of steroids from the adrenal capsule were measured. The ACTH-Z treatment caused a dose-dependent increase in corticosterone and a decrease in aldosterone in both plasma and adrenal capsule experiments, as well as an increase in adrenal weights. For the following study 5 micrograms/100 g body weight of ACTH-Z was used. Administration of RU486 alone caused no change in plasma aldosterone level compared to controls, even though the steroid type II receptor was blocked, as evidenced by significant increases in plasma ACTH and corticosterone levels. Concomitant administration of RU486 and ACTH-Z increased both plasma corticosterone and aldosterone levels (p < 0.01) but decreased adrenal capsule corticosterone production (p < 0.05) compared to the rats treated with ACTH-Z alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of aldosterone turn-off phenomenon following chronic adrenocorticotropin treatment with in vivo administration of antiglucocorticoid and antioxidants in rats. 758 88

In 2 studies, plasma, erythrocyte, and neutrophil alpha-tocopherol concentrations were monitored in beef cattle after shipping, handling, and sample collection. On the basis of alpha-tocopherol results, an additional 2 studies were designed to measure the effects of administration of adrenocorticotropic hormone (ACTH) and epinephrine on the alpha-tocopherol concentration in the aforementioned blood constituents and on creatine kinase (CK) activity in Holstein calves. In the first of these studies, 15 beef cattle that had recently arrived at the feedlot consumed feed supplemented daily with 1,000 IU of dl-alpha-tocopheryl acetate. Values for initial blood samples indicated that CK activity was high. Although plasma alpha-tocopherol concentration indicated that vitamin supplementation was adequate, RBC and neutrophil alpha-tocopherol values were generally nondetectable. After 4 weeks of supplementation, plasma alpha-tocopherol concentration increased (P < 0.05), and neutrophil and RBC alpha-tocopherol values became measurable in most of the cattle. In the second study, 6 beef heifers had decreased (P < 0.05) plasma, RBC, and neutrophil alpha-tocopherol values after multiple periods of handling and blood sample collection. In the third and fourth studies, 10 tamed Holstein heifer calves, 5 of which were administered ACTH and epinephrine to simulate stress effects on blood alpha-tocopherol concentrations and CK activity. In study 3, the vitamin E-adequate heifers had increased blood CK (P < 0.001) activity and cortisol (P < 0.01) concentration, and decreased (P < 0.05) neutrophil alpha-tocopherol concentration after hormone injections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of shipping, handling, adrenocorticotropic hormone, and epinephrine on alpha-tocopherol content of bovine blood. 821 97

Sulfated glycoprotein-2 (SGP-2 or clusterin) is a complex multifunctional molecule that has been recently been implicated in neuronal degeneration and remodeling. We have shown that estradiol treatment results in a selective destruction of beta-endorphin neurons in the hypothalamic arcuate nucleus. We have used immunocytochemistry to determine the distribution of SGP-2 immunoreactivity in the rat hypothalamus and to assess the effects of the estradiol-induced destruction of beta-endorphin neurons on SGP-2 expression. We have found that SGP-2-immunopositive neurons normally occur in the medial preoptic area (MPOA), supraoptic nucleus (SON), paraventricular nucleus (PVN), dorsomedial nucleus (DM), and the lateral hypothalamic area (LHA) in both males and females. The neuropil appears free of label. Treatment with estradiol valerate results in the appearance of immunopositive punctate deposits in the neuropil in the MPOA, PVN and DM. The number and distribution of SGP-2-positive neurons are unaffected by estradiol treatment except in the MPOA, where there are twice as many SGP-2-positive neurons as in controls. These effects are precluded by treatment with vitamin E, with blocks the cytotoxic action of estradiol on beta-endorphin neurons. Thus, we interpret these changes as responses to the loss of beta-endorphin afferents.
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PMID:The effect of estradiol-induced hypothalamic pathology on sulfated glycoprotein-2 (clusterin) expression in the hypothalamus. 903 92

The present experiment was conducted to study the effects of dietary vitamin E on plasma corticosterone (CTC) concentration and adrenal steroid syntheses in chickens treated with adrenocorticotropic hormone (ACTH). Chickens were divided into ACTH(-) and ACTH(+) groups, and each group was further divided into three subgroups administered with vitamin E (500 or 5,000 mg/kg diet) and without the vitamin. Vitamin E (DL-alpha-tocopheryl acetate) was mixed with the basal diet at levels of 500 and 5,000 mg/kg and fed for 6 d. ACTH (20 IU/kg body weight) was given daily by intraperitoneal injection for 5 d. alpha-Tocopherol levels in the plasma and adrenal gland were markedly elevated by vitamin E feeding, and the level of adrenal free cholesterol (CHOL), which is used for steroid synthesis, was significantly decreased by vitamin E feeding in a dose-dependent manner. However, the level of adrenal CHOL ester was unchanged by any treatment. The elevations of pregnenolone, progesterone and CTC levels in the adrenal gland of chickens with ACTH treatment were decreased by vitamin E administration. The elevation of plasma CTC concentration in the ACTH(+) group was dramatically decreased by vitamin E administration, while that concentration was not influenced by the vitamin administration in the ACTH(-) group. These findings indicate that vitamin E suppresses the elevation of the plasma CTC concentration due to ACTH in chickens, possibly by inhibiting the conversion of CHOL ester to free CHOL in the adrenal gland.
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PMID:A high dose of vitamin E inhibits adrenal corticosterone synthesis in chickens treated with ACTH. 1134 89

This study was conducted to determine the effects of vitamin C (L-ascorbic acid) and vitamin E (alpha-tocopherol acetate) on serum concentrations of lipid peroxidation (MDA) and triiodothyronine (T3), thyroxine (T4), adrenocorticotropic hormone (ACTH), and some metabolite and mineral in laying hens reared at high ambient temperatures ranging from 25 degrees C to 35 degrees C. One hundred twenty laying hens (18 wk old; Hy-Line) were divided into 4 groups, 30 hens per group. The laying hens were fed either a basal diet (control) or the basal diet supplemented with either 250 mg of L-ascorbic acid/kg of diet (vitamin C), 250 mg of alpha-tocopherol acetate/kg of diet (vitamin E), or 250 mg of L-ascorbic acid plus 250 mg alpha-tocopherol acetate/kg of diet (combination). Separately or as a combination vitamins C and E increased serum vitamin C and vitamin E concentrations (p < 0.001) but decreased serum MDA concentration (p < 0.05). Serum concentrations of vitamin E and vitamin C were found highest but serum MDA concentration was lowest in the combination group. Supplemental vitamins C and E either separately or in a combination increased serum T3 and T4 concentrations (p < 0.05), whereas decreased serum ACTH concentration (p < 0.01). Serum glucose and cholesterol concentrations decreased, whereas serum protein concentration increased (p < 0.05) when vitamins C and E singly or together were added to the diet. Vitamin C and vitamin E supplementation resulted in an increase in serum concentrations of Ca, P, and K (p < 0.01) but a decrease in serum concentration of Na (p < 0.05). The results of the present study suggest that supplemental vitamin C and vitamin E alter serum lipid peroxidation, vitamin C, vitamin E and metabolite status, and diets supplemented with a combination of these two vitamins offer a good management practice in laying hens reared at high temperatures. In addition, the results suggest that dietary vitamin C and vitamin E act synergistically.
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PMID:Effects of vitamin C and vitamin E on lipid peroxidation, blood serum metabolites, and mineral concentrations of laying hens reared at high ambient temperature. 1188 97

This study was conducted to determine the effects of dietary vitamin C (L-ascorbic acid) and vitamin E (alpha-tocopherol acetate) on lipid peroxidation status measured as MDA and serum triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), as well as some other serum metabolite and mineral concentrations of Japanese quails reared under heat stress (34 degrees C). One hundred-eighty 10-day-old Japanese quails were randomly assigned to six treatment groups, three replicates of 10 birds each. Using a 2 x 3 factorial design, the birds received two levels of vitamin C (100 and 200 mg/kg of diet) or three levels of vitamin E (125, 250, or 500 mg/kg of diet). Greater dietary vitamin E and vitamin C resulted in a greater serum T3, T4, and TSH (p = 0.001), but lower ACTH (p = 0.001) concentrations. Serum concentrations of T4 and TSH increased to a greater extent by increasing dietary vitamin C when greater vitamin E levels were fed (interaction, p = 0.001). Serum glucose, urea, triglycerides, and cholesterol concentrations decreased (p = 0.001), while protein and albumin concentrations increased (p = 0.001) when both dietary vitamin C and vitamin E were increased. Serum activities of SGOT and SGPT were not influenced by dietary vitamin C and vitamin E (p > 0.43). However, serum activity of AP increased (p = 0.001) by increasing both dietary vitamin C and vitamin E. Increasing both dietary vitamin C and vitamin E caused an increase in serum concentrations of Ca, P, K (p = 0.001), Fe, and Zn (p = 0.01) but a decrease in serum concentrations of Na (p = 0.001) and Cu (p = 0.01). Interactions between vitamin C and vitamin E were detected for Ca, P, Na, and K (p = 0.001). Greater dietary vitamin C and vitamin E resulted in a greater serum and liver vitamin E, C, and A (p < or = 0.05), but lower MDA (p = 0.001) concentrations. Results of the present study conclude that supplementing a combination of dietary vitamin C (200 mg) and vitamin E (250-500 mg) offers a good management practice to reduce heat stress-related decreases in performance of Japanese quails.
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PMID:Effects of vitamin C and vitamin E on lipid peroxidation status, serum hormone, metabolite, and mineral concentrations of Japanese quails reared under heat stress (34 degrees C). 1194

Retrolental fibroplasia is today the principal cause of blindness in children of preschool age, exceeding all other causes combined. The disease occurs in infants of low weight at birth, commonly those born prematurely. The incidence of the disease is rising at an alarming rate. Vitamin E deficiency, corticotropin (ACTH) deficiency, the use of cow's milk in place of mother's milk, and improper oxygenation have been suggested as etiologic factors but the cause remains a mystery. Often the incidence is high in institutions in which maximal care is given premature infants.Clinically, the disease advances through an "active" phase during which regression is possible, and a "subsiding" or "cicatricial" phase which terminates with the formation of a disorganized opaque mass behind the lens. The earliest manifestations are noted in the fundi. Hemorrhages, neovascularization, transudation commencing in the periphery, and retinal separation contribute to the formation of the characteristic retrolental membrane. The diagnosis may be made when the retrolental membrane is observed in the eye of an infant whose weight at birth was low. Differential diagnosis is required occasionally. Thus far, no form of therapy has prevented or reversed the pathologic changes successfully. Use of vitamin E, corticotropin and mother's milk has not influenced the incidence of the disease. Avoidance of premature delivery if possible is indicated.
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PMID:Retrolental fibroplasia; blindness in infants of low weight at birth. 1300 70


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