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)

Excessive oxidative stress and associated macromolecular damage are considered to be key features of aging, and appear to contribute to the age-related decline in steroid hormone production in adrenal and testicular Leydig cells. The current studies were initiated to examine the potential mechanism by which excessive oxidative stress during aging attenuates the functional expression of the oxidant-responsive transcription factor Activator protein-1. Chronic oxidative stress was induced in vivo by maintaining groups of rats on a diet deficient in vitamin E for 6 months. Plasma, liver, and adrenal tissues from vitamin E-deficient animals had negligible levels of this vitamin and showed high susceptibility to in vitro lipid peroxidation. Synthesis and secretion of corticosterone in response to corticotropin (ACTH), dibutyryl-cAMP, or 20alpha-hydroxycholesterol in vitro was significantly reduced in adrenocortical cells prepared cells from rats deficient in vitamin E. AP-1 DNA-binding activity was diminished approximately 55 % in adrenal extracts from vitamin E-deficient rats with no corresponding change in the binding activity of SP-1. The vitamin E deficiency-mediated loss of AP-1 activity was not due to an alteration in the dimeric composition of constituent proteins, but rather to a general down-regulation of steady-state levels of members of the Fos and Jun families of proteins. Interestingly, vitamin E deficiency also reduced the expression of the redox-regulated Ref-1 protein. Collectively these data demonstrate that chronic oxidative stress specifically down-regulates essential components of the AP-1 transcription factor complex, and suggest that aberrancies in AP-1 expression may adversely affect processes crucial for intracellular cholesterol transport and steroid hormone production.
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PMID:Suppression of steroidogenesis and activator protein-1 transcription factor activity in rat adrenals by vitamin E deficiency-induced chronic oxidative stress. 1506 14

1. Differences in blood lipids, glucose, insulin, amylin, adrenocorticotropic hormone (ACTH), cortisol, aldosterone, angiotensin II, metabolites of nitric oxide (nitrate, nitrite), asymmetric dimethyl arginine, endothelial leucocyte adhesion molecule-1, vascular cell adhesion molecule-1, C-reactive protein, homocysteine and oxidative status (urate, vitamin A, vitamin E, beta-carotene and total anti-oxidant capacity) were investigated in men (aged 18-25 years) with (+) or without (-) a family history (FH) of hypertension. 2. In the present study, FH+ was defined as having at least one parent or grandparent taking medication for hypertension. Blood (60 mL) was sampled (0800-1000 hours) from a cannulated forearm vein after an overnight fast and 24 h abstinence from caffeine-containing products and alcohol. 3. Comparing FH+ with FH-, systolic blood pressure (124 +/- 1 vs 117 + 3 mmHg, respectively; n = 50 and 14, respectively; P < 0.05) and plasma cortisol (377 +/- 23 vs 298 +/- 24 nmol/L, respectively; n = 43 and 12, respectively; P < 0.05) were found to be significantly higher in the former group. 4. No significant difference was found between the two groups for body mass index, resting heart rate, diastolic and mean blood pressures or any of the biochemical measures studied. 5. A significant correlation was found between cortisol and ACTH (r = 0.73). No correlation was found between cortisol and any other parameter measured. 6. These data indicate that elevated cortisol levels are characteristic of young lean normotensive FH+ men. The future impact of this on their vascular health and hypertension remains to be determined.
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PMID:Elevated levels of circulating cortisol in young normotensive adult men with a family history of hypertension. 1806 96


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