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)

In order to investigate the involvement of opioid peptides and prolactin in stress-facilitated mammary cancer, we studied the effect of chronic restraint stress on dimethylbenz[a]-anthracene (DMBA)-induced mammary tumorigenesis and the effect of an opiate antagonist, naltrexone, on this process. Female Fischer-344 rats (n = 160) were administered 15 mg DMBA/ml of sesame oil/rat by intragastric intubation. Eighty rats were subjected to daily 30 min restraint stress in a plastic cylinder, and 80 rats served as control not subjected to the stressor. Half of the rats from each group received naltrexone (1 mg/kg, i.p. daily). Five rats from each group (restraint stress +/- naltrexone and control +/- naltrexone) were killed every 2-3 weeks. Rats subjected to restraint stress developed a greater number of tumors earlier. Naltrexone decreased the tumor incidence in the stressed animals from 32 to 12% (P less than 0.001) and in unstressed rats from 27 to 15% (P less than 0.001) at the end of 18 weeks. Stressed rats showed a decrease of 48% (P less than 0.001) in the level of hypothalamic beta-endorphin. Plasma prolactin increased from 4-13 ng/ml in the control rats to 109-396 ng/ml (P less than 0.001) in the stressed rats throughout the 18 week period. The beneficial effect of naltrexone was associated with 42% (P less than 0.01) increase in T cell proliferation, but greater than 90% (P less than 0.001) decrease in plasma prolactin level was observed in naltrexone-treated rats compared to the untreated animals. Rats subjected to restraint stress showed a 15% (P less than 0.001) decrease in weight gain at the end of the experiment (18 weeks). Neither restraint stress nor naltrexone administration affected the caloric intake of rats during this period. Thus, we believe that restraint stress facilitates DMBA-induced mammary tumors by releasing beta-endorphin and prolactin, and naltrexone shows a beneficial effect by opposing the effect of beta-endorphin on prolactin release in the stressed animals.
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PMID:Facilitation of dimethylbenz[a]anthracene-induced rat mammary tumorigenesis by restraint stress: role of beta-endorphin, prolactin and naltrexone. 190 24

A new transplantable rat pituitary tumor was induced in F344 female rats with dimethylbenz(a)anthracene and estrogen (MtT/F-DMBA) and studied for 20 serial transplant generations. The tumor grew without estrogen supplements in female rats by the second transplant generation. Sensitivity to estrogens, as indicated by a prolonged latency period for tumor development, was seen at the 20th, but not the 5th transplant generation. MtT/F-DMBA tumors expressed prolactin (PRL), growth hormone (GH), and adrenocorticotropin (ACTH) mRNAs. A decrease in the percentage of cells expressing PRL mRNA, PRL protein, and in the number of secretory granules per cell occurred with serial transplantation. S-100 protein-positive folliculostellate cells were present in the hyperplastic pituitary but not in the transplantable tumors. Estrogen treatment at the 20th transplant generation prolonged the tumor latency period, increased the number of cells expressing PRL mRNA greater than 5-fold by in situ hybridization analysis (14 +/- 2% versus 77 +/- 5%), increased PRL secretion (132 +/- 40 ng/ml versus 3762 +/- 890 ng/ml), and increased the number of cytoplasmic secretory granules per cell. These results indicate that hyperplastic pituitary and true pituitary neoplasms differ in their ability to grow readily after transplantation. The presence of S-100 protein-positive folliculostellate cells, which are present in hyperplastic but not in neoplastic pituitary tissues, may serve as a morphologic marker to separate hyperplastic and neoplastic rat pituitary tissues. Transplantable tumors remained responsive to estrogen with expression of a more differentiated phenotype, including an increased number of cells expressing PRL mRNA and increased numbers of PRL secretory granules.
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PMID:Regulation of prolactin gene expression in a DMBA-estrogen-induced transplantable rat pituitary tumor. 212 15

Mammary tumors were induced in female Sprague-Dawley rats by giving a single oral dose of 20 mg 7,12-dimethylbenz[a]anthracene (DMBA). Animals were killed after full development of tumors 4 months after the ingestion of DMBA. Opioid peptides in various tissues were estimated by radioimmunoassay (RIA). Tumor-bearing rats (n = 5) had higher (P less than 0.05) contents of beta-endorphin in pituitary (+60%), striatum (+52%) and midbrain (+85%) compared to animals with no tumors. However, tumor-bearing rats showed a decrease of 35% in striatal met-enkephalin content. Dynorphin level decreased (P less than 0.05) in pituitary (-49%) and hypothalamus (-29%) of tumor-bearing rats. Thus for the first time, we report the alteration in the level of these neuropeptides during the process of chemical carcinogenesis.
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PMID:Effect of 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis on the opioid peptide levels in the rat central nervous system. 287 Jul 95

In cultured fetal human adrenocortical cells, metabolism of the carcinogen benzo[a]pyrene was found to be unresponsive to the xenobiotic inducers 3-methylcholanthrene, benz[a]anthracene and 2,3,7,8-tetrachlorodibenzo-p-dioxin. However, exposure of cultures to the hormone adrenocorticotropin (ACTH) for 48 hours stimulated benzo[a]pyrene metabolism 3-fold. The major metabolite was the 7,8-diol. Other compounds which stimulate the production of adrenocortical cell cyclic AMP (forskolin and cholera toxin) as well as monobutyryl cyclic AMP also increased benzo[a]pyrene metabolism. Human adrenocortical cells thus provide an unusual example of hormonal regulation of the metabolism of a carcinogen.
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PMID:Hormonal regulation of benzo[a]pyrene metabolism in human adrenocortical cell cultures. 299 46

The major cytochrome P450 (P450EF) in the mouse embryo fibroblast C3H/10T1/2CL8 (10T1/2) cell line, which is very active in polycyclic aromatic hydrocarbon metabolism, is immunologically distinct from known P450 families but shares homology with an adrenocorticotropin hormone-regulated P450 from rat adrenal glands (P450RAP). P450EF is more effectively induced by benz[a]anthracene (BA) than by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which is anomalous for aryl hydrocarbon receptor (AhR)-mediated transcriptional activation. Evidence is presented here that induction of P450EF is consistent with mediation by the AhR but also involves an additional selective stabilization of P450EF by BA. P450EF-specific mRNA was measured by in vitro translation of 10T1/2 mRNA and subsequent immunoprecipitation with antibodies that recognize P450EF. P450EF mRNA was equally stimulated (> 10-fold) by BA (10 microM) and TCDD (10 nM) after 6 hr of induction in 10T1/2 cells. This equal stimulation of P450EF by BA and TCDD is consistent with transcriptional activation of the gene by the AhR. BA induction of mRNA declined 3-fold between 6 and 18 hr, due to metabolism of BA. Steady state P450EF mRNA levels declined quickly once this stimulation was removed, whereas total P450EF protein levels, measured by immunoblotting, continued to increase. During a 6-hr inhibition of protein synthesis with cycloheximide, both total P450EF and functional cytochrome, measured by polycyclic aromatic hydrocarbon metabolism, decreased by 60% in uninduced and TCDD-induced transformed 10T1/2 cells. This is consistent with relatively rapid degradation of P450EF (t1/2 = 4 hr). No such decline was seen when BA was present, indicating a stabilization of P450EF, which can explain the additional effectiveness of BA in enhancing the level of P450EF.
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PMID:Dual regulation of cytochrome P450EF expression via the aryl hydrocarbon receptor and protein stabilization in C3H/10T1/2 cells. 802 8