Estradiol regulates class I alcohol dehydrogenase gene expression in renal medulla of male rats by a post-transcriptional mechanism

Qulali, Mona; Crabb, David W.

doi:10.1016/0003-9861(92)90673-k

Cited by 18 publications

(9 citation statements)

References 31 publications

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“…17␤-Estradiol (␤E) and testosterone enanthate were dissolved in corn oil and given subcutaneously for 7 days daily. Testosterone and ␤E were given 7 days postgonadectomy to rats at 2 or 100 ng ⅐ kg Ϫ1 ⅐ day Ϫ1 , as previously described (10,56,65), respectively. All agents except for bovine growth hormone were purchased from Sigma and were the highest purity available.…”

Section: Methodsmentioning

confidence: 99%

Hormonal regulation of hepatic multidrug resistance-associated protein 2 (Abcc2) primarily involves the pattern of growth hormone secretion

Simon¹,

Iwahashi²,

Hu³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Biliary excretion is the rate-limiting step in transfer of bilirubin, other organic anions, and xenobiotics across the liver. Multidrug resistance-associated protein 2 (Mrp2, Abcc2) is the major transporter for conjugated endo- and xenobiotic-conjugated compounds into bile. Hormones regulate bilirubin and xenobiotic secretion into bile, which have dimorphic differences. Therefore, we examined the possible role of sex steroids and growth hormone in the regulation of Mrp2. In ∼8-wk-old rats, mRNA, transcriptional activity, and hepatic content of Mrp2 were selectively increased fourfold ( P < 0.001) in females compared with males. In males, estrogens increased and testosterone decreased Mrp2 mRNA and protein, whereas no significant effect was measured in females, suggesting either a direct effect on the liver or an alteration in growth hormone secretory pattern. After hypophysectomy, Mrp2 mRNA was markedly reduced and the effects of estrogens and testosterone on Mrp2 were prevented, supporting the role of pituitary hormones in controlling Mrp2 expression. Mrp2 increased following growth hormone infusion in males. Mrp2 mRNA was decreased in growth hormone-deficient “Little” mice. Growth hormone infusions in hypophysectomized rats partially restored Mrp2 levels, whereas thyroxine addition returned Mrp2 mRNA and protein to basal levels. Morphology as well as biochemical measurements demonstrated that Mrp2 was localized to the bile canaliculus in equal density in both genders, whereas hormone replacements increased Mrp2 in hypophysectomized animals. In cultured hepatocytes, thyroxine did not have an effect, but growth hormone alone and combined with thyroxine increased Mrp2 mRNA levels. In conclusion, Mrp2 levels are regulated by the combination of thyroxine and different growth hormone secretory patterns.

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Section: Methodsmentioning

confidence: 99%

Hormonal regulation of hepatic multidrug resistance-associated protein 2 (Abcc2) primarily involves the pattern of growth hormone secretion

Simon¹,

Iwahashi²,

Hu³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…A greater capability for ethanol oxidation and less ability to remove acetaldehyde may lead to its accumulation in endometrium, contributing to cancer development. In addition, some reports have shown that the expression of ADH I gene is regulated by sex hormones, which elevated level is noted at women who consume ethanol, what also can be associated with carcinogenesis in uterus [53]. The analyses of ADH isoenzymes activity in the sera of endometrial cancer patients reveal similar correlations.…”

Section: Adh and Aldh In Malignant Diseasesmentioning

confidence: 80%

Alcohol dehydrogenase and aldehyde dehydrogenase in malignant neoplasms

Orywal

Szmitkowski

2016

Clin Exp Med

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According to International Agency for Research on Cancer, ethanol and acetaldehyde belong to group 1 of human carcinogens. The accurate mechanism by which alcohol consumption enhances carcinogenesis is still unexplained. Alcohol is oxidized primarily by alcohol dehydrogenase (ADH) to acetaldehyde, a substance capable of initiating carcinogenesis by forming adducts with proteins and DNA and causing mutations. Next, acetaldehyde is metabolized by aldehyde dehydrogenase (ALDH) to acetate. In tissues of many cancers, we can observe significantly higher activity of total alcohol dehydrogenase with any change in aldehyde dehydrogenase activity in comparison with healthy cells. Moreover, in malignant diseases of digestive system, significantly increased activity of ADH isoenzymes class I, III and IV was found. The gynecological, brain and renal cancers exhibit increased activity of class I ADH. ADH and ALDH can play also a crucial regulatory role in initiation and progression of malignant diseases by participation in retinoic acid synthesis and elimination of toxic acetaldehyde. Besides, changes of enzymes activities in tumor cells are reflected in serum of cancer patients, which create the possibilities of application ADH isoenzymes as cancer markers.

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“…It was reported that ADH class I transcript in mouse kidney was stimulated by testosterone treatment, whereas ADH class I transcript in mouse adrenal gland was reduced to less than 5% [41]. Estrogen treatment induced the expression of ADH class I mRNA in rat kidney [12,13] and rat liver [42]. Harada et al demonstrated that the administration of estrogen and progesterone increased ADH activities in rat liver, while that of testosterone decreased ADH activities [43].…”

Section: Discussionmentioning

confidence: 99%

“…Detection of ADH activity was performed essentially as described previously [12,13]. Briefly, tissues were homogenized in a double volume of 50 mM Hepes, pH 8.4 containing 0.5 mM dithiothreitol, using glassteflon homogenizer.…”

Section: Detection Of Alcohol Dehydrogenase Activitymentioning

confidence: 99%

Evidence for the Expression of Alcohol Dehydrogenase Class I Gene in Rat Uterus and Its Up-regulation by Progesterone

et al. 2008

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Abstract. The endometrium is one of the target tissues of the ovarian steroid hormones, estrogen and progesterone. In order to elucidate the mechanism of gene regulation in the endometrium, suppressive subtraction hybridization was performed to isolate the candidate genes controlled by progesterone in rat uterus. Alcohol dehydrogenase (ADH) class I gene was one of the candidate genes. Here we investigated the expression and regulation of ADH class I gene in rat uterus. The mRNA of ADH class I was detected in uterus by RT-PCR using specific primers. Using specific probe for ADH class I, in situ hybridization was performed to investigate localization in rat uterus. Positive signals were detected in the endometrial stromal cells of rat uterus by in situ hybridization and were not detected in endometrial epithelial cells and myometrium in rat uterus. Ovariectomized rats were treated with 17-β estradiol and progesterone and the uteri of these rats were used for Northern blot analysis and assay of the ADH activity. Northern blot analysis revealed that the expression of ADH class I mRNA in rat uteri was up-regulated approximately two-fold after progesterone treatment, but not estrogen. Likewise, ADH activity was approximately two-fold higher in progesterone-treated rat uteri compared with controls. This study demonstrated that ADH class I gene is progesterone-responsive in the uterus. This implies that progesterone might be involved with retinoic acid synthesis in the uterus, since ADH is the key enzyme for retinoic acid synthesis.

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Estradiol regulates class I alcohol dehydrogenase gene expression in renal medulla of male rats by a post-transcriptional mechanism

Cited by 18 publications

References 31 publications

Hormonal regulation of hepatic multidrug resistance-associated protein 2 (Abcc2) primarily involves the pattern of growth hormone secretion

Hormonal regulation of hepatic multidrug resistance-associated protein 2 (Abcc2) primarily involves the pattern of growth hormone secretion

Alcohol dehydrogenase and aldehyde dehydrogenase in malignant neoplasms

Evidence for the Expression of Alcohol Dehydrogenase Class I Gene in Rat Uterus and Its Up-regulation by Progesterone

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