Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To analyze the mechanism by which nitric oxide (NO) exerts its antisteroidogenic action, human luteal cells were cultured during 24 and 48 h with L-arginine (L-Arg, 1 mmol/L); 1,2(2-trifluoromethylphenyl)imidazole (TRIM) (50 micromol/L and 1 mmol/L) and cyclic guanosine monophosphate (cGMP) analog (8-Br-cGMP, 1 mmol/L). Estradiol, nitrite, and P450 AROM activity were determined in culture media. Total cGMP concentration was evaluated in the cells and culture media by radioimmunoassay, and NADPH diaphorase was used as a histochemical marker for NO synthase (NOS) activity. During the corpus luteum (CL) life-span, NO affected estradiol secretion in an age-dependent manner, with an inhibition in mid-CL (37%; p < 0.05) in agreement with our previous results, and no significant modification in early and late CL. Basal nitrite concentration in 24 and 48 h of midluteal cell cultures (42 and 93 pmol/10(6) cells, respectively) was increased by L-Arg (53% and 88%) and inhibited by the two TRIM concentrations; also, an intense diaphorase reactivity was observed in endothelial cells and luteal parenchyma. Total cGMP was not detected in cell cultures and 8-Br-cGMP did not modify estradiol secretion, whereas aromatase activity was strongly inhibited by L-Arg (70%, p < .05). These results suggest that both NOS isoforms are active in midluteal cells, and the mechanism of action for NO on in vitro estradiol secretion may be an inhibition of P450 AROM activity.
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PMID:Antisteroidogenic action of nitric oxide on human corpus luteum in vitro: mechanism of action. 1066 38

This study examined the effects of variety and quantity of dietary fat consumed by rats during pregnancy and lactation on female offspring's response to chemically induced mammary cancer. Groups of six female rats were fed diets containing 7% corn oil (7-CO), 15% CO (15-CO), 7% olive oil (7-OO), or 15% OO (15-OO) for 5 wk prior to, and during, pregnancy and lactation. Female offspring (n = 15 per group) were fed a 7-CO diet, and mammary cancer was induced with 7,12-dimethylbenz[a]anthracene (DMBA). Three months following cancer induction tumor incidence and size were recorded, and markers of apoptosis, serum estrogen concentrations, and hepatic phase II enzymes were measured. Tumor incidence was 47% in offspring born to mothers fed the 7-OO diet, rose to 67% in 7-CO and 15-OO offspring, and reached 86% in 15-CO. A trend toward smaller tumors was observed in the 7-OO group, and offspring of mothers fed high-fat diets had significantly more tumors. Estradiol levels at the end of lactation were significantly lower in mothers fed 7-OO but were similar in all groups of offspring. In tumor tissue, Bcl-2 expression was highest in the 15-CO offspring, and Bak expression was significantly higher in rats exposed to OO. A distinct trend toward increased caspase-3 expression (20 kDa) was observed in the 7-OO offspring, and both low-fat diets significantly elevated caspase activity. In healthy mammary tissue, rats exposed to low-fat diets had significantly higher caspase-3 (32-kDa) levels, and caspase-3 activity was significantly higher in the healthy tissue from both OO groups. Hepatic quinone reductase activity was significantly lower in offspring of mothers fed the low-fat diets. These results indicate that perinatal exposure to OO may have a protective effect against future development of mammary cancer in female offspring, whereas high-fat diets fed to pregnant and lactating rats, in particular CO, may be deleterious.
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PMID:Olive oil consumption during pregnancy and lactation in rats influences mammary cancer development in female offspring. 1292 5

Estradiol (E2) has been linked to both, protection against damage associated with chronic diseases or exposure to chemicals, and to the incidence of cancer. In its protective role, E2 appears to attenuate oxidative stress while as a carcinogen, E2 damages macromolecules via formation of reactive catechol metabolites. Alterations in the expression of antioxidant and xenobiotic metabolizing enzymes upon administration of pharmacological doses of E2 have been previously identified, but the effect of chronic exposure to low concentrations of E2 on activities of those enzymes in liver is unclear. The August-Copenhagen Irish (ACI) rat is more sensitive to estrogen-induced carcinogenesis than the Sprague-Dawley rat. Accordingly, the effect of treatment of female ACI and Sprague-Dawley rats for 6 weeks with E2 on activities of NAD(P)H quinone oxidoreductase 1 (NQO1), glutathione peroxidase, glutathione S-transferase (GST), phenol sulfotransferase (SULT1A1), cytochrome P450 (CYP450) and UDP-glucuronosyltransferase (UGT) was studied. Basal expression of these enzymes was similar in livers from both strains prior to exposure to E2. However, only NQO1 and GST activity was increased (3- and 2.5-fold, respectively) in liver cytosol of ACI rats treated with E2. In contrast, only NQO1 activity was increased modestly in livers of Sprague-Dawley rats. Other enzymes were not significantly affected in the livers of ACI or Sprague-Dawley rats following chronic treatment with E2. The selective induction of NQO1 and GST activity suggests that under physiological conditions, E2 may protect against oxidative stress via elevation of these antioxidant enzymes. The marked induction of NQO1 and GST in the ACI rat indicates a potential for this strain to be used as a model to study the E2-mediated modulation of these enzymes in tissues that are either sensitive to E2 carcinogenesis or to its protective effects.
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PMID:Induction of NAD(P)H quinone oxidoreductase and glutathione S-transferase activities in livers of female August-Copenhagen Irish rats treated chronically with estradiol: comparison with the Sprague-Dawley rat. 1467 40