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Overweight male rats received oral oleoyl-estrone (OE) for 10 days, and were compared with controls. The expression of 17ß-hydroxysteroid dehydrogenase (17ßHSDH) isoenzymes, and other proteins related to sex hormone metabolism, were analyzed in testicle, liver, adrenals and two white adipose sites: subcutaneous inguinal and epididymal pads using a semiquantitative RT-PCR method. Androstenedione, testosterone, estrone and estradiol levels were measured by HPLC-MS/MS. Isoenzyme expressions were grouped according to their main physiological function (oxidative or reductive) and preferred substrate (androgen or estrogen). As expected, testicle was the main site for synthesis of testosterone and estradiol, and the liver the main organ oxidizing them to androstenedione and estrone. Overall oxidative capacity was 6.5-fold higher than the reductive, and estradiol synthesis and oxidation potential were higher than for testosterone. OE decreased serum androgens, and increased estrone, but not estradiol. This was due to decreased testicle ability to produce testosterone, because of smaller size and decreased 17ßHSDH3 expression, but also to lower availability of precursors. High estrone availability (from OE hydrolysis) does not translate into higher estradiol because of decreased testicle reductive 17ßHSDH expression and decreased aromatase. In consequence, we can assume that OE effects on androgens, and the hypothalamic-pituitary-gonadal axis are limited to testicles.
The objective of this study was to determine the effect of oxidative stress caused by exposure to ozone on the activity of 17-β-hydroxysteroid dehydrogenase and alkaline phosphatase, and testosterone concentrations in male rats, and to investigate the possible protective effect of easily available antioxidants such as vitamins E and C. The experiment was conducted on adult Wistar-Hannover rats. One group of animals was exposed to ozone without vitamin cover, and the remaining animals were administered vitamins E and C in various combinations and doses. Ozone exposure in the group of rats not receiving vitamin injections caused oxidative stress manifested by elevated MDA concentrations in the blood plasma and testicular tissue. An increase in MDA levels was also observed in the group of animals administered vitamins, excluding the animals receiving low- and average-dose combinations of vitamins E and C. A drop in the activity of 17-β-hydroxysteroid dehydrogenase was reported in animals exposed to ozone, but this effect was not noted in the groups exposed to ozone and receiving vitamins. The lowest blood testosterone levels were observed in rats exposed to ozone and in the groups receiving low- and average-dose combinations of vitamins E and C.
The aim of the study was to determine whether consumption of diets containing different fat (rapeseed oil or lard-rich), supplemented with a high level of cholesterol (3% w/w) and/or vitamin E (500 mg/kg of diet) for 6 weeks influenced 17beta-hydroxysteroid dehydrogenase (17β-HSD) type 3 activity (measured in vitro), testosterone (Tt) content in testes and plasma testosterone (Tp) concentration (measured by ELISA and RIA, respectively) in male rats. 17β-HSD activity was shown to depend on dietary fat type. Supplementation of vitamin E influenced Tt value, whereas none of the investigated dietary factors had effects on Tp. Significant differences between the investigated factors were observed only for groups fed rapeseed oil-rich diets with marked increases of Tt and Tp in rats fed vitamin E-rich diet.
W pracy przedstawiono wpływ zwiększonej koncentracji ozonu w powietrzu na poziom testosteronu w osoczu krwi oraz na aktywność w jądrach dehydrogenazy 17-ß-hydroksy-steroidowej i fosfatazy alkalicznej u dojrzałych płciowo szczurów. Sprawdzono również, w jakim stopniu witamina E jest w stanie zapobiec ewentualnym zmianom patologicznym.
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