Nickel is a ubiquitous environmental pollutant, which has various effects on reproductive endocrinology. In this study, human adrenocortical carcinoma (NCI-H295R) cell line was used as an in vitro biological model to study the effect of nickel chloride (NiCl2) on the viability and steroidogenesis. The cells were exposed to different concentrations (3.90; 7.80; 15.60; 31.20; 62.50; 125; 250 and 500 microM) of NiCl2 and compared with control group (culture medium without NiCl2). The cell viability was measured by the metabolic activity assay. Production of sexual steroid hormones was quantified by enzyme linked immunosorbent assay. Following 48 h culture of the cells in the presence of NiCl2 a dose-dependent depletion of progesterone release was observed even at the lower concentrations. In fact, lower levels of progesterone were detected in groups with higher doses (>/=125 microM) of NiCl2 (P<0.01), which also elicited cytotoxic action. A more prominent decrease in testosterone production (P<0.01) was also noted in comparison to that of progesterone. On the other hand, the release of 17beta-estradiol was substantially increased at low concentrations (3.90 to 62.50 microM) of NiCl2. The cell viability remained relatively unaltered up to 125 microM (P>0.05) and slightly decreased from 250 microM of NiCl2 (P<0.05). Our results indicate endocrine disruptive effect of NiCl2 on the release of progesterone and testosterone in the NCI-H295R cell line. Although no detrimental effect of NiCl2 (

• MeSH
• adrenokortikální karcinom metabolismus   patologie   MeSH
• adrenokortikální nádory metabolismus   patologie   MeSH
• endokrinní disruptory farmakologie   MeSH
• estradiol metabolismus   MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• nikl farmakologie   MeSH
• progesteron metabolismus   MeSH
• techniky in vitro MeSH
• testosteron metabolismus   MeSH
• viabilita buněk MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• endokrinní disruptory MeSH
• estradiol MeSH
• nikl MeSH
• progesteron MeSH
• testosteron MeSH

In mammalian ovaries, follicular atresia occurs periodically and destroys almost all the follicles in the ovary. Follicle-stimulating hormone (FSH) acts as the primary survival factor during follicular atresia by preventing apoptosis in granulosa cells (GCs). Many studies have demonstrated that oxidative stress-induced apoptosis is a main cause of follicular atresia. Reactive oxygen species (ROS)-induced GCs apoptosis is regulated by a variety of signaling pathways involving numerous genes and transcription factors. Therefore, we examined whether FSH inhibits the expression of p53 up-regulated modulator of apoptosis (PUMA) induced by reactive oxygen species (ROS) through phosphoinositide 3-kinase (PI3K) / protein kinase B (AKT) in mouse GCs. In vivo study: thirty-two-mice were randomly assigned to four groups and given FSH. We found that FSH can inhibit the 3-nitropropionic acid (3-NP) induced apoptosis and PUMA expression in mRNA level. Moreover, In vitro experiment, we found that FSH can inhibit the H(2)O(2)-induced apoptosis and PUMA expression in mRNA level. Additionally, we also found that PI3K/AKT inhibitor LY294002 abolished the downregulation of PUMA mRNA by FSH in vitro, In conclusion, FSH inhibit the expression of PUMA induced by ROS through PI3K/AKT pathway in vivo and vitro.

• MeSH
• apoptóza fyziologie   MeSH
• folikulární buňky účinky léků   metabolismus   MeSH
• folikuly stimulující hormon farmakologie   MeSH
• fosfatidylinositol-3-kinasy třídy I metabolismus   MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední ICR MeSH
• myši MeSH
• nádorové supresorové proteiny metabolismus   MeSH
• ovariální folikul účinky léků   metabolismus   MeSH
• primární buněčná kultura MeSH
• proteiny regulující apoptózu metabolismus   MeSH
• protoonkogenní proteiny c-akt metabolismus   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• signální transdukce MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• Akt1 protein, mouse MeSH Prohlížeč
• folikuly stimulující hormon MeSH
• fosfatidylinositol-3-kinasy třídy I MeSH
• nádorové supresorové proteiny MeSH
• Pik3ca protein, mouse MeSH Prohlížeč
• proteiny regulující apoptózu MeSH
• protoonkogenní proteiny c-akt MeSH
• PUMA protein, mouse MeSH Prohlížeč
• reaktivní formy kyslíku MeSH