In vitro assessment of the impact of nickel on the viability and steroidogenesis in the human adrenocortical carcinoma (NCI-H295R) cell line
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
32901497
PubMed Central
PMC8549914
DOI
10.33549/physiolres.934452
PII: 934452
Knihovny.cz E-zdroje
- 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
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 (
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