Apoptotic effects of 25-hydroxycholesterol in immature rat Sertoli cells: prevention by 17beta-estradiol.
Reprod Toxicol
; 21(3): 329-34, 2006 Apr.
Article
em En
| MEDLINE
| ID: mdl-16260115
ABSTRACT
The aim of the present study was to determine whether or not apoptosis occurs in Sertoli cells in presence of 25-hydroxycholesterol, an oxysterol derived from cholesterol-containing foods or endogenous oxidation. Here, we provide evidence that 25-hydroxycholesterol can induce cultured Sertoli cells of immature rat to undergo apoptosis. The cell death was identified by analysis of fragmented DNA detected using enzyme-immunoassay. After 48 h of treatment with 50 microM of 25-hydroxycholesterol, apoptosis increased by 70% in Sertoli cells. Moreover, 50 microM of 25-hydroxycholesterol inhibited the incorporation of [14C] acetate into cholesterol by 70%. Addition of mevanolate to prevent isoprenoid deficiency do not inhibit the apoptosis generated by 25-hydroxycholesterol. In contrast, this increase of DNA fragmentation was reversed by addition of caspase-3 inhibitors as Ac-DEVD-CHO or Ac-ESMD-CHO. Bcl-2 mRNA level in the Sertoli cells decreased by 60% after 24 h exposure to 25-hydroxycholesterol. In parallel, Bax mRNA level increased by 40% in the Sertoli cells incubated in presence of 50 microM of 25-hydroxycholesterol. Physiological concentrations of 17beta-estradiol (10 or 100 nM) elicited a significant protection on apoptosis generated by 25-hydroxycholesterol in Sertoli cells. Our results show that the 25-hydroxycholesterol would control the cholesterol synthesis without toxic effect in immature rat Sertoli cells, these cells being able to protect themselves by estradiol production.
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Base de dados:
MEDLINE
Assunto principal:
Células de Sertoli
/
Apoptose
/
Estradiol
/
Inibidores de Caspase
/
Hidroxicolesteróis
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2006
Tipo de documento:
Article