文化大學機構典藏 CCUR:Item 987654321/20877
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    題名: Effects and Mechanisms of Nonylphenol on Corticosterone Release in Rat Zona Fasciculata-Reticularis Cells
    作者: Chang, LL (Chang, Ling-Ling)
    Wun, WSA (Wun, Wan-Song Alfred)
    Wang, PS (Wang, Paulus S.)
    貢獻者: 化材系
    關鍵詞: ACTIVATED PROTEIN-KINASE
    ACUTE REGULATORY PROTEIN
    ENDOCRINE-DISRUPTING CHEMICALS
    NITRIC-OXIDE SYNTHASES
    LEYDIG TUMOR-CELLS
    ALKYLPHENOL ETHOXYLATES
    OVARIECTOMIZED RATS
    METABOLIC SYNDROME
    GLOMERULOSA CELLS
    L-ARGININE
    日期: 2010-12
    上傳時間: 2011-12-08 15:37:00 (UTC+8)
    摘要: Alkylphenol ethoxylate, consisting of similar to 80% nonylphenol ethoxylate (NPEO), is a major group of nonionic surfactant. The primary degradation product of NPEO, nonylphenol (NP), interferes with reproduction, induces cell death in gonads, and leads to changes in other reproductive parameters. With such apparent stress, NP is believed to induce stress response mechanism, i.e., adrenal cortical hormone. However, the effects and action mechanisms of NP on rat adrenal zona fasciculata-reticularis (ZFR) cells are still unclear. This study explored the effects of NP on corticosterone release. ZFR cells were incubated with NP in the presence or absence of adrenocorticotropin (ACTH), 8-bromo-cyclic 3',5'-adenosine monophosphate (8-Br-cAMP), forskolin (FSK), 25-hydroxyl cholesterol (25-OH-cholesterol), pregnenolone, progesterone, or deoxycorticosterone at 37 degrees C for 1 h. The concentrations of corticosterone or pregnenolone in the spent media were measured by radioimmunoassay. The expressions of steroidogenic acute regulatory (StAR) protein, cytochrome P450 side-chain cleavage (P450scc) protein, and 11 beta-hydroxylase in the cells were measured by Western blot. The data demonstrated that (1) NP stimulated corticosterone release induced by ACTH, 8-Br-cAMP, FSK, 25-OH-cholesterol, pregnenolone, progesterone, or deoxycorticosterone; (2) NP significantly increased pregnenolone release in the control, 25-OH-cholesterol, trilostane, and 25-OH-cholesterol + trilostane groups; (3) NP-stimulated corticosterone release was estrogen receptor dependent, but mediated by nitric oxide and p38 mitogen-activated protein kinase pathway independent; and (4) NP did not affect StAR, 11 beta-hydroxylase, or P450scc protein expression. These results suggest that NP acts directly on rat ZFR cells to stimulate corticosterone release and that the stimulation mechanism of NP mediates through post-cAMP corticosterone manufacture enzymes, i.e., P450scc and 11 beta-hydroxylase.
    顯示於類別:[化學工程與材料工程學系暨碩士班] 期刊論文

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