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Expression of the genes for 3p-hydroxysteroid dehydrogenase type 1 and cytochrome P450scc during syncytium formation by human placental cytotrophoblast cells in culture and the regulation by progesterone and estradiol.
At the end of the incubation, the medium was collected from the 24-well plates and stored at -20[degrees]C for testosterone measurements, and cells were collected for the measurements of StAR, P450scc and 3[beta]-HSD-1 mRNA.
BPA exposure resulted in a significant downregulation of StAR expression, but P450scc and 3[beta]-HSD levels were apparently unaffected (Figure 3D,E).
Immunoreactive StAR, P450scc, or 3[beta]-HSD proteins were visualized with an avidin-biotin-enhanced horseradish peroxidase method (Vector Laboratories, Burlingame, CA, USA) using diaminobenzadine as the substrate, followed by a light nuclear counter-stain with Gill's hematoxylin.
Reduced testosterone levels were accompanied by the decreased expression of StAR (steroidogenic acute regulatory protein) and 3[beta]-HSD (3[beta]-hydroxysteroid dehydrogenase), as well as increased levels of P450scc (cytochrome P450 side chain cleavage), in Leydig cells.
The up-regulation of P450scc expression after exposure to B[alpha]P appears to be associated with a compensatory mechanism for producing the maximum amount of pregnenolone with the minimum amount of transported cholesterol by StAR; the down-regulation of 3[beta]-HSD may occur because B[alpha]P can negatively target 3[beta]-HSD, which is required for testosterone production.
Testicular cytochrome P450scc and LHR as possible targets of 2,3,7,8-tetrachlorodibenzo-p-dioxvn (TCDD) in the mouse.
Cycling conditions for P450scc were the same except the annealing/extension was carried out at 55.
Thus, DBP exposure in utero reduces expression of genes encoding proteins involved in cholesterol uptake and transport into the mitochondrion, as well as suppressing P450scc and P45017-hydroxylase (Barlow et al.
In rodent Leydig cells, TCDD has been shown to decrease the secretion of testosterone through interference with LH receptor expression, impairment of the cholesterol mobilization to mitochondrial cytochrome P450scc, or reduction of the activity of this enzyme, thus interfering with the first steps in testosterone production (Fukuzawa et al.
For Leydig cell function, we evaluated immunoexpression of two protein markers: P450scc and 3[beta]-hydroxysteroid dehydrogenase (3[beta]-HSD).
Immunolocalization of steroidogenic enzymes p450scc, 3-beta-hsd, p450c17 and p450arom in the corpus-luteum of the Hokkaido brown bear (Ursus arctos Yesoensis) in relation to delayed implantation.
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