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Microgram-order ammonium perfluorooctanoate may activate mouse peroxisome proliferator-activated receptor alpha, but not human PPARalpha.
TLDR
Human PPARalpha may be less responsive to PFOA than that of mice when a relatively low dose is applied, and this information may be very valuable in considering whether P FOA influences the lipid metabolism in humans. Expand
Bisphenol A may cause testosterone reduction by adversely affecting both testis and pituitary systems similar to estradiol.
TLDR
BPA directly affects not only the Leydig cells but also the pituitary gland, but the former may be impaired at lower exposure concentrations than the latter, as observed at lower levels of exposure to BPA or E2. Expand
Molecular mechanism of trichloroethylene-induced hepatotoxicity mediated by CYP2E1.
TLDR
This study directly demonstrates that CYP2E1 was the major P450 involved in the first step of the TRI metabolism, and the metabolites produced may have two opposing roles: one inducing hepatotoxicity and the other protecting against the toxicity. Expand
Nanoparticle-rich diesel exhaust may disrupt testosterone biosynthesis and metabolism via growth hormone.
TLDR
Disruption of testosterone biosynthesis by NR-DE exposure may be a mode of action for reproductive toxicity, which may, in part, be regulated by increasing StAR and P450scc expressions via GH signalling. Expand
Differential Response to Trichloroethylene-Induced Hepatosteatosis in Wild-Type and PPARα-Humanized Mice
TLDR
TRI exposure elevated nuclear factor-kappa B p52 mRNA and protein in all mice regardless of PPARα genotype, and NFκB-p52 is a candidate molecular marker for inflammation caused by TRI, and PPAR α may be involved in TRI-induced hepatosteatosis. Expand
Modulation of ammonium perfluorooctanoate-induced hepatic damage by genetically different PPARα in mice
TLDR
Milligram-order APFO activated both mouse and human PPARα in a different manner, which may reflect histopathologically different types of hepatic damage. Expand
Hepatic peroxisome proliferator-activated receptor α may have an important role in the toxic effects of di(2-ethylhexyl)phthalate on offspring of mice.
TLDR
Taking together, PPARα expression is required for the toxicity of DEHP in fetuses and pups and altered plasma triglyceride levels, through regulation of MTP may be important in mPPARα mice and not in hPPAR α mice. Expand
Plasticizers May Activate Human Hepatic Peroxisome Proliferator-Activated Receptor α Less Than That of a Mouse but May Activate Constitutive Androstane Receptor in Liver
TLDR
Generally, hepatic PPARα of mPPAR α mice was more strongly activated than that of hPPARα mice when several target genes involving β-oxidation of fatty acids were evaluated, and all plasticizers also activated hepatic constitutive androstane receptor (CAR) more in hPParα mice than in mPP ARα mice. Expand
Environmental and Occupational Risk Factors Associated with Chronic Kidney Disease of Unknown Etiology in West Javanese Rice Farmers, Indonesia
TLDR
A prevalence estimate of CKDu in male rice farmers in West Java, Indonesia is obtained and the relationship between CKDu and environmental and occupational factors is analyzed to investigate more on the association of those environmental and Occupational factors with CKDu. Expand
Ammonium perfluorooctanoate may cause testosterone reduction by adversely affecting testis in relation to PPARα.
TLDR
It is suggested that APFO may disrupt testosterone biosynthesis by lowering the delivery of cholesterol into the mitochondria and decreasing the conversion of cholesterol to pregnenolone and androstandione in the testis of mPPAR α and hPPARα mice, which may, in part, be related to APFO-induced mitochondrial damage. Expand
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