Co-induction of microsomal cytochrome P-452 and the peroxisomal fatty acid β-oxidation pathway in the rat by clofibrate and di-(2-ethylhexyl)phthalate: Dose-response studies
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Integrated physiology and systems biology of PPARα
2014, Molecular MetabolismCitation Excerpt :The stimulatory effect of in vivo fibrate treatment on fatty acid oxidation and oxidative enzymes can be detected in isolated mitochondria and peroxisomes [73–76]. Besides mitochondrial and peroxisomal fatty acid oxidation, fibrates also stimulate hepatic microsomal omega-hydroxylation of fatty acids [75,77–79]. In addition, fibrates markedly induce ketogenesis in cultured hepatocytes and rodent livers [68,73,80–82].
Effect of placental fatty acid metabolism and regulation by peroxisome proliferator activated receptor on pregnancy and fetal outcomes
2007, Journal of Pharmaceutical SciencesCitation Excerpt :Upon activation, PPARs generally regulate the transcription of fatty acid homeostasis‐related target genes by binding as heterodimers with retinoic acid X receptors to the PPAR response elements (PPRE, 5′‐AACT AGGNCA A AGGTCA‐3′, direct repeat with one nucleotide spacing two half sites, DR1) in the promoter region28 (Fig. 4). Some of the translated proteins are involved in the fatty acid/lipid transport and metabolism pathways, as summarized in Table 3.80–127 All three isoforms of PPAR have been detected in the human placenta, predominantly in the syncytiotrophoblast layer,128,129 suggesting their roles in regulating fatty acid transport and metabolism.
Protective effect of bezafibrate on streptozotocin-induced oxidative stress and toxicity in rats
2007, ToxicologyCitation Excerpt :Roles for β-cell necrosis and apoptosis are the core of the pathophysiology of diabetes mellitus. A link between the hypertrophic (peroxisome and microsome proliferation, increases in the activities of peroxisomal β-oxidation and the microsomal cytochrome P450 4A) and hyperplastic (increase in DNA synthesis, inhibition of apoptosis) markers in hepatocytes (Foxworthy and Eacho, 1986; Sharma et al., 1988; Foxworthy et al., 1990) effects of peroxisome proliferators (PPs) is indeed not to be excluded. The STZ diabetic animals (group II) exhibited persistent hyperglycemia.
Pretranslational upregulation of microsomal CYP4A in rat liver by intake of a high-sucrose, lipid-devoid diet containing orotic acid
2005, Biochemical PharmacologyCitation Excerpt :It is feasible that the observed effects of clofibric acid may be due in part to greater hepatic PPARα expression after treatment with the chemical. Early studies suggested that CYP4A and peroxisomal β-oxidation enzymes are coregulated by clofibric acid and other PP chemicals [26,32]. However, the differential responsiveness of PPARα-inducible genes to PPARα ligands has been documented more recently [29,33].
Profiling of hepatic gene expression in rats treated with fibric acid analogs
2004, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisBlood burden of di(2-ethylhexyl) phthalate and its primary metabolite mono(2-ethylhexyl) phthalate in pregnant and nonpregnant rats and marmosets
2004, Toxicology and Applied Pharmacology