Briefly, primers were designed for ACOX, apolipoprotein A-1 (APO-A1), cate-cholamine O-methyltransferase (COMT), cytochrome P450 4A1 (CYP4A1), cytosolic epoxide hydrolase (CEH), hydroxyacyl-CoA dehydrogenase (HCD), paraoxonase 1 (PON1), PPAR[alpha], and phosphoenolpyruvate carboxykinase (PEPCK) with Primer Express software (PerkinElmer Applied Biosystems, Foster City, CA, USA) following the manufacturer's advice for optimal primer design for the TaqMan reactions.
In both in vivo studies, an increase in ACOX activity 2-3 times that of the control was demonstrated at the high-dose (250 mg/kg/day) level only (Figure 1).
HCD, 3-ketoacyl-CoA thiolase A + B (3KCTA+B), ACOX, aldehyde dehydrogenase 1 (ADH1), and CYP4A1].
ACOX, 3KCTA+B) and metabolism of bile acids were also seen at 3 days as well as genes representative of peroxisome biogenesis.
For example, at days 3 and 7, there was variance in the percentage of liver weight increase, which was also reflected in levels of ACOX activity.
2001), and it has been shown that PPs such as clofibrate induce expression of genes encoding ACOX, enoyl-CoA hydratase, HCD (multifunctional enzyme), and ketoacyl-CoA thiolase, all of which are responsible for very long-chain fatty acid [beta]-oxidation in peroxisomes (Amacher et al.