Similar results were found with intestinal alkaline

phosphatase activity. In addition, Na+/K+-ATPase activity was found to be aggravated in diabetic rats by MCP treatment. Oxidative stress markers showed similar degree of change in both MCP and diabetic rats while MCP aggravated oxidative stress condition in diabetic rats. Scanning electron microscopy CSF-1R inhibitor and histological analysis of the small intestine revealed increased length of villi, congestion, goblet cell hyperplasia and infiltration of inflammatory cells in MCP and diabetic rats while MCP also induced necrotic lesions in diabetic rats. Collectively, our findings provide evidence that multiple doses of MCP has the propensity to augment diabetes associated intestinal dysfunctions in rats. (c) 2014 Elsevier Ireland Ltd. All rights reserved.”
“Active derivatives of vitamin A are essential in physiological processes such as cell growth, differentiation, morphogenesis and development. The biological functions of vitamin A are mediated through the retinoid acid receptors (RARs) and retinoid X receptors (RXRs). Aryl hydrocarbon receptor (AhR) agonists such as planar halogenated compounds are known to interfere with vitamin A homeostasis in both field and laboratory CYT387 studies. In this study, we have investigated the molecular

interactions between vitamin A and AhR signalling pathways using juvenile Atlantic salmon and agonists for both receptor pathways. Groups of juvenile salmon were treated with all-trans- and 9-cis-retinoic acid mixture (7:3 ratio) dissolved in DMSO (dimethyl

sulfoxide) at 0.1, 1 and 10 mg/kg fish weight. The mixture was force fed singly or in combination with 0.1 mg 3,3′,4,4′-tetrachlorobiphenyl (co-planar congener 77)/kg fish weight dissolved in DMSO. Liver samples were collected 3 days after PCB-77 exposure. A separate group exposed to combined retinoic acid (1 mg/kg for 5 days) and PCB-77, was sampled at 3, 7 and 14 days after PCB-77 exposure. Liver samples collected from all exposure groups were analyzed for gene (RARce, AhR2 alpha, AhR2 beta, CYP1A1, UGT1 and GST pi) expression using real-time PCR and activity (7-ethoxyresorufin O-deethylase (EROD), UGT and GST) MX69 cell line using biochemical methods with specific substrates. Our data showed that exposure to RA alone did not produce a significant increase of RAR alpha mRNA levels, and the presence of PCB-77 attenuated the expression of RAR alpha in RA dose- and time-specific manner. In addition, RA produced a dose-dependent increase of CYP1A1 mRNA and activity (EROD) levels without concomitant increase in AhR2 isoforms. When administered alone, PCB-77 produced increased CYP1A1, UGT1 and GST pi mRNA and enzyme levels. The PCB-77-induced CYP1A1, UGT1 and GST pi (mRNA and activity) levels were modulated by RA, in a parameter and dose-specific manner.