Project description:Mixed MCBA PBFM dosing of wild-type C57BL/6Crl mice. 80 mg/kg total bile acid dose (10 mg/kg individual MCBA). MCBAs included in the dosing included AlaCA, AspCA, GluCA, LeuCA, PheCA, SerCA, ThrCA, and TyrCA.
Project description:Mixed MCBA PBFM dosing of wild-type C57BL/6Crl mice. 80 mg/kg total bile acid dose (10 mg/kg individual MCBA). MCBAs included in the dosing included AlaCA, AspCA, GluCA, LeuCA, PheCA, SerCA, ThrCA, and TyrCA.
Project description:The modes of triazole reproductive toxicity have been characterized by an observed increased in serum testosterone and reduced insemination and fertility indices. The key events involved in the disruption in testosterone homeostasis and reduced fertility remain unclear. Gene expression analysis was conducted on liver from Sprague Dawley rats dosed with myclobutanil (300 mg/kg/day), propiconazole (300 mg/kg/day), or triadimefon (175 mg/kg/day) for 72 hours. Pathway-based analysis highlighted key biological processes affected by all three triazoles in the liver including fatty acid catabolism, steroid metabolism, and xenobiotic metabolism. Within the pathways identified in the liver, specific genes involved in phase I-III metabolism and fatty acid metabolism were affected by all three triazoles. These modulated genes are part of a network of lipid and testosterone homeostasis pathways regulated by the constitutive androstane (CAR) and pregnane X (PXR) receptors. Gene expression profiles from this study indicate triazoles activate CAR and PXR; increase fatty acid catabolism and steroid metabolism in the liver; constituting a plausible series of key events contributing to the observed disruption in testosterone homeostasis. Experiment Overall Design: A total of 12 liver samples were analyzed. Three biological replicates each for the controls, 300 mg/kg/day myclobutanil, 300 mg/kg/day propiconazole, and 175 mg/kg/day triadimefon.
Project description:In this time course pregnant CD-1 (outbred) dams were exposed to MeHg as monomethylmercuric chloride intraperitoneally on 9 d.p.c. The test dose of 5.0 mg/kg MeHg was selected as a dose with an estimated 20% increased risk for encephalopathy in term fetuses, with no evidence of maternal toxicosis. Sampling intervals ranged from 1.5h to 24.0h post-exposure. All measurements were on RNA from the embryonic forebrain (prosencephalon) using contemporous control embryos as a reference. Keywords = time series Keywords = mercury Keywords = embryo Keywords = Fetal Minamata Disease Keywords: time-course
Project description:C57BL/6Crl mice were fed 10 mg/kg BA or control for 13 days. Samples collected on day 14. Treatment groups included serocholate, serine + cholate, phenylalanocholate, phenylalanine + cholate, taurocholate, taurine + cholate, and a mock control.
Fecal, F; Colon, CL; Cecum, CE; Duodenum, DD; Gallbladder, GB; Ileum, IL; Liver, L
Project description:In this time course pregnant CD-1 (outbred) dams were exposed to the 2-chloro analogue of 2'-deoxyadenosine (a metabolic toxin) on 8 d.p.c. The test dose of 2.5 mg/kg 2CdA was modeled for a 5% increased risk of microphthalmia in term fetuses. Sampling intervals were anchored to the conditional biomarker (p53 protein induction) expressed in 2CdA-treated embryos between 3.0- and 4.5h post-exposure. Since p53 protein induction has been defined as a critical event in 2CdA-induced micropthalmia, these sampling intervals represent times before (3.0h), during (4.5h), and after (6.0h) this critical event. All measurements were on RNA from the embryonic headfold. Keywords = time series Keywords = 2-chloro-2'-deoxyadenosine Keywords = embryo Keywords = p53 protein induction Keywords = microphthalmia Keywords: time-course