A novel cysteine sulfinic Acid decarboxylase knock-out mouse: comparison between newborn and weanling mice.

摘要: We developed a novel cysteine sulfinic acid decarboxylase knockout mouse (CSAD KO) to investigate the critical roles of taurine. The absence CSAD gene was confirmed using Southern, northern and western blotting; homozygous (CSAD−/−) heterozygous (CSAD+/-) animals were identified PCR. Plasma taurine concentrations decreased by 86 % in CSAD−/− animals. Reproductive performance poor second later generations but restored supplementing drinking water with 0.05 Taurine at postnatal day 1 (PD1) generation (G1) close normal presumably due transport through placenta from CSAD+/− dam. In contrast, brain liver G2, G3, G4 very low birth. At month age (1 M), week after weaning, G1 concentration same level as CSAD−/−. all M reduced 44 WT 5 liver. supplementation levels 76 had little effect on Gene expression compared PD1 M. Expression prolactin receptor lactoferrin genes both Metabolic including serine dehydratase uridine phosphorylase 2 increased significantly not An oxidative stress gene, glutathioneperoxidase 3 KO−/− metabolism genes, dioxygenase (Cdo), cysteamine transporter (TauT) unaffected PD1. M, however, TauT twofold, while Cdo WT. These data indicate that KO is powerful model for exploring role deficiency various disorders especially since requirement can be supplied food or water.