Effect of Lecithin on <Emphasis Type="SmallCaps">d</Emphasis>-Galactosamine Induced Hepatotoxicity Through Mitochondrial Pathway Involving Bcl-2 and Bax

Twenty four Wistar strain albino rats were used for the investigations. Lecithin 50 and 100 mg/kg b wt was administered for 1 week by oral route. Liver damage was induced by intra peritoneal administration of 400 mg/kg b wt d-galactosamine on the last day. At the end of the study animals were sacrificed and liver enzyme levels, histopathology, mitochondrial integrity, expression of p53, Bax and Bcl-2 mRNA levels were studied. Increases in the liver enzyme levels by d-GalN were significantly inhibited by pretreatment with lecithin. Histopathological observation further confirmed the hepatoprotective effect of lecithin. In addition, the disruption of mitochondrial membrane, up regulation of Bax and down regulation of Bcl-2 mRNA levels in the liver of d-GalN intoxicated rats were effectively prevented by pretreatment with lecithin. The results of the present study validate our conviction that d-GalN causes hepatic damage via mitochondrial pathway involving Bax and Bcl-2.     

Tapping into existing information flows: The transformation to compliance by design in business-to-government information exchange

Transforming Business-to-Government (B2G) information exchange is a next frontier for reducing government spending while improving performance. This paper examines two different B2G information exchange architectures that reflect continuing transformations that empower some government agencies to do better compliance monitoring tasks with fewer resources. The win for the reporting companies is the lower cost of compliance. Instead of focusing on collecting compliance information from individual companies, the government agencies in this study focus on collecting information on the supply chain level, allowing for automated data reconciliation. Our findings reveal that pushing controls (automated checks) upstream (in company software and data sources) results in more efficiency, higher information quality and reduces redundant controls. The examined architectures exhibit high levels of compliance by design, meaning that many control objectives are by default encompassed in the design. This requires a well-aligned combination of data standardization (using shared syntax and semantics) and automated information processing (using an intelligent gateway between businesses and government agencies). However, achieving such an alignment is a difficult challenge; especially when taking into account that such transformations require solid governance, trust and high initial investments — prerequisites that are rare in many public-private partnerships.     

Effect of Lecithin and silymarin on D-galactosamine induced toxicity in isolated hepatocytes and rats

To investigate Lecithin for its hepatoprotective activity against D-galactosamine (D-GalN) induced toxicity in freshly isolated rat hepatocytes and animal models. Freshly isolated rat hepatocytes were exposed to Dgalactosamine (30 mM) along with/without lecithin (100 μg/ml) and the levels of selected liver enzymes were measured. Thirty six Wistar strain albino rats were used for the in vivo investigations. Lecithin 50 and 100 mg/kg.b.wt were administered for one week by oral route. Liver damage was induced by intra peritoneal administration of 400 mg/kg b.wt D-galactosamine. The antihepatotoxic effect of lecithin was observed in freshly isolated rat hepatocytes at concentration 100 μg/ml and was found to be similar to that of the standard silymarin used. Its in vivo hepatoprotective effect at 100 mg/kg b.wt was comparable with that of the standard silymarin at 100 mg/kg body weight. Lecithin was able to normalise the biochemical levels which were altered due to D-galactosamine intoxication in freshly isolated rat hepatocytes and also in animal models.     

Protective Role of Catechin on <Emphasis Type="SmallCaps">d</Emphasis>-Galactosamine Induced Hepatotoxicity Through a p53 Dependent Pathway

Objective of this study was to obtain a better understanding of the mechanism responsible for the d-galactosamine (d-GalN) induced hepatotoxicity and to study the effect of catechin against d-GalN induced hepatotoxicity. Catechin 50 and 100 mg/kg b.wt was administered for 1 week by oral route. Liver damage was induced by intra-peritoneal administration of 400 mg/kg b.wt d-galactosamine on the last day of catechin treatment. At the end of treatment all animals were killed and liver enzyme levels were estimated. Dissected hepatic samples were used for histopathology, RNA isolation, expression studies of Bax, Bcl-2 and p53 mRNA levels and mitochondrial membrane potential studies. We found that increases in the liver enzyme activity and decrease in antioxidant enzyme activity by d-GalN were significantly restricted by oral pretreatment with catechin. Disruption of mitochondrial membrane potential, up regulation of p53, Bax and down regulation of Bcl-2 mRNA levels in the liver of d-GalN intoxicated rats were effectively prevented by pretreatment with catechin.