Effect of cytidine and uridine on regeneration of the liver in rats poisoned with carbon tetrachloride

Bushma, M. I.; Parkhovchenko, É. I.; Peschanskii, V. S.

doi:10.1007/bf00830369

Cited by 3 publications

(2 citation statements)

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“…34 In addition, administration of uridine or cytidine suppresses liver hexosamine and collagen and reduces ornithine carbamyl transferase activity in liver, thus preventing the liver cell necrosis and fibrosis. 35 Therefore, the increased uridine was likely to prevent the DBR-induced liver damage. Our results revealed that pyrimidine metabolism was critical for the hepatotoxicity process, and it might represent a potentially novel metabolic pathway involved in the mechanism of DBR-induced liver injury.…”

Section: ■ Discussionmentioning

confidence: 99%

“…Uridine, a pyrimidine nucleoside containing uracil and ribose, can exert protective effects against drug-induced hepatotoxicity and psychiatric disorders . In addition, administration of uridine or cytidine suppresses liver hexosamine and collagen and reduces ornithine carbamyl transferase activity in liver, thus preventing the liver cell necrosis and fibrosis . Therefore, the increased uridine was likely to prevent the DBR-induced liver damage.…”

Section: Discussionmentioning

confidence: 99%

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Integrated Metabolomics and Proteomics Approach To Identify Metabolic Abnormalities in Rats with Dioscorea bulbifera Rhizome-Induced Hepatotoxicity

Dong-sheng

Jiang

Wang

et al. 2018

Chem. Res. Toxicol.

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Previous studies have shown that Dioscorea bulbifera rhizome (DBR) can induce hepatotoxicity in clinical practice. However, its underlying mechanisms remain largely unexplored. In the present study, we investigated the global effect of DBR exposure on the proteomic and metabolomic profiles in rats over a 12-week administration using an integrated proteomics and metabolomics approach. The abundance of 1366 proteins and 58 metabolites in the liver of rats after subchronic exposure to DBR was dose-dependently altered. The results indicated that DBR mainly damaged hepatic cells through the aberrant regulation of multiple systems mainly including purine metabolism, pyrimidine metabolism, taurine and hypotaurine metabolism, and bile acid metabolism. Notably, the deregulated proteins including Pnp, Dpyd, Upp1, and Tymp and the differential metabolites including uridine, uracil, cytidine, thymine, adenine, adenosine, adenosine 3'-monophosphate, and deoxycytidine were well correlated to purine and pyrimidine metabolism, which might be novel pathways involved in metabolic abnormalities in rats with DBR-induced liver damage. Collectively, these findings not only contributed to understanding the mechanisms underlying the hepatotoxicity of DBR, but also illustrated the power of integrated proteomics and metabolomics approaches to improve the identification of metabolic pathways and biomarkers indicative of herb-induced liver injury.

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Section: ■ Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%