An approximate method has been established to calculate the depth of the potential acting on an electron in a molecule at the saddle point along a chemical bond, denoted by Dpb. It is a new indicator which can be used...An approximate method has been established to calculate the depth of the potential acting on an electron in a molecule at the saddle point along a chemical bond, denoted by Dpb. It is a new indicator which can be used for predicting the strength of a chemical bond. In this work, as a practical application for demonstrating this method, we calculated the Dpb of deoxyribonucleosides and ribonucleosides along all C-H and N-H chemical bonds using the method. The results are in fair agreement with those results of previously reported experimental and theoretical observations,展开更多
New ribonucleoside analogues containing thio-substituted 1,3,4-triazole as heterocyclic base have been synthesized via condensation of the central intermediate 1 with various acids, esters, amides, and anhydrides in a...New ribonucleoside analogues containing thio-substituted 1,3,4-triazole as heterocyclic base have been synthesized via condensation of the central intermediate 1 with various acids, esters, amides, and anhydrides in anhydrous solvent followed by deprotection.展开更多
In the present study, the effect of 5-aminoimidazole-4-carboxamide ribonucleoside （AICAR） on long-chain fatty acid oxidation by hepatocytes isolated from suckled neonatal pig liver （a low ketogenic and lipogenic ti...In the present study, the effect of 5-aminoimidazole-4-carboxamide ribonucleoside （AICAR） on long-chain fatty acid oxidation by hepatocytes isolated from suckled neonatal pig liver （a low ketogenic and lipogenic tissue） was tested Incubation of hepatocytes with AICAR （0.5 raM） in the presence of ] mM of carnitine and 10 mM of glucose for 1 hour at 37℃ had no significant effect on total [1-14C]-palrnitate （0.5 mM） oxidation （14CO2 and 14C-Acid soluble products （ASP））. Consistent with the fatty acid oxidation, carnitine palmitoyltransferase I activity and inhibition of its activity by malonyI-CoA （10 MM） assayed in cell homogenate also remained constant. However, addition of AICAR to the hepatocytes decreased 14CO2 production by 18% compared to control （p 〈 0.06）. The reduction of labeled carboxylic carbon accumulated in C02 caused a significant difference in distribution of oxidative products between 14C02 and 14C-ASP （p 〈 0.03） compared with the control. It was also noticed that acetyI-CoA carboxylase （ACC） was increased by AICAR （p 〈 0.03）, indicating that ACC might drive acetyI-CoA toward fatty acid synthesis pathway and induce an increase in distribution of fatty acid carbon to 14C-ASP. Addition of insulin to hepatocyte incubations with AICAR did not change the oxidative product distribution between CO2 and ASP, but further promoted ACC activity. The increased ACC activity was 70% higher than in the control group when citrate was absent in the reaction medium and was 30% higher when citrate was present in the medium. Our results suggest that AICAR may affect the distribution of metabolic products from fatty acid oxidation by changing ACC activity in hepatocyte isolated from suckled neonatal piglets; however, the basis for the increase in ACC activity elicited by AICAR is not apparent.展开更多
基金supported by the National Natural Science Foundation of China(Nos.21073080 and 21133005)
文摘An approximate method has been established to calculate the depth of the potential acting on an electron in a molecule at the saddle point along a chemical bond, denoted by Dpb. It is a new indicator which can be used for predicting the strength of a chemical bond. In this work, as a practical application for demonstrating this method, we calculated the Dpb of deoxyribonucleosides and ribonucleosides along all C-H and N-H chemical bonds using the method. The results are in fair agreement with those results of previously reported experimental and theoretical observations,
文摘New ribonucleoside analogues containing thio-substituted 1,3,4-triazole as heterocyclic base have been synthesized via condensation of the central intermediate 1 with various acids, esters, amides, and anhydrides in anhydrous solvent followed by deprotection.
基金supported by National Research Initiative Competitive Grant no. 2007-35206-17897 from the USDA National Institute of Food and Agriculture
文摘In the present study, the effect of 5-aminoimidazole-4-carboxamide ribonucleoside （AICAR） on long-chain fatty acid oxidation by hepatocytes isolated from suckled neonatal pig liver （a low ketogenic and lipogenic tissue） was tested Incubation of hepatocytes with AICAR （0.5 raM） in the presence of ] mM of carnitine and 10 mM of glucose for 1 hour at 37℃ had no significant effect on total [1-14C]-palrnitate （0.5 mM） oxidation （14CO2 and 14C-Acid soluble products （ASP））. Consistent with the fatty acid oxidation, carnitine palmitoyltransferase I activity and inhibition of its activity by malonyI-CoA （10 MM） assayed in cell homogenate also remained constant. However, addition of AICAR to the hepatocytes decreased 14CO2 production by 18% compared to control （p 〈 0.06）. The reduction of labeled carboxylic carbon accumulated in C02 caused a significant difference in distribution of oxidative products between 14C02 and 14C-ASP （p 〈 0.03） compared with the control. It was also noticed that acetyI-CoA carboxylase （ACC） was increased by AICAR （p 〈 0.03）, indicating that ACC might drive acetyI-CoA toward fatty acid synthesis pathway and induce an increase in distribution of fatty acid carbon to 14C-ASP. Addition of insulin to hepatocyte incubations with AICAR did not change the oxidative product distribution between CO2 and ASP, but further promoted ACC activity. The increased ACC activity was 70% higher than in the control group when citrate was absent in the reaction medium and was 30% higher when citrate was present in the medium. Our results suggest that AICAR may affect the distribution of metabolic products from fatty acid oxidation by changing ACC activity in hepatocyte isolated from suckled neonatal piglets; however, the basis for the increase in ACC activity elicited by AICAR is not apparent.
