@article {Chavezjpet.116.239301, author = {Enrique Chavez and Maria Guadalupe Lozano-Rosas and Mariana Dominguez-Lopez and Gabriela Velasco-Loyden and Jesus Rafael Rodriguez-Aguilera and Concepcion Jose-Nunez and Marietta Tuena de Gomez-Puyou and Victoria Chagoya de Sanchez}, title = {Functional, metabolic, and dynamic mitochondrial changes in the rat cirrhosis-hepatocellular carcinoma model and the protective effect of IFC-305.}, elocation-id = {jpet.116.239301}, year = {2017}, doi = {10.1124/jpet.116.239301}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {Background: Mitochondrion is an important metabolic and energetic organelle which regulates several cellular processes. Mitochondrial dysfunction has been related with liver diseases including hepatocellular carcinoma. As a result, the energetic demand is not properly supplied and mitochondrial morphologic changes has been observed resulting in an altered metabolism. We previously demonstrated the chemopreventive effect of the hepatoprotector IFC-305. Aim: In this work we aimed to evaluate the functional, metabolic, and dynamic mitochondrial alterations in the sequential model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats and the possible beneficial effect of IFC-305. Methods: Experimental groups of rats were formed to induce cirrhosis-hepatocellular carcinoma and to assess the IFC-305 effect during cancer development and progression through the evaluation of functional, metabolic and dynamic mitochondrial parameters. Results: In this experimental model, dysfunctional mitochondria were observed and suspension of the diethylnitrosamine treatment was not enough to restore them. Administration of IFC-305 maintained and restored the mitochondrial function and regulated parameters implicated in metabolism as well as the mitochondrial dynamics modified by diethylnitrosamine intoxication. Conclusion: This study supports IFC-305 as a potential hepatocellular carcinoma treatment or as an adjuvant in chemotherapy.}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/early/2017/02/16/jpet.116.239301}, eprint = {https://jpet.aspetjournals.org/content/early/2017/02/16/jpet.116.239301.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }