High fat diet induces coenzyme Q10 depletion and dysregulation of mitochondrial complexes in rat liver cells

FRANCISCO BAEZ; DAMIAN SORIA; MARIO CONTIN ; LAURA VALDEZ; CAROLINA CANIFFI; VALERIA TRIPODI

Congreso; REUNIÓN CONJUNTA SAIC SAI&FAIC SAFIS 2022; 2022

High-fat diet induces metabolic syndrome, oxidative stress, proin-flammatory and prothrombotic state, hypertension, central obesity,and cardiovascular disease. Coenzyme Q (CoQ), is an endogenouspotent antioxidant located in the mitochondria with a key role in theATP production in the electron transport chain (ETC). Our aim is toassess the status of CoQ along with oxidized and reduced gluta-thione (GSSG and GSH), 2-thiobarbituric acid reactive substances(TBARS), mitochondrial complex activity (I-III and II-III), and serumlipidic profile in high-fat diet (HFD) fed rats. Wistar rats (n=20) wereequally and randomly divided at weaning (21 days), into two groupsthat received HFD or control diet (CD) until 14 weeks of age. The di-ets used differ only in fat content (60% of total calories came from fatin HFD and 16% in CD). After sacrifice, plasmatic CoQ and TBARSand CoQ, GSSG and GSH in liver homogenate were chromatogra-phycally determined together with the activity of liver mitochondrialcomplexes by spectrophotometry. In liver homogenate, CoQ andGSH were highly reduced in HFD respect to CD (CoQ: 0.7±0.2 vs1.4±0.7uM and GSH: 38±3 vs 54±3μmol/mg protein, respectively,p<0.05, mean±SEM). In mitochondria, complex activities were high-er for both complexes in HFD respect to CD (I-III: 134±10 vs 102±13and II-III: 24±2 vs 19±2nmol/min/mg protein, respectively, p<0.05,mean±SEM). Lipidic profile was consistent with an obesity model.Plasmatic CoQ and TBARS results reveal no changes between di-ets. HFD promotes a prooxidant imbalance with significative CoQdepletion in liver and a probable vicious circle in which higher ETCactivity increase mitochondrial reactive oxygen species generationand thus a higher antioxidant consumption.