Yildiz, AzibeDemiralp, TugbaVardi, NigarOtlu, GulTaslidere, ElifCirik, HilalGurel, Elif2024-08-042024-08-0420220040-8166https://doi.org/10.1016/j.tice.2022.101824https://hdl.handle.net/11616/100682Exposure to various organic compounds including several environmental pollutants and drugs can cause cellular damage through the generation of lipid peroxidation products. Carbon tetrachloride (CCl4) is a potent toxic agent that causes peroxidative degeneration in many tissues. Dexpanthenol (Dxp) is a member of the B complex vitamins that exhibits antioxidant effects against lipid peroxidation products. This study was designed to evaluate the cardioprotective effect of Dxp against CCl4-induced myocardial toxicity in rats. Administration of a single dose of CCl4 caused cardiotoxicity by the increase in lipid peroxidation and histopathological changes (cardiomyocytes degeneration, interstitial edema) in the myocardial tissue. Moreover, CCl4 caused a decrease in lactate dehydrogenase (LDH) and troponin-I immunoreactivities, while significantly increasing tumor necrosis factor-alpha (TNF-alpha) and caspase-3 immunoreactivities. On the other hand, administration of Dxp improved biochemical, histopathological, and immunohistochemical parameters compared to the CCl4 treated group. Overall, this study suggests that Dxp is effective in inhibiting CCl4-induced lipid peroxidation, and that administration of Dxp may help prevent CCl4 related inflammation, necrosis, and apoptosis on the cardiac tissue.eninfo:eu-repo/semantics/closedAccessCarbon tetrachlorideCardiotoxicityDexpanthenolHistopathologyImmunohistochemistrylipid peroxidationArticle773565390710.1016/j.tice.2022.1018242-s2.0-85131128444Q2WOS:000807877200003Q1