Erguc, AliAlbayrak, GokayMuhammed, Muhammed TilahunKarakus, FuatArzuk, EgeInce-Erguc, Elif2025-05-102025-05-1020251120-009X1973-947810.1080/1120009X.2025.24711542-s2.0-85218688627https://doi.org/10.1080/1120009X.2025.2471154https://hdl.handle.net/20.500.14720/12390Doxorubicin (DOX) and lapatinib (LAP) have been reported to cause liver toxicity. The roles of mitochondrial and cellular responses in DOX and LAP mediated-hepatotoxicity have not been investigated with or without quercetin (QUE) in HepG2 cells sensitive to mitochondrial damage (high-glucose or galactose media) in addition to in silico studies. Our results revealed that cytosolic pathways might play role a in DOX-induced cytotoxicity rather than mitochondria. QUE exacerbated DOX-induced ATP depletion in both environments. Our data also indicated that cytosolic and mitochondrial pathways might play a role in LAP-induced cytotoxicity. Incubating QUE with LAP increased ATP levels in high-glucose media. Therefore, QUE might have protective effect against LAP-induced cytotoxicity resulting from cytosolic pathways. The findings from in vitro experiments that QUE increased DOX or LAP-induced mitochondrial dysfunction were confirmed by the results from in silico studies indicating that QUE incubated with LAP or DOX might increase mitochondrial dysfunction.eninfo:eu-repo/semantics/closedAccessDoxorubicinLapatinibQuercetinMitochondrial DysfunctionIn SilicoArticleQ4Q339988777WOS:001432909100001