Exploring the role of quercetin on doxorubicin and lapatinib-mediated cellular and mitochondrial responses using <i>in vitro</i> and <i>in silico</i> studies

Ergüç A., Albayrak G., Muhammed M. T., Karakuş F., Arzuk E., İnce-Ergüç E.

JOURNAL OF CHEMOTHERAPY, vol.38, no.1, pp.32-46, 2026 (SCI-Expanded, Scopus) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 38 Issue: 1
  • Publication Date: 2026
  • Doi Number: 10.1080/1120009x.2025.2471154
  • Journal Name: JOURNAL OF CHEMOTHERAPY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE
  • Page Numbers: pp.32-46
  • Ondokuz Mayıs University Affiliated: Yes

Abstract

Doxorubicin (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.