Ketamine Induces Mitochondrial Fission and Dysfunction in Cervical Cancer Cells via RhoA‐Dependent DRP‐1 Activation
Journal of Biochemical and Molecular Toxicology September 21, 2025 Yanfang Zhou, Guangming Chen, Ye Zhu 2 citations
Ketamine, an anesthetic, kills C33A cervical cancer cells by damaging their mitochondria. It causes dose-dependent increases in GGT and LDH release and reduces cell viability. At 100 μM, ketamine lowers Complex IV activity, mitochondrial membrane potential, and ATP production, and triggers mitochondrial fragmentation. It raises levels of mitochondrial p-Drp1 and enhances expression of CaMK II and RhoA, but not Rac1/Cdc42. Blocking RhoA, but not CaMK II, reduces ketamine's effects on mitochondrial DRP-1 activation, fragmentation, and dysfunction, indicating RhoA as a key mediator. This suggests ketamine could be developed as a therapy targeting mitochondrial dynamics in cervical cancer.