The effect of the degree of oxidation and the molecular structure of cobalt complexes with imidazole on the metabolic profiles of CCD 841 CoN and HT-29 cells

Colorectal cancer is among the most prevalent causes of cancer-related morbidity and mortality on a global scale, underscoring the necessity of novel chemotherapeutic strategies that exhibit enhanced selectivity and diminished systemic toxicity. The present study investigates the biological impact of three structurally diverse cobalt complexes bearing imidazole: the polymeric [Co(II)(imid)₂], the dimeric [Co(III)(Himid)(L-(α)-histidine)₂]₂O₂^2-, and the mononuclear Co(II)(Himid)₂(H₂O)₂CO_3. The first complex, [Co(II)(imid)₂]_n, is regarded as a paradigm of a coordination compound that crystallizes in an infinitely polymeric network, wherein each cobalt atom is linked via imidazole bridges to four adjacent cobalt atoms. The second complex, [Co(III)(Himid)(L-(α)-histidine)₂]₂O₂^2-, is a dimeric, diamagnetic complex with an O₂ molecule coordinated in the peroxide form with an O₂^2- (μ-peroxo) bridge between two cobalt ions oxidized to Co(III). The third complex, Co(II)(Himid)₂(H₂O)₂CO₃, represents the first documented instance of a carbonate group functioning as a bidentate ligand in a solid cobalt complex. The biological effects of the aforementioned compounds were evaluated against normal human colon epithelial cells (CCD 841 CoN) and colonic adenocarcinoma cells (HT-29). MTT assays revealed that the dimeric Co(III) complex exhibited no cytotoxic effect on either cell line. In contrast, both the polymeric and mononuclear Co(II) compounds elicited a substantial, concentration-dependent enhancement in cell viability in HT-29 cells, reaching up to 400 % relative to the control, and a non-significant cytotoxic effect in CCD 841 CoN cells. The results suggest that both Co(II) complexes might trigger a pseudohypoxic metabolic shift in colorectal cancer cells, whereas the Co(III) complex remains biologically inert.