TY - JOUR
T1 - Visible-light-induced CO-releasing properties and cytotoxicity of a Ru(II) carbonyl complex containing 2-(pyridin-2-yl)-quinoxaline
AU - Khaled, Rabaa M.
AU - Abo-Elfadl, Mahmoud T.
AU - Radacki, Krzysztof
AU - Abo Zeid, Mona A.M.
AU - Shehab, Ola R.
AU - Abdel-Kader, Nora S.
AU - Mostafa, Gamal A.E.
AU - Ali, Essam A.
AU - Al Neyadi, Shaikha S.
AU - Mansour, Ahmed M.
N1 - Publisher Copyright:
© The Royal Society of Chemistry 2025.
PY - 2025/1/3
Y1 - 2025/1/3
N2 - The photo-induced CO-releasing properties of the dark-stable complex [RuCl2(CO)2L] (L = 2-(pyridin-2-yl)quinoxaline) were investigated under 468 nm light exposure in the presence and absence of biomolecules such as histidine, calf thymus DNA and hen egg white lysozyme. The CO release kinetics were consistent regardless of the presence of these biomolecules, suggesting that they did not influence the CO release mechanism. The quinoxaline ligand demonstrated exceptional cytotoxicity against human acute monocytic leukemia cells (THP-1), with evidence of potential DNA damage ascertained by comet assay, while it remained non-toxic to normal kidney epithelial cells derived from African green monkey (Vero) cell lines. In contrast, upon light activation, the Ru(II) complex showed no toxicity against THP-1 cells but was detrimental to Vero cells. In human colorectal carcinoma (HCT-116) cells, the ligand and the Ru(II) complex produced ROS under light and dark conditions. However, HCT-116 cells retained their ability to consume oxygen and produce ATP following CO treatment, suggesting that the ROS levels were insufficient to cause significant cellular damage. Morphological features of apoptosis, including apoptotic bodies, chromatin condensation, cell shrinkage, and membrane leakage, were observed in the presence of both the ligand and its complex, irrespective of light exposure.
AB - The photo-induced CO-releasing properties of the dark-stable complex [RuCl2(CO)2L] (L = 2-(pyridin-2-yl)quinoxaline) were investigated under 468 nm light exposure in the presence and absence of biomolecules such as histidine, calf thymus DNA and hen egg white lysozyme. The CO release kinetics were consistent regardless of the presence of these biomolecules, suggesting that they did not influence the CO release mechanism. The quinoxaline ligand demonstrated exceptional cytotoxicity against human acute monocytic leukemia cells (THP-1), with evidence of potential DNA damage ascertained by comet assay, while it remained non-toxic to normal kidney epithelial cells derived from African green monkey (Vero) cell lines. In contrast, upon light activation, the Ru(II) complex showed no toxicity against THP-1 cells but was detrimental to Vero cells. In human colorectal carcinoma (HCT-116) cells, the ligand and the Ru(II) complex produced ROS under light and dark conditions. However, HCT-116 cells retained their ability to consume oxygen and produce ATP following CO treatment, suggesting that the ROS levels were insufficient to cause significant cellular damage. Morphological features of apoptosis, including apoptotic bodies, chromatin condensation, cell shrinkage, and membrane leakage, were observed in the presence of both the ligand and its complex, irrespective of light exposure.
UR - https://www.scopus.com/pages/publications/85216981675
UR - https://www.scopus.com/pages/publications/85216981675#tab=citedBy
U2 - 10.1039/d4dt03082f
DO - 10.1039/d4dt03082f
M3 - Article
C2 - 39751836
AN - SCOPUS:85216981675
SN - 1477-9226
VL - 54
SP - 2529
EP - 2539
JO - Dalton Transactions
JF - Dalton Transactions
IS - 6
ER -