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DOI 10.1016/j.tiv.2024.105988

Медицинская библиотека · Toxicology in vitro : an international journal published in association with BIBRA · 2024

Essential oil from Ocimum carnosum induces ROS mediated mitochondrial dysfunction and intrinsic apoptosis in HL-60 cells.

Agrawal Madhunika, Saxena A K, Agrawal Satyam Kumar

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Аннотация

The present study demonstrates that essential oil from Ocimum carnosum (EOC), possesses potent cytotoxic properties against human promyelocytic leukemia HL-60 cells. The results demonstrated a concentration- and time-dependent reduction in cell viability, with an IC50 value of 0.029 μl/ml after 24 h. Further mechanistic studies revealed that EOC induces apoptosis, a regulated form of cell death in HL-60 cells. This was evidenced by morphological changes characteristic of apoptosis, including cell shrinkage, membrane blebbing, and nuclear condensation. Additionally, flow cytometric analysis demonstrated a significant increase in the sub-G0 cell population, indicative of DNA fragmentation. The mitochondrial pathway of apoptosis appears to be involved in EOC-induced cell death. A loss of mitochondrial membrane potential and the subsequent release of cytochrome c into the cytosol were observed. Pronounced quantity of cytosolic cytochrome c was associated with Bcl-2 depletion. Moreover, cytochrome c, in conjunction with other apoptotic factors, activates caspases, a family of cysteine proteases that execute cell death. These findings collectively indicate that EOC possesses promising anti-cancer properties through the induction of apoptosis via a mitochondrial-dependent pathway. However, further studies are required to elucidate the precise molecular mechanisms underlying EOC's cytotoxic effects and to evaluate its therapeutic potential in vivo.

Для цитирования: Agrawal Madhunika, Saxena A K, Agrawal Satyam Kumar. Essential oil from Ocimum carnosum induces ROS mediated mitochondrial dysfunction and intrinsic apoptosis in HL-60 cells.. Toxicology in vitro : an international journal published in association with BIBRA. 2024. DOI: 10.1016/j.tiv.2024.105988.

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