The present work describes the anticancer activity of cantharidin isolated from red-headed blister beetles, Epicauta hirticornis
and its possible mode of action involving induction of apoptosis, oxidative stress and decrease in glutathione against murine ascites
Dalton’s lymphoma. The structure of isolated compound was confirmed as cantharidin by X-ray diffraction method. Cantharidin
treatment showed potent anticancer activity with an increase in life span (~ 87%) of tumor-bearing mice. Cantharidin treatment induced
apoptosis in Dalton’s lymphoma cells and also caused an oxidative stress due to generation of reactive oxygen species (ROS) and an
increase in lipid peroxidation. The observed canthardin-mediated decrease in glutathione and glutathione related enzymes activities in the
tumor cells may weaken the cellular antioxidant system. Moreover, cantharidin treatment also caused a significant decrease in
mitochondrial cytochrome c and simultaneous increase in cytosolic cytochrome c which ultimately facilitates activation of caspase 9 and
3 to augment mitochondrial apoptotic pathway causing cancer cell death. Based on the present findings, it may be suggested that
cantharidin-mediated anticancer activity could be due to decrease in the protective ability of cancer cells by ROS and subsequent
activation of effecter caspases leading to apoptotic cell death.
Keywords: Antioxidant, Cytotoxicity, Docking, Glutathione reductase, Glutathione-S-transferase, Glutathione peroxidase.
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