Selective cytotoxicity of standardised n-hexane extract of black soldier flies' larvae on cancerous skin cells mitochondria isolated from rat model of melanoma.

Introduction: Melanoma is known as a highly lethal cancer. In melanoma cells, apoptosis signalling which relies heavily on the acute activity of mitochondria and reactive oxygen species (ROS) formation is suppressed. Our previous studies on natural compounds on melanoma suggested that mitochondria are a potential target for the melanoma treatment by selective cytotoxic effect of them. The black soldier fly is an important environmental protectant insect that based on recent studies induces apoptosis in liver and colorectal carcinoma cells through the activation of caspase 3, 8, and 9 and ultimately inhibits the growth of cancer cells.
Purpose: This study was designed to evaluate the selective apoptotic effect of the n-hexane BSFL extract (BSFLE) on skin mitochondria.
Materials and Methods: The mitochondria isolated from melanoma cells were treated with various concentrations (1500, 3000, and 6000 µg/ml) of n-hexane BSFLE Then MTT viability assay, ROS determination, Mitochondrial Membrane Potential (MMP), mitochondrial swelling, cytochrome c release determination, and % apoptosis were performed.
Results: MTT assay showed that different concentrations of n-hexane BSFLE significantly ( P  < 0.05) decreased the SDH activity in cancerous skin mitochondria with the IC50. The ROS production and mitochondrial swelling results also showed that all concentrations of BSFL extracts significantly increased. MMP decline and the release of cytochrome c in cancer groups mitochondria. BSFLE increased apoptosis on melanoma cells.
Discussion and Conclusion: It is suggested that n-hexane BSFLE compounds selectively induce a cascade of proapoptotic events that are probably defective in cancer cells. Most of these compounds target the mitochondrial transient pore caused by disruption of the mitochondrial respiratory chain. These events lead to disruption of the temporary permeability of mitochondria, swelling of mitochondria and finally the formation of apoptosome in the cytosol.