Event Title

Cannabinoid Mediated Inhibition of Ovarian Cancer Cell Proliferation is Mediated via Oxidative stress

Location

124 Science & Nursing Building

Start Date

27-4-2018 9:30 AM

End Date

27-4-2018 9:55 AM

Description

I hypothesized that the cytotoxic effects of cannabinoids will be mediated via cannabinoid (CB) receptors and cannabinoids will increase the cellular reactive oxygen species (ROS). SKOV3 cell viability was determined in the presence of WST-1 reagent. Mitochondrial morphology and membrane potential (Δψm) were observed with Mitotracker Green FM and tetramethylrhodamine methyl ester (TMRM). ROS were visualized with 5-(and 6)-chloromethyl-2’,7’-dichlorohydrofluorescein diacetate (CM-H2DCFDA) and dihydroethidium (DHE). The plasma membrane of the cells became permeable to Nuclear Green Dead dye. ROS was also increased in the cannabinoid-treated cells but the cytotoxic effects were not reverse by either CB1 (Rimonabant) or CB2 (AM630) receptor antagonist. Although the antioxidant α-tocopherol (vitamin E) was able to prevent the induction of cytotoxicity, water-soluble Trolox and ascorbic acid were unable to do so.

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Apr 27th, 9:30 AM Apr 27th, 9:55 AM

Cannabinoid Mediated Inhibition of Ovarian Cancer Cell Proliferation is Mediated via Oxidative stress

124 Science & Nursing Building

I hypothesized that the cytotoxic effects of cannabinoids will be mediated via cannabinoid (CB) receptors and cannabinoids will increase the cellular reactive oxygen species (ROS). SKOV3 cell viability was determined in the presence of WST-1 reagent. Mitochondrial morphology and membrane potential (Δψm) were observed with Mitotracker Green FM and tetramethylrhodamine methyl ester (TMRM). ROS were visualized with 5-(and 6)-chloromethyl-2’,7’-dichlorohydrofluorescein diacetate (CM-H2DCFDA) and dihydroethidium (DHE). The plasma membrane of the cells became permeable to Nuclear Green Dead dye. ROS was also increased in the cannabinoid-treated cells but the cytotoxic effects were not reverse by either CB1 (Rimonabant) or CB2 (AM630) receptor antagonist. Although the antioxidant α-tocopherol (vitamin E) was able to prevent the induction of cytotoxicity, water-soluble Trolox and ascorbic acid were unable to do so.