Evaluation of differential cytotoxic effects of the oil spill dispersant Corexit 9500

Abstract

AimsThe British Petroleum (BP) oil spill has raised several ecological and health concerns. As the first response, BP used a chemical dispersant, Corexit-9500, to disperse the crude oil in the Gulf of Mexico to limit shoreline contamination problems. Nevertheless, portions of this oil/Corexit mixture reached the shoreline and still remain in various Gulf shore environments. The use of Corexit itself has become a significant concern since its impacts on human health and environment is unclear. Main methodsIn this study, in vitro cytotoxic effects of Corexit were evaluated using different mammalian cells. Key findingsUnder serum free conditions, the LC50 value for Corexit in BL16/BL6 cell was 16ppm, in 1321N1 cell was 33ppm, in H19-7 cell was 70ppm, in HEK293 was 93ppm, and in HK-2 cell was 95ppm. With regard to the mechanisms of cytotoxicity, we hypothesize that Corexit can possibly induce cytotoxicity in mammalian cells by altering the intracellular oxidative balance and inhibiting mitochondrial functions. Corexit induced increased reactive oxygen species and lipid peroxide levels; also, it depleted glutathione content and altered catalase activity in H19-7 cells. In addition, there was mitochondrial complex-I inhibition and increase in the pro-apoptotic factors including caspase-3 and BAX expression. SignificanceThe experimental results show changes in intracellular oxidative radicals leading to mitochondrial dysfunctions and apoptosis in Corexit treatments, possibly contributing to cell death. Our findings raise concerns about using large volumes of Corexit, a potential environmental toxin, in sensitive ocean environments.