Thymoquinone supplementation and its effect on kidney tubule epithelial cells in vitro

Reactive oxygen species (ROS) play a major role in the progression of renal disease. Vitamins can be used to attenuate the production of ROS and potentially slow or stop the progression of renal disease. In both renal transplant rejection and acute glomerulonephritis, there is an increase in polymophonuclear cells which lead to increases in local production of H2O2, and ultimately to large amounts of ROS and cellular damage. Decreasing ROS will lead to better graft survival and resolution of acute inflammation. Black seed has free radical scavenging properties and inhibits lipid peroxidation. Thymoquinone has been documented to have a cytocidal effect on cancer cells and reduced the cytotoxicity of standard antineoplastic drugs. Thymoquinone has also been documented to protect renal tissue by significantly reducing the side effect of nephrotoxicity associated with various medications. The hepatoprotective property of thymoquinone may be attributed to the preservation of intracellular glutathione or may be related to the inhibition of thromboxane B2 production. The overall goal of this study was to define a dose of TQ which will increase cellular glutathione levels without cytotoxic effects. Thirty-five wells were plated with RMKEC and sub-divided into five equal groups. Group 2-4 was treated with 10microM TQ, 50 microM TQ, or 100 microM of TQ respectively. Data obtained suggests that: (1) TQ does not act as a prooxidant at higher concentrations, which would induce cellular damage leading to cell death, and (2) at 72 hours in culture there was a significant increase in glutathione levels in all treatment groups when compared with control cells suggesting possible protective effects of this compound. The data suggests that further studies need to be conducted to determine the full impact of thymoquinone on kidney epithelial function as a means of cellular protection against oxidative damage.