Mercury is one of the most environmentally abundant toxic metals, and is known to produce cellular injury in the kidneys. The kidneys serve as a target organ for toxins due to its extremely high blood flow (20 - 25%) of the cardiac output. Hence, heavy metals such as mercury that enter the blood stream will travel to the kidneys. The primary function of the kidneys is to concentrate waste products, including heavy metals such as mercury. Transport and binding sites in the kidneys are present in the proximal tubules, and mercury may alter the structure and function of the proteins and membranes in these cells. These changes may result in long term residual effects. Heavy metals such as mercury elicit adverse effects in the proximal tubule and it is the epithelial cells of the proximal tubule that reabsorbs the mercury that is filtered out of the glomerulus. This research was therefore designed to evaluate the dose response relationship in human renal proximal tubule cells following exposure to mercury. Cytotoxicity was evaluated using the MTT-assay for cell viability. The Annexin-V assay was performed by flow cytometry to determine the extent of phosphatidylserine externalization in HK-2 cells exposed to mercury. Cells were exposed to mercury for 24 hours at doses of 0, 1, 2, 3, 4, 5, and 6 mu g/mL. Cytotoxicity experiments yielded a LD50 value of 4.65 +/- 0.6 mu g/mL upon 24 hours of exposure, indicating that mercury is highly toxic. The percentage of cells undergoing early apoptosis were 0.70 +/- 0.03%, 10.0 +/- 0.02%, 11.70 +/- 0.03%, 15.20 +/- 0.02%, 16.70 +/- 0.03%, 24.20 +/- 0.02%, and 25.60 +/- 0.04% for 0, 1, 2, 3, 4, 5, and 6 mu g/mL of mercury respectively, indicating a dose response relationship with regards to mercury induced cytotoxicity, and early apoptosis in HK-2 cells.
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