Abstract
Previously we showed that hepatocyte lysis induced by Hg +2 or Cd +2 could be partly attributed to mitochondrial toxicity [1,2]. Similar changes in Na + homeostasis induced when Cd +2 or Hg +2 was incubated with hepatocytes. Cd +2 or Hg +2 induced cytotoxicity were prevented by Na + omission from the media or by the addition of the Na + / H + exchange inhibitor 5-(N,N-dimethyl)-amiloride. Furthermore the omission of Cl - from the media or addition of glycine, a Cl - channel blocker also prevented Cd +2 or Hg +2 induced hepatocyte toxicity. A hypotonic media also increased Cd +2 or Hg +2 induced hepatocyte cytotoxicity. This suggests that Cd +2 or Hg +2 cytotoxicity could be partly attributed to disruption of cell volume regulation mechanisms. The increased osmotic load caused by the uncontrolled accumulation of intracellular Na + in Cd +2 or Hg +2 treated hepatocytes likely resulted from the activation of Na + / H + exchanger and the Na + / HCO3 - cotransporter by the acidosis and ATP depletion caused by mitochondrial toxicity.
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