Elsevier

Toxicology Letters

Volume 74, Issue 2, November 1994, Pages 149-155
Toxicology Letters

bcl-2 expression decreases methyl mercury-induced free-radical generation and cell killing in a neural cell line

https://doi.org/10.1016/0378-4274(94)90093-0Get rights and content

Abstract

Methyl mercury neurotoxicity is associated with a broad range of neuropathologic and biochemical disturbances which include induction of oxidative injury. Treatment of the hypothalamic neural cell line GT1-7 with 10 μM methyl mercury (MeHg) for 3 h resulted in increased formation of reactive oxygen species (ROS), and decreased levels of reduced glutathione (GSH), associated with 20% cell death. Cells transfected with an expression construct for the anti-apoptotic proto-oncogene, bcl-2, displayed attenuated ROS induction and negligible cell death. Twenty-four-h exposure to 5 μM MeHg killed 56% of control cells, but only 19% of bcl-2-transfected cells. By using diethyl maleate to deplete cells of GSH, we demonstrate that the differential sensitivity to MeHg was not due solely to intrinsically different GSH levels. The data suggest that MeHg-mediated cell killing correlates more closely with ROS generation than with GSH levels and that bcl-2 protects MeHg-treated cells by suppressing ROS generation.

References (25)

  • T. Suzuki et al.

    Advances in Mercury Toxicology

    (1991)
  • S.D. Welch

    The protective effect of vitamin E and N,N'-diphenyl-p-phenylenediamine (DDPD) against methyl mercury toxicity in the rat

    J. Nutr.

    (1979)
  • Cited by (0)

    View full text