2,3,7,8-tetrachlorodibenzo-p-dioxin regulates bovine herpesvirus type 1 induced apoptosis by modulating Bcl-2 family members

Apoptosis. 2008 Oct;13(10):1243-52. doi: 10.1007/s10495-008-0249-y.

Abstract

Exposure to environmental contaminants, like 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to an increased susceptibility to infectious agents. Infection of bovine cells (MDBK) with Bovine Herpesvirus 1 (BHV-1) anticipates virus-induced apoptosis, suggesting an involvement of TCDD in virus infection. Herein we analyzed the effects of TCDD on apoptotic pathway in MDBK cells infected with BHV-1. After 12 h of infection, TCDD induced a significant increase in apoptotic cells. TCDD caused a dose-dependent up-regulation and anticipated activation of caspases 3, 8 and 9, with respect to unexposed groups. TCDD anticipated cleavage of PARP, compared to controls. Furthermore TCDD increased Bax and Bid levels, and decreased Bcl-2 and Bcl-XL levels. Such events took place earlier in exposed than unexposed cells. These results showed that TCDD influences BHV-1 induced apoptosis through members of Bcl-2 family and up-regulating activation of caspases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Caspases / metabolism
  • Cattle
  • Cell Count
  • Cell Line
  • Cell Membrane Permeability / drug effects
  • Enzyme Activation / drug effects
  • Herpesvirus 1, Bovine / drug effects
  • Herpesvirus 1, Bovine / physiology*
  • Poly(ADP-ribose) Polymerases / metabolism
  • Polychlorinated Dibenzodioxins / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*

Substances

  • Polychlorinated Dibenzodioxins
  • Proto-Oncogene Proteins c-bcl-2
  • Poly(ADP-ribose) Polymerases
  • Caspases