2,3,7,8-Tetrachlorodibenzo-p-dioxin regulates Bovine Herpesvirus type 1 induced apoptosis by modulating Bcl-2 family members

Filomena Fiorito, Gabriella Marfè, Emma De Blasio, Giovanna Elvira Granato, Marco Tafani, Luisa De Martino, Serena Montagnaro, Salvatore Florio, Ugo Pagnini

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1243-1252
Number of pages10
Issue number10
Publication statusPublished - Oct 2008


  • Bcl-2
  • BHV-1
  • Caspases
  • PARP
  • TCDD

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Cell Biology


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