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Benzo[a]pyrene metabolites: effects on viral interferon induction.
Journal of Interferon Research
|October 1, 1986
Summary
Metabolites of Benzo[a]pyrene (BaP), when enzymatically activated, significantly inhibit influenza virus-induced interferon-alpha/beta (IFN-alpha/beta) in mammalian cells. This finding suggests a link between BaP metabolite mutagenicity and their impact on the immune response.
Area of Science:
- Environmental Toxicology
- Immunology
- Virology
Background:
- Benzo[a]pyrene (BaP) is a polycyclic aromatic hydrocarbon with known mutagenic and carcinogenic properties.
- Interferon-alpha/beta (IFN-alpha/beta) plays a crucial role in the innate immune response against viral infections, including influenza.
- Understanding how environmental pollutants affect viral defense mechanisms is critical for public health.
Purpose of the Study:
- To investigate the inhibitory effects of Benzo[a]pyrene (BaP) metabolites on influenza virus-induced interferon-alpha/beta (IFN-alpha/beta) production.
- To determine the role of enzymatic activation (using rat liver S9 fraction) in the observed inhibitory activities.
- To explore the correlation between the mutagenicity of BaP metabolites and their immunomodulatory effects.
Main Methods:
- Mammalian cell cultures (LLC-MK2) were exposed to influenza virus.
- Benzo[a]pyrene (BaP) and its various metabolites were tested for their effects on IFN-alpha/beta induction, both with and without enzymatic activation by rat liver S9.
- Inhibitory activity was quantified, and comparisons were made between different metabolite classes (phenols, diols, quinones, epoxides, tetrols, triols).
Main Results:
- Benzo[a]pyrene (BaP) itself did not inhibit viral IFN-alpha/beta induction.
- Enzymatically activated BaP metabolites significantly reduced viral IFN induction by approximately 80%.
- Specific metabolites like BaP diol epoxides showed direct inhibitory activity, while others required S9 activation to exhibit significant effects. Microbial mutagenicity correlated with IFN inhibition.
Conclusions:
- Enzymatic activation is crucial for the potent inhibition of viral IFN induction by BaP metabolites.
- BaP metabolites can interfere with the innate immune response to influenza virus, suggesting a potential mechanism for increased susceptibility to infections.
- The study validates the use of this cell-based assay for assessing the immunomodulatory potential of suspect mutacarcinogens.