Abstract
We investigated whether treatment with the interferon inducer polyinosinic-polycytidylic acid and other cytokines (interleukin-1, tumor necrosis factor) or the cytokine inducer lipopolysaccharide modified O6-alkylguanine-DNA alkyltransferase (AT) in rat liver. AT levels were determined in liver extracts using N-[3H]methyl-N-nitrosourea alkylated calf thymus DNA as substrate and an HPLC procedure to measure O6-methylguanine. Doses as low as 0.1 mg/kg i.p. of polyinosinic-polycytidylic acid caused a highly significant increase (P <0.01) in AT levels in the liver, evident either 24 or 48 h after treatment. Lipopolysaccharide at the dose of 80 μg/kg i.p. also induced AT whereas interleukin-1 (60 μg/kg) or tumor necrosis factor (60 μg/kg) were inactive. Treatment with human recombinant interferon alpha A/D caused a highly significant increase in AT levels, thus confirming the hypothesis that interferon was probably responsible for the observed effect. These results suggest a link between the immune response and DNA repair mechanisms.
| Original language | English |
|---|---|
| Pages (from-to) | 181-183 |
| Number of pages | 3 |
| Journal | Carcinogenesis |
| Volume | 11 |
| Issue number | 1 |
| Publication status | Published - Jan 1990 |
ASJC Scopus subject areas
- Cancer Research
- Statistics, Probability and Uncertainty
- Applied Mathematics
- Physiology (medical)
- Physiology
- Behavioral Neuroscience