| First Author | Jeong TC | Year | 1996 |
| Journal | Immunopharmacol Immunotoxicol | Volume | 18 |
| Issue | 1 | Pages | 91-103 |
| PubMed ID | 8683041 | Mgi Jnum | J:32164 |
| Mgi Id | MGI:79669 | Doi | 10.3109/08923979609007112 |
| Citation | Jeong TC, et al. (1996) Effects of ethyl carbamate and its metabolites on the antibody response in splenocyte cultures from female Balb/C mice. Immunopharmacol Immunotoxicol 18(1):91-103 |
| abstractText | To investigate a possible role by cytochrome P450 (P450) in ethyl carbamate-induced immunosuppression, an attempt to assess the ability of ethyl carbamate, its metabolites produced by P450 (i.e., ethyl N-hydroxycarbamate and vinyl carbamate), and methyl carbamate to suppress the polyclonal antibody response induced by bacterial lipopolysaccharide was made in splenocyte cultures isolated from female Balb/C mice. The results showed that vinyl carbamate and ethyl N-hydroxycarbamate were more immunosuppressive compared to ethyl carbamate. A structurally related analogue, methyl carbamate, did not suppress the antibody response. These results indicate that metabolism of ethyl carbamate by P450 may produce more immunosuppressive metabolites as in ethyl carbamate-induced carcinogenicity. A pre-incubation study with phenobarbital-induced liver microsomes in the presence of NADPH-generating system showed that the antibody response was suppressed by ethyl carbamate when splenocytes were pre-incubated with ethyl carbamate and microsomes simultaneously. Moreover, the suppression was completely recovered by the addition of a P450 inhibitor, aminoacetonitrile, in the pre-incubation. Taken together, the present results indicate that metabolism of ethyl carbamate by P450 enzyme(s) may be an important pathway to cause immunosuppression. |
