Common viral infection affects pentabrominated diphenyl ether (PBDE) distribution and metabolic and hormonal activities in mice.

A murine model infection with the human coxsackievirus B3 (CB3) has been shown to change uptake and tissue distribution of several environmental pollutants, in some cases followed by an aggravated disease. In this study, the model was tested for polybrominated diphenyl ethers (PBDEs), which we know are absorbed from the gastro-intestinal tract and further distributed throughout the body. On day 0, female Balb/c mice were infected with CB3; on day 1 of the infection, they were dosed orally with approximately 200 microg/kgbody weight (bw) (ca. 0.52 microCi) of 14C-labelled 2,2',4,4',5-pentabromodiphenyl ether (14C-BDE-99); and on day 3 of the infection, they were sacrificed for studies of 14C-BDE-99 distribution. In comparison with control values, 14C-BDE-99 concentrations were altered in the liver (186%, p < 0.05), lungs (47%, p < 0.05) and pancreas (51%, p < 0.05), but no change was seen in the blood, brain, heart, spleen, thymus or kidneys. Moreover, on day 3, plasma thyroxine (T4) levels (33%, p < 0.001), as well as ethoxyresorufin-O-dealkylase (EROD) (17%, p < 0.001) and pentoxyresorufin O-dealkylase (PROD) (31%, p < 0.001) activities were much lower in infected compared to non-infected control mice. It is suggested that the change in tissue distribution of 14C-BDE-99 as a result of the infection may be caused by an infection-induced specific change in the hepatic enzyme activities affecting this PBDE congener. The mechanism for virally induced T4 changes remains, however, unclear. The presented infection-induced alteration in distribution, which is different from other environmental pollutants (e.g., dioxin, acrylamide and cadmium), may have consequences for PBDEs toxicity, especially in relation to microsomal enzyme and thyroid hormone activities.