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.