Redistribution of accumulated 2,3,7,8-tetrachlorodibenzo- p-dioxin during coxsackievirus B3 infection in the mouse

Abstract

The tissue redistribution of accumulated 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) during infection was studied in adult male A/J mice using a common human virus coxsackievirus B3. Before infection (day 1), all mice were injected intraperitoneally (i.p.) with 1 μCi 3H-TCDD, corresponding to 0.5 μg TCDD kg −1. One group was sacrificed before virus inoculation (day 0). Of the remaining mice, one subgroup was inoculated i.p. with CB3 virus while the other subgroup served as a noninfected control. On days 0, 4 and 7, the spleen, thymus, heart, pancreas, liver, white and brown adipose tissue, skeletal muscle, lung, kidney, brain, adrenals, thyroid, testes, epididymis and blood were sampled from infected and noninfected groups. Liquid scintillation was used to determine the 3H-TCDD-content of the tissues. The results showed that the accumulated TCDD was redistributed due to infection. The major changes occurred in the organs involved in the infectious process. In the target organs for coxsackievirus B3 (the pancreas and heart), the TCDD concentration peaked in relation to noninfected control values, concurrent with the development of inflammatory lesions ( P<0.001 and 0.01, respectively for the heart and pancreas). The TCDD levels in the thymus increased three-fold during the infection to an estimated 0.5 pmol g −1 tissue on day 7 of the infection, whereas the levels in noninfected mice did not change markedly ( P<0.001). In the brain of infected mice, the TCDD concentration increased significantly with time, at day 7 reaching two-fold levels in comparison with noninfected controls ( P<0.001). The findings suggest that a common infection causes redistribution of a previously accumulated environmental pollutant, resulting in increased concentrations and potentially increased toxicity in selected target tissues.