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

Citation
E. Funseth et al., Redistribution of accumulated 2,3,7,8-tetrachlorodibenzo-p-dioxin during coxsackievirus B3 infection in the mouse, TOX LETT, 116(1-2), 2000, pp. 131-141
Citations number
36
Categorie Soggetti
Pharmacology & Toxicology
Journal title
TOXICOLOGY LETTERS
ISSN journal
03784274 → ACNP
Volume
116
Issue
1-2
Year of publication
2000
Pages
131 - 141
Database
ISI
SICI code
0378-4274(20000727)116:1-2<131:ROA2DC>2.0.ZU;2-H
Abstract
The tissue redistribution of accumulated 2,3,7,8-tetrachlorodibenzo-p-dioxi n (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 inj ected intraperitoneally (i.p.) with 1 mu Ci H-3-TCDD, corresponding to 0.5 mu g 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 wh ile 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, epididym is and blood were sampled from infected and noninfected groups. Liquid scin tillation was used to determine the H-3-TCDD-content of the tissues. The re sults 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, concur rent with the development of inflammatory lesions (P < 0.001 and 0.01, resp ectively for the heart and pancreas). The TCDD levels in the thymus increas ed 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 cha nge markedly (P<0.001). In the brain of infected mice, the TCDD concentrati on 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 envir onmental pollutant, resulting in increased concentrations and potentially i ncreased toxicity in selected target tissues. (C) 2000 Published by Elsevie r Science Ireland Ltd. All rights reserved.