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Human & Experimental Toxicology
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Cellular and molecular aspects of organotin-induced thymus atrophy

Raymond H.H. Pieters

Research Institute of Toxicology, Immunotoxicology Section, Utrecht University, Utrecht

Marianne Bol

Research Institute of Toxicology, Immunotoxicology Section, Utrecht University, Utrecht

Willem Seinen

Research Institute of Toxicology, Immunotoxicology Section, Utrecht University, Utrecht

André H. Penninks

TNO-Nutrition and Food Institute, Zeist, The Netherlands

1 Organotin compounds, di-n-butyltin dichloride (DBTC) in particular, have been shown to cause Thymus atrophy in the rat.

2 DBTC-induced thymus atrophy results from a depletion of small CD4+CD8+ thymocytes which is caused by a diminished production of immature CD4-CD8+ and CD4+CD8+ thymoblasts.

3 DBTC inhibits the activation, but not the differentiation of immature CD4-CD8+ thymocytes in vitro and in vivo suggesting a selective anti-proliferative activity of DBTC.

4 DBTC inhibits the adhesion molecule-mediated binding of thymocytes to thymic epithelial cells.

5 DBTC enhances the Ca2+ release elicited by cross-linking of the T cell receptor complex (TcR{alpha}β-CD3) on thymocytes and moreover delays cap formation of the TcR{alpha}β-CD3 receptor.

6 It is concluded that DBTC possibly interferes with the functioning of the cytoskeleton. The relation of the in vitro findings to the inhibition of immature CD4-CD8+ thymocyte activation and the induction of thymus atrophy is unknown as yet.

Human & Experimental Toxicology, Vol. 13, No. 12, 876-879 (1994)
DOI: 10.1177/096032719401301210
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