Dialkyltin compounds such as dibutyltin and dioctyltin induce a severe thymus atrophy and a concurrent cellular immunodeficiency. However, this atrophy is recovered by a long-term exposure (5 ~ 8 weeks), that is, a tolerance for the dibutyltin-induced thymus atrophy has become apparent. This tolerance is not due to inducing the generation of degradation enzyme working in the dealkylation of organotins. Rather it appears to be caused by inducing the generation of a dibutyltin-binding substance or an unknown substance which is capable of preventing the dibutyltin-induced suppressive effects, specifically, antiproliferation and death of the thymocytes.
