Tin - Toxicology of Metals - page 835

The mitotic activity of these compounds increases
with increasing their lipophilicity. The highest muta-
genicity has been shown for tributyltin compounds,
whereas no evidence of mutagenicity has been found
for dimethyltin and dibutyltin in the SOS chromot-
est with E. coli PQ37 and in PHA-stimulated human
lymphocytes (Hamasaki et al ., 1992). Triphenyltin com-
pounds induce micronuclei in cultured Chinese ham-
ster ovary cells (Chao et al ., 1999). The increase in sister
chromatid exchange level has been seen in CHO cells
exposed to organotins by adding S9 microsomal frac-
tions. Triphenyltins given orally at doses 2.5-25 mg/kg
to mice induce an increase in micronucleated reticulo-
cytes. Triphenyltin has been reported positive in both
the Ames test and the mouse lymphoma TK+/muta-
tion assay (Oshiro et al ., 1991). These data indicate that
these chemicals are potential chromosome mutagens.
The carcinogenic potential of some butyltin compounds
includes inhibition of the ability of natural killer cells
to bind to tumor cells, thereby predisposing to malig-
nancy (Whalen et al ., 1999). The toxic effects of butyltin
compounds include immune suppression in rodents
(Penninks, 1993). The immunotoxicity of tributyltin
may be due to the primary action of dibutyltin on the
maturation of immature thymocytes. The toxic effect of
triphenyltin is also explained by depolymerization of
thymocyte F-actin (Chow and Orrenius, 1994). Moreo-
ver, immunotoxic effects of organotin compounds may
involve cytoskeletal modifi cation in addition to the
perturbation of thymocyte calcium homeostasis.
However, despite several studies on organotin com-
pound toxicity, the molecular targets of organotins
have not yet been identifi ed.

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Acknowledgment

We wish to dedicate this chapter to the late Dr. Magnus Piscator,
who wrote the Tin chapter in the second edition of this topic.

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