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Synthesis and characterization of diorganotin(IV) complexes of N ‐(2‐pyridylmethylene)arylamines and mutagenicity testing in vivo of Et 2 SnCl 2 ·[L 4 = N ‐(2‐pyridylmethylene)‐4‐toluidine]
Author(s) -
Baul Swarnali Basu,
Baul Tushar S. Basu,
Rivarola Eleonora,
Dakternieks Dainis,
Tiekink Edward R. T.,
Syngai Christine,
Chatterjee Anupam
Publication year - 1998
Publication title -
applied organometallic chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.53
H-Index - 71
eISSN - 1099-0739
pISSN - 0268-2605
DOI - 10.1002/(sici)1099-0739(199807)12:7<503::aid-aoc746>3.0.co;2-p
Subject(s) - chemistry , in vivo , adduct , dna , stereochemistry , glutathione , sister chromatid exchange , biochemistry , enzyme , organic chemistry , microbiology and biotechnology , biology
Diorganotin(IV) dichloride complexes of the type R 2 SnCl 2 ·L (R = methyl, ethyl, vinyl, t‐butyl, n‐butyl or phenyl; L = N ‐(2‐pyridylmethylene)arylamine) have been synthesized and characterized on the basis of IR, NMR and 119 Sn Mössbauer studies. Investigation of the complexes indicated that N ‐(2‐pyridylmethylene)arylamines form distorted trans ‐octahedral complexes with R 2 SnCl 2 similar to the well‐known R 2 SnCl 2 ·L. Cytogenetic toxicology testing has been performed for Et 2 SnCl 2 ·L 4 [L 4 = N ‐(2‐pyridylmethylene)‐4‐toluidine] in mouse bone‐marrow cells in vivo since such testing is a regulatory requirement before new drugs are released. This tin compound induced delay in cell‐cycle kinetics and sister chromatid exchanges (SCEs) significantly. The effect of Et 2 SnCl 2 ·L 4 was greater when endogenous glutathione (GSH) was depleted by buthionine sulphoximine (BSO). It seems that Et 2 SnCl 2 ·L 4 induces SCEs due to formation of adduct by binding on DNA which could interfere in DNA synthesis and cause delay in cell proliferation. Depletion of GSH could reduce the shielding effect of GSH on chromatin and allows more Et 2 SnCl 2 ·L 4 to bind on DNA. © 1998 John Wiley & Sons, Ltd.