6533b7d4fe1ef96bd1262674
RESEARCH PRODUCT
Synthesis and characterization of diorganotin(IV) complexes ofN-(2-pyridylmethylene)arylamines and mutagenicity testingin vivo of Et2SnCl2�[L4=N-(2-pyridylmethylene)-4-toluidine]
Eleonora RivarolaTushar S. Basu BaulAnupam ChatterjeeEdward R. T. TiekinkChristine Syng-aiSwarnali Basu BaulSwarnali Basu BaulSwarnali Basu BaulDainis Dakterniekssubject
DNA synthesisStereochemistrySister chromatid exchangeMutagenGeneral ChemistryGlutathionemedicine.disease_causeChemical synthesisAdductInorganic Chemistrychemistry.chemical_compoundchemistryIn vivomedicineDNAdescription
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 Mossbauer 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.
year | journal | country | edition | language |
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1998-07-01 | Applied Organometallic Chemistry |