Bacterial screening employing the agar diffusion test on triphenyltin carboxylates containing various functional residues in the ester moiety revealed appreciable differences in their activities relative to triphenyltin acetate. Among these, [3-(Diethylphosphono)propionato] triphenyltin (1) and [N-cyclohexylcarbamoyl) glycinato] triphenyltin displayed activities comparable to tri-n-butyltin cinnamate (2) towards both Gram-positive and Gram-negative bacteria; the latter compound was the most active among the eleven triorganotin compounds tested, which included cyclopentyldiphenyltin hydroxide (3) and its methacrylate derivative. Applying the more quantitative plate count and optical density tests on compounds 1-3, it was shown that their inhibitory activity ranked in the order 2 > 3 >1. Significantly, 3 caused around 90% inhibition of both Eschechia coli (-) and Pseudomonas aeruginosa (-) when incubated for 24 h at 37+/-1 at the 10.0 mug/ mL concentration level. Compound 2 was less effective against P.aeruginosa than against E.coli. While the Gram-positive bacteria were all readily inhibited, Bacillus subtilis (+) appeared to the most susceptible among them towards the test compounds.
Triphenyltin coumarin-3-carboxylate and its coordination complexes with ethanol, triphenylphosphine oxide, triphenylarsine oxide, diphenylcyclopropenone and quinoline N-oxide exhibited high in vitro cytotoxicity (LC(50) values in the range 0.25-3.4 mug/mL) when tested against EBV-DNA positive Raji cells and P-388 leukaemia cells, compared to the standard drug 5-Fluorouracil, which showed LC(50) values of 11 and >50 mug/mL, respectively, against these cells. Additional tests performed on the Raji cells incubated with the quinoline N-oxide complex in the presence of the tumour promoters, TPA and sodium butyrate, revealed that the diffused and restricted protein components of the early antigen complex were suppressed relative to the control containing only the promoters, indicating impaired function of the genes involved as transactivators in the early lytic cycle of the EBV. The failure of the restriction enzymes Eco R1 and Hind III to cleave the extracted DNA from such treated cells in contrast to the control, coupled with the amplification of the BMLF-1 gene by the PCR technique which was realised only with the DNA of the control and not of the treated sample, point to a punitive interaction of the organotin with the nuclear DNA of the Raji cells.
Features of pesticide synergism and acetylcholinesterase (AChE) inhibition (in vitro) were studied using a selected range of organotin compounds against the early 4th instar larvae of a highly resistant strain of the diamondback moth (DBM), Plutella xylostella, a major universal pest of cruciferous vegetables.Fourteen triorganotin compounds were evaluated for their ability to enhance the toxicity of the microbial insecticide, Bacillus thuringiensis (BT) and of the commercial insecticide, Malathion to Plutella xylostella larvae. Supplemental synergism was observed with triphenyl- and tricyclopentyltin hydroxides in combinations with Bacillus thuringiensis. Increased synergism was observed with an increase in the number of cyclopentyl groups on tin in the mixed series, Cyp(n) Ph(3-n) SnX, where X = OH, and 1-(1,2,4-triazolyl). The combination of (p-chlorophenyl)diphenyltin N,N-dimethyldithiocarbamate at LD(10) and LD(25) concentrations with sublethal concentrations of Malathion as well as of tricyclohexyltin methanesulphonate at the 0.01% (w/v) concentration with Malathion exerted strong synergistic effects (supplemental synergism) with toxicity index (T.I) values of 7.2, 19.8 and 10.1, respectively.Studies on the in vitro inhibition of acetylcholinesterase prepared from the DBM larvae showed that while most of the triorganotin Compounds tested were without effect on the enzyme, compounds containing the thiocarbamylacetate or the dithiocarbamylacetate moieties demonstrated appreciable levels of inhibition, being comparable in efficacy to commercial grades of Malathion and Methomyl.