6533b7d8fe1ef96bd126a2ae

RESEARCH PRODUCT

Effect of tin and lead chlorotriphenyl analogues on selected living cells.

Ewa Boniewska-bernackaMałgorzata A. BrodaRudolf SłotaDariusz Man

subject

Models Molecularfood.ingredientCell SurvivalHealth Toxicology and MutagenesisCellMolecular Conformationchemistry.chemical_elementSaccharomyces cerevisiaeToxicologyCleavage (embryo)BiochemistryLecithinCell wallfoodLecithinsmedicineEscherichia coliOrganometallic CompoundsOrganotin CompoundsHumansChlorotriphenyltinLipid bilayerMolecular BiologyLiposomeElectron Spin Resonance SpectroscopyGeneral MedicineYeastChlorotriphenylleadElectron Paramagnetic Resonancemedicine.anatomical_structureMembraneHEK293 CellsBiochemistrychemistryLeadHuman Embryonic Kidney CellsLiposomesMolecular MedicineTin

description

Three kinds of living cells, human embryonic kidney cells, Saccharomyces cerevisiae, and Escherichia coli, were tested for their sensitivity to chlorotriphenyltin and chlorotriphenyllead. The tin compound proved definitely more toxic than the lead derivative, particularly in the case of the human embryonic kidney cells devoid of any protective cell wall. Electron paramagnetic resonance (EPR) comparative studies carried out by using a natural model liposome system (egg yolk lecithin) confirmed considerable changes within the lipid bilayer upon doping by the aforementioned additives, which may be crucial to the mechanism of the observed cell cleavage. The individual dopants revealed diverse impact upon the membrane's condition, chlorotriphenyltin distinctly fluidized the lipid system, whereas chlorotriphenyllead stiffened the medium within the membrane. A theoretical approach concerning such different behaviors of studied tin and lead analogues because of their high toxicity in living cells has been presented. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 25:231–237, 2011; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.20380

10.1002/jbt.20380https://pubmed.ncbi.nlm.nih.gov/21812073