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Published on: November 1, 2013
Effect of tin and lead chlorotriphenyl analogues on selected living cells
Ewa Boniewska-Bernacka1, Dariusz Man, Rudolf Słota
1Department of Biotechnology and Molecular Biology, Opole University, 45-035 Opole, ul. Kominka 4, Poland.
Abstract:
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.
Insights
Chlorotriphenyltin is more toxic to human cells than chlorotriphenyllead, affecting cell membranes differently. This study explores organotin and organolead toxicity mechanisms.
Area of Science:
- Environmental Toxicology
- Cell Biology
- Biochemistry
Background:
- Organotin and organolead compounds exhibit toxicity.
- Understanding their cellular mechanisms is crucial for risk assessment.
- Cellular protective mechanisms, like cell walls, can influence sensitivity.
Purpose of the Study:
- To compare the toxicity of chlorotriphenyltin and chlorotriphenyllead across different cell types.
- To investigate the impact of these compounds on cell membrane structure and function.
- To elucidate the potential mechanisms behind their observed cellular toxicity.
Main Methods:
- Testing the sensitivity of human embryonic kidney cells, Saccharomyces cerevisiae, and Escherichia coli to chlorotriphenyltin and chlorotriphenyllead.
- Utilizing Electron Paramagnetic Resonance (EPR) spectroscopy with a liposome model (egg yolk lecithin).
- Conducting theoretical analysis of the observed toxicological and membrane-modifying effects.
Main Results:
- Chlorotriphenyltin demonstrated significantly higher toxicity than chlorotriphenyllead, especially in human cells lacking cell walls.
- EPR studies revealed distinct alterations in the lipid bilayer of the liposome model upon exposure to both compounds.
- Chlorotriphenyltin fluidized the lipid system, while chlorotriphenyllead induced stiffening of the membrane.
Conclusions:
- The differential toxicity of chlorotriphenyltin and chlorotriphenyllead is linked to their distinct effects on cell membrane fluidity.
- Membrane perturbation is a key factor in the mechanism of organotin and organolead-induced cytotoxicity.
- Further theoretical and experimental studies are warranted to fully understand these toxicological profiles.
