Glutathione and cysteines suppress cytotoxicity of gas phase of cigarette smoke by direct reacting with unsaturated carbonyl compounds in the gas phase.

  title={Glutathione and cysteines suppress cytotoxicity of gas phase of cigarette smoke by direct reacting with unsaturated carbonyl compounds in the gas phase.},
  author={T. Higashi and Enas Elmeligy and Y. Mai and Y. Noya and K. Terada and Y. Mazaki and Y. Kuge and S. Miwa},
  journal={Biochemical and biophysical research communications},
  volume={509 4},
Unsaturated carbonyl compounds, such as acrolein (ACR) and methyl vinyl ketone (MVK), are environmental pollutants, and are contained in smoke, automobile exhaust, and heated oil. We have previously reported that major cytotoxic factors in the gas phase of cigarette smoke are ACR and MVK. ACR and MVK induce cell damage by reactive oxygen species generation via protein kinase C and NADPH oxidases, and antioxidants, such as glutathione (GSH) and N-acetylcysteine (NAC), can effectively suppress… Expand
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Intracellular Metabolism of α,β-Unsaturated Carbonyl Compounds, Acrolein, Crotonaldehyde and Methyl Vinyl Ketone, Active Toxicants in Cigarette Smoke: Participation of Glutathione Conjugation Ability and Aldehyde-Ketone Sensitive Reductase Activity.
The results show that the GSH adducts of α,β-unsaturated aldehydes, CA and ACR, are quickly reduced by certain intracellular carbonyl reductase(s) and excreted from the cells, unlike the G SH-MVK adduct, which might be related to differences in the cytotoxicity ofα, β-uns saturated aldeHydes and ketones. Expand
Intracellular Ca2+ is an essential factor for cell damage induced by unsaturated carbonyl compounds.
It is suggested that intracellular Ca2+ is an essential factor for cell damage caused by both PKC-dependent andPKC-independent pathways, and mobilization of Ca 2+ from intrACEllular Ca1+ stores is induced by ACR or MVK. Expand
Identification of stable cytotoxic factors in the gas phase extract of cigarette smoke and pharmacological characterization of their cytotoxicity.
Results show that acrolein and MVK areresponsible for the acute cytotoxicity of the CSE through PKC/NOX-dependent and -independent mechanisms, whereas CPO is responsible for the delayed cytot toxicity of theCSE through a PKC or NOX-independent mechanism. Expand
Aldehyde-induced protein modifications in human plasma: protection by glutathione and dihydrolipoic acid.
Aldehydes present in CS did not cause a depletion of plasma antioxidants such as ascorbic acid or alpha-tocopherol and did not induce plasma lipid peroxidation, but Aldehydes decreased plasma protein sulfhydryl concentrations but increased protein carbonyls. Expand
Protein kinase C-dependent cell damage by unsaturated carbonyl compounds in vascular cells.
Results indicate that the unsaturated carbonyl compounds might affect the vascular system by damaging smooth muscle cells via PKC activation, because blood vessels are easily exposed to these compounds. Expand
Nicotine- and tar-free cigarette smoke induces cell damage through reactive oxygen species newly generated by PKC-dependent activation of NADPH oxidase.
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Oxidants in the gas phase of cigarette smoke pass through the lung alveolar wall and raise systemic oxidative stress.
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Acrolein: sources, metabolism, and biomolecular interactions relevant to human health and disease.
The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Expand
Molecular mechanism of glyceraldehyde-3-phosphate dehydrogenase inactivation by α,β-unsaturated carbonyl derivatives.
A general cytotoxic mechanism in which electrophilic α,β-unsaturated carbonyls selectively form adducts with reactive nucleophilic cysteine residues specifically associated with the active sites of proteins is suggested. Expand
Protein modification by acrolein: relevance to pathological conditions and inhibition by aldehyde sequestering agents.
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