Abstract
How pH(i) changes, more specifically alkalinization, affect the apoptotic cascade has yet to be determined. The aim of the present work was to test the involvement of mitochondria in the apoptotic cascade triggered by benzo(a)pyrene [B(a)P] and to determine the role of pH(i) changes and p53 relative to mitochondria. Our results indicate that B(a)P-induced apoptosis might rely upon a p53-dependent and a pH-sensitive mitochondrial dysfunction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Apoptosis / physiology*
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Benzo(a)pyrene / toxicity*
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Benzothiazoles
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Bongkrekic Acid / pharmacology
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Cell Line
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Epithelial Cells / cytology*
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Epithelial Cells / drug effects
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Epithelial Cells / physiology
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Guanidines / pharmacology
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Hydrogen-Ion Concentration*
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Liver / cytology*
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Liver / drug effects
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Mitochondria / drug effects
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Mitochondria / physiology*
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Mitochondria / ultrastructure*
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Rats
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Sulfones / pharmacology
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Thiazoles / pharmacology
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Toluene / analogs & derivatives*
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Toluene / pharmacology
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Tumor Suppressor Protein p53 / drug effects
Substances
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Benzothiazoles
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Guanidines
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Sulfones
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Thiazoles
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Tumor Suppressor Protein p53
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Bongkrekic Acid
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Benzo(a)pyrene
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Toluene
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cariporide
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pifithrin