Pyrogallol Induces Apoptosis in Human Platelets
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
29871735
DOI
10.14712/fb2018064010023
PII: file/5864/fb2018a0004.pdf
Knihovny.cz E-resources
- MeSH
- Apoptosis drug effects MeSH
- Biomarkers metabolism MeSH
- Borates pharmacology MeSH
- Cytochromes c metabolism MeSH
- Glutathione pharmacology MeSH
- Humans MeSH
- Membrane Potential, Mitochondrial drug effects MeSH
- Pyrogallol pharmacology MeSH
- Serine pharmacology MeSH
- Blood Platelets cytology drug effects metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Biomarkers MeSH
- Borates MeSH
- Cytochromes c MeSH
- Glutathione MeSH
- Pyrogallol MeSH
- Serine MeSH
- serine-borate complex MeSH Browser
Pyrogallol is a polyphenol that generates the superoxide anion. In this study, we investigated the influence of pyrogallol on human platelets. Our data showed that exposure of platelets to pyrogallol induced numerous manifestations of apoptosis including depolarization of mitochondrial inner membrane and release of cytochrome c from the mitochondria. Pyrogallol also induced downstream extra-mitochondrial apoptotic responses, including activation of caspase-3 and phosphatidylserine exposure on the outer leaflet of the plasma membrane. Addition of glutathione significantly rescued cells from pyrogallol- induced apoptosis, as evidenced by a decrease of all markers of apoptosis. Thus, pyrogallol appears to produce depletion of intracellular glutathione content in platelets, the main non-protein antioxidant in the cells. Furthermore, inhibition of γ-glutamyl transpeptidase, an enzyme that plays the main role in the cellular supply of glutathione, reverted the glutathione (GSH) protection over platelet apoptosis. Our results indicate that pyrogallol induces apoptosis by suppressing the natural anti-oxidation in human platelets.
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