Effects of Epigallocatechin Gallate on Tert-Butyl Hydroperoxide-Induced Mitochondrial Dysfunction in Rat Liver Mitochondria and Hepatocytes
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
PubMed
28074116
PubMed Central
PMC5198192
DOI
10.1155/2016/7573131
Knihovny.cz E-zdroje
- MeSH
- hepatocyty cytologie účinky léků metabolismus MeSH
- jaterní mitochondrie účinky léků metabolismus MeSH
- katechin analogy a deriváty farmakologie MeSH
- krysa rodu Rattus MeSH
- kultivované buňky MeSH
- membránový potenciál mitochondrií účinky léků MeSH
- peroxid vodíku metabolismus MeSH
- potkani Wistar MeSH
- spotřeba kyslíku účinky léků MeSH
- terc-butylhydroperoxid toxicita MeSH
- vápník metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- epigallocatechin gallate MeSH Prohlížeč
- katechin MeSH
- peroxid vodíku MeSH
- terc-butylhydroperoxid MeSH
- vápník MeSH
Epigallocatechin gallate (EGCG) is a green tea antioxidant with adverse effects on rat liver mitochondria and hepatocytes at high doses. Here, we assessed whether low doses of EGCG would protect these systems from damage induced by tert-butyl hydroperoxide (tBHP). Rat liver mitochondria or permeabilized rat hepatocytes were pretreated with EGCG and then exposed to tBHP. Oxygen consumption, mitochondrial membrane potential (MMP), and mitochondrial retention capacity for calcium were measured. First, 50 μM EGCG or 0.25 mM tBHP alone increased State 4 Complex I-driven respiration, thus demonstrating uncoupling effects; tBHP also inhibited State 3 ADP-stimulated respiration. Then, the coexposure to 0.25 mM tBHP and 50 μM EGCG induced a trend of further decline in the respiratory control ratio beyond that observed upon tBHP exposure alone. EGCG had no effect on MMP and no effect, in concentrations up to 50 μM, on mitochondrial calcium retention capacity. tBHP led to a decline in both MMP and mitochondrial retention capacity for calcium; these effects were not changed by pretreatment with EGCG. In addition, EGCG dose-dependently enhanced hydrogen peroxide formation in a cell- and mitochondria-free medium. Conclusion. Moderate nontoxic doses of EGCG were not able to protect rat liver mitochondria and hepatocytes from tBHP-induced mitochondrial dysfunction.
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