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EFFECT OF TRANS‐RESVERATROL IN RAT HEART MITOCHONDRIA IN HYPOXIA‐REOXYGENATION
Author(s) -
GutiérrezPérez Areli,
CortésRojo Christian,
ClementeGuerrero Mónica,
CalderónCortés Elizabeth,
SaavedraMolina Alfredo
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a922-c
Subject(s) - resveratrol , mitochondrion , reactive oxygen species , mitochondrial permeability transition pore , chemistry , tbars , antioxidant , mitochondrial ros , polyphenol , pharmacology , oxidative stress , biochemistry , hypoxia (environmental) , programmed cell death , oxygen , apoptosis , lipid peroxidation , biology , organic chemistry
The trans‐resveratrol (3,4′,5 ‐trihydroxystilbene) is a polyphenol that can be found in the red wine. Its ingestion has been related with cardio protective activity as potent antioxidant. Mitochondria consume about 90% oxygen and generate reactive oxygen species (ROS) in the respiratory chain. The aim of this work was to assess the trans‐resveratrol effects on rat heart mitochondria under hypoxia‐reoxygenation conditions. Trans‐resveratrol did not promote mitochondrial permeability transition. While, in the presence of cyclosporine A, trans‐resveratrol still promoting swelling of heart mitochondria suggesting the transport of the polyphenolic compound to mitochondria. Test of mitochondrial lipoperoxidation were performed by the TBARS assay. We observed that the resveratrol pre‐treatment in the absence of Fe/ascorbate oxidant system diminished the lipoperoxidation levels compared with the basal values without the oxidants. These results suggest that the trans‐resveratrol prevent lipoperoxidation induced for the high production of free radicals in many stressed conditions and therefore could protect against cell damage and cell death. Acknowledgements The authors appreciate the partial economic support of grants from CONACYT (43705) and CIC‐UMSNH (2.16‐2005).