NecroX-5 prevents hypoxia/reoxygenation injury by inhibiting the mitochondrial calcium uniporter.

Abstract

AIMS:

Preservation of mitochondrial function is essential to limit myocardial damage in ischaemic heart disease. We examined the protective effects and mechanism of a new compound, NecroX-5, on rat heart mitochondria in a hypoxia/reoxygenation (HR) model.

METHODS AND RESULTS:

NecroX-5 reduced mitochondrial oxidative stress, prevented the collapse in mitochondrial membrane potential, improved mitochondrial oxygen consumption, and suppressed mitochondrial Ca(2+) overload during reoxygenation in an in vitro rat heart HR model. Furthermore, NecroX-5 reduced the ouabain- or histamine-induced increase in mitochondrial Ca(2+).

CONCLUSION:

These findings suggest that NecroX-5 may act as a mitochondrial Ca(2+) uniporter inhibitor to protect cardiac mitochondria against HR damage.

• Authors: Vu Thi Thu, Hyoung-Kyu Kim, Le Thanh Long, Sung-Ryul Lee, Tran My Hanh, Tae Hee Ko, Hye-Jin Heo, Nari Kim, Soon Ha Kim, Kyung Soo Ko, Byoung Doo Rhee, Jin Han
• Journal: Cardiovascular research (Cardiovasc Res) Vol. 94 Issue 2 Pg. 342-50 (May 01 2012) ISSN: 1755-3245 [Electronic] England
• PMID: 22425903 (Publication Type: Journal Article)

Chemical References

• Antioxidants
• Calcium Channels
• Heterocyclic Compounds, 4 or More Rings
• NecroX-5
• Reactive Oxygen Species
• Sulfones
• mitochondrial calcium uniporter
• Calcium

Topics

• Animals
• Antioxidants (pharmacology)
• Calcium (metabolism)
• Calcium Channels (drug effects)
• Heart (drug effects, physiology)
• Heterocyclic Compounds, 4 or More Rings (pharmacology, therapeutic use)
• Male
• Membrane Potentials (drug effects)
• Mitochondria, Heart (drug effects, metabolism)
• Myocardial Reperfusion Injury (metabolism, prevention & control)
• Myocardium (metabolism)
• Oxidative Stress (drug effects)
• Oxygen Consumption (drug effects)
• Rats
• Rats, Sprague-Dawley
• Reactive Oxygen Species (metabolism)
• Sulfones (pharmacology, therapeutic use)