Hydroxysafflor Yellow A Inhibits Rat Brain Mitochondrial Permeability Transition Pores by a Free Radical Scavenging Action

Pharmacology ◽  
2008 ◽  
Vol 82 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Jingwei Tian ◽  
Guisheng Li ◽  
Zhifeng Liu ◽  
Fenghua Fu
Keyword(s):  
Free Radical ◽  
Rat Brain ◽  
Mitochondrial Permeability Transition ◽  
Radical Scavenging ◽  
Permeability Transition ◽  
Free Radical Scavenging ◽  
Hydroxysafflor Yellow A ◽  
Mitochondrial Permeability ◽  
Permeability Transition Pores

Free radical scavenging systems in developing rat brain

1991 ◽  
Vol 9 (2) ◽  
pp. 181-185 ◽  
Author(s):  
Bangalore R. Shivakumar ◽  
Hindupur K. Anandatheerthavarada ◽  
Vijayalakshmi Ravindranath
Keyword(s):  
Free Radical ◽  
Rat Brain ◽  
Radical Scavenging ◽  
Free Radical Scavenging ◽  
Developing Rat

scholarly journals Effect of complexes of precursors and modulators of coenzyme q biosynthesis on functional state of old rats' heart mitochondria

2010 ◽  
Vol 56 (2) ◽  
pp. 244-256 ◽  
Author(s):  
E.B. Kuchmenko ◽  
D.N. Petukhov ◽  
G.V. Donchenko ◽  
L.S. Mkhitaryan ◽  
S.V. Tymoshchuk ◽  
...  
Keyword(s):  
Free Radical ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Coenzyme Q ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Biologically Active ◽  
Mitochondrial Permeability ◽  
Old Rats ◽  
Enzyme Complexes

Our research demonstrate that ageing leads to changes in activity of electron-transporting enzyme complexes in myocardial mitochondria of old rats and to increased sensitivity of mitochondrial permeability transition pore to inductors of its opening - Ca2+ and phenylarsine oxide. We also observed activation of lipid and protein free-radical peroxidation processes. Administration of a complex of biologically active substances that included precursors and modulators of coenzyme Q biosynthesis (α-tocopherol acetate, 4-hydroxybenzoic acid, and methionine) we observed the increase in coenzyme Q content, correction of functional activity of mitochondrial electron-transport chain enzyme complexes, the decrease in intensivity of lipid and protein free-radical peroxidation in the heart and the decrease in sensitivity of mitochondrial permeability transition pore to inductors of its opening. This complex may be used to treat mitochondrial dysfunction under numerous pathologies of cardiovascular system, as well as in ageing.

scholarly journals Quantification of active mitochondrial permeability transition pores using GNX-4975 inhibitor titrations provides insights into molecular identity

2016 ◽  
Vol 473 (9) ◽  
pp. 1129-1140 ◽  
Author(s):  
Andrew P. Richardson ◽  
Andrew P. Halestrap
Keyword(s):  
Cell Death ◽  
Membrane Proteins ◽  
Mitochondrial Membrane ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Mitochondrial Permeability ◽  
Molecular Identity ◽  
Permeability Transition Pores

The molecular identity of the mitochondrial permeability transition pore (MPTP), a key player in cell death, remains controversial. Here we use a novel MPTP inhibitor to demonstrate that formation of the pore involves native mitochondrial membrane proteins adopting novel conformations.

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