scholarly journals Ефект попередників і модуляторів біосинтезу убіхінону на вміст і функціонування убіхінону та оксидативний статус у серці при введенні адреналіну

2011 ◽  
Vol 2 (1) ◽  
pp. 68-74
Author(s):  
O. B. Kuchmenko ◽  
D. M. Petukhov ◽  
I. N. Yevstratova ◽  
L. S. Mkhitaryan ◽  
G. V. Donchenko

Preventive and/or subsequent application of precursors and modulators complexes of ubiquinone biosynthesis under the adrenaline treatment reduces free-radical lipid and protein peroxidation intensity, but increases superoxide dismutase activity and improves activities of the mitochondrial electron-transport chain complexes. EPM and EPMD complexes can be effective anti-hypoxic remedies that promote normalization of the energy metabolism in ischemic heart.

1999 ◽  
Vol 277 (6) ◽  
pp. H2240-H2246 ◽  
Author(s):  
Lance B. Becker ◽  
Terry L. vanden Hoek ◽  
Zuo-Hui Shao ◽  
Chang-Qing Li ◽  
Paul T. Schumacker

Although a burst of oxidants has been well described with reperfusion, less is known about the oxidants generated by the highly reduced redox state and low O2 of ischemia. This study aimed to further identify the species and source of these oxidants. Cardiomyocytes were exposed to 1 h of simulated ischemia while oxidant generation was assessed by intracellular dihydroethidine (DHE) oxidation. Ischemia increased DHE oxidation significantly (0.7 ± 0.1 to 2.3 ± 0.3) after 1 h. Myxothiazol (mitochondrial site III inhibitor) attenuated oxidation to 1.3 ± 0.1, as did the site I inhibitors rotenone (1.0 ± 0.1), amytal (1.1 ± 0.1), and the flavoprotein oxidase inhibitor diphenyleneiodonium (0.9 ± 0.1). By contrast, the site IV inhibitor cyanide, as well as inhibitors of xanthine oxidase (allopurinol), nitric oxide synthase (nitro-l-arginine methyl ester), and NADPH oxidase (apocynin), had no effect. Finally, DHE oxidation increased with Cu- and Zn-containing superoxide dismutase (SOD) inhibition using diethyldithiocarbamate (2.7 ± 0.1) and decreased with exogenous SOD (1.1 ± 0.1). We conclude that significant superoxide generation occurs during ischemia before reperfusion from the ubisemiquinone site of the mitochondrial electron transport chain.


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