scholarly journals Cytochromes and some respiratory enzymes in mitochondria from the spadix of Arum maculatum

1958 ◽  
Vol 70 (3) ◽  
pp. 381-390 ◽  
Author(s):  
D. S. Bendall
Keyword(s):  
Respiratory Enzymes ◽  
Arum Maculatum

New aspects of the energy-tropic action of mexidol

2018 ◽  
pp. 36-40
Author(s):  
Ю.И. Кирова ◽  
Э.Л. Германова
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cerebral Cortex ◽  
Growth Factor ◽  
Atp Synthase ◽  
Oxygen Deficiency ◽  
Vascular Endothelial ◽  
Cyt B ◽  
Respiratory Enzymes ◽  
Catalytic Subunits ◽  
Endothelial Growth Factor

Митохондриогенез и ангиогенез являются ключевыми нейропротекторными механизмами, повышающими устойчивость нервной ткани к условиям гипоксии/ишемии. В настоящее время фармакологическая индукция биогенеза митохондрий является одним из наиболее перспективных и активно разрабатываемых подходов к коррекции ишемических и постишемических нарушений, нейродегенеративных заболеваний и кардиопатий. Выявление факта стимуляции митохондриогенеза эталонными нейропротекторными препаратами позволит существенно расширить представление об их терапевтическом потенциале и принципах применения. Цель исследования - изучение влияния нейропротекторного сукцинатсодержащего препарата мексидол на экспрессию каталитических субъединиц дыхательных ферментов митохондрий, АТФ-синтазы и фактора роста эндотелия сосудов в коре головного мозга крыс с врожденными различиями в устойчивости к дефициту кислорода. Методика. Исследование выполнено на белых беспородных крысах-самцах. Инъекции мексидола (40 мг/кг, внутрибрюшинно) выполняли ежедневно на протяжении 20 сут. Уровень экспрессии каталитических субъединиц дыхательных ферментов митохондрий и АТФ-синтазы, фактора роста эндотелия сосудов и сукцинатного рецептора в ткани коры головного мозга оценивали методом иммуноблоттинга. Общую резистентность организма к острой гипоксии тестировали в гипобарической камере проточного типа при разрежении атмосферы, соответствующем 190 мм рт. ст. (3% О). Результаты. В ходе курса применения мексидола происходило увеличение уровня каталитических субъединиц дыхательных ферментов митохондрий (NDUFV2, SDHA, cyt b, COX1), АТФ-синтазы (ATP5A), фактора роста эндотелия сосудов (VEGF) и сукцинатного рецептора (SUCNR1), особенно выраженное у неустойчивых к гипоксии особей. Заключение. Впервые показана вовлеченность сукцинатсодержащего препарата мексидол в механизмы индукции ферментов энергопродуцирующей системы митохондрий коры головного мозга, что существенно расширяет сложившиеся представления о механизмах его энерготропного действия. Mitochondriogenesis and angiogenesis are crucial neuroprotective mechanisms that increase the resistance of nervous tissue to hypoxia/ischemia conditions. Currently, pharmacological induction of mitochondrial biogenesis is one of the most promising and actively developed approaches for the correction of ischemic and post-ischemic disorders, neurodegenerative diseases and cardiopathies. Revealing the fact of stimulation of mitochondriogenesis with standard neuroprotective drugs will significantly expand the understanding of their therapeutic potential and principles of application. The aim of the research was to study the effect of the neuroprotective succinate-containing drug mexidol on the expression of catalytic subunits of the respiratory enzymes of mitochondria, ATP-synthase and vascular endothelial growth factor in the cerebral cortex of rats with inborn differences in resistance to oxygen deficiency. Methods. The study was carried out on white mongrel rats-males injections of mexidol (40 mg/kg, intraperitoneally) were performed daily for 20 days. The expression level of the catalytic subunits of the respiratory enzymes of mitochondria and ATP-synthase, vascular endothelial growth factor and succinate receptor in the tissue of the cerebral cortex was assessed by immunoblotting. The total resistance of the organism to acute hypoxia was tested in a hypobaric chamber with an atmosphere underpressure corresponding to 190 mm Hg (3% O). Results. During the injection course of mexidol, there was an increase in the level of catalytic subunits of the respiratory enzymes of mitochondria (NDUFV2, SDHA, cyt b, COX1), ATP-synthase (ATP5A), vascular endothelial growth factor (VEGF) and succinate receptor (SUCNR1), especially pronounced in rats with low-resistance to hypoxia. Conclusion. The study revealed for the first time the involvement of the succinate-containing drug mexidol in the mechanisms of induction of enzymes of the energy-producing system of the mitochondria of the cerebral cortex, which significantly expands the existing ideas about the mechanisms of its energy-tropic action.

scholarly journals THE ASSAY OF ANIMAL TISSUES FOR RESPIRATORY ENZYMES

1948 ◽  
Vol 175 (2) ◽  
pp. 619-634 ◽  
Author(s):  
Van R. Potter ◽  
G.A. LePage ◽  
H.L. Klug
Keyword(s):  
Animal Tissues ◽  
Respiratory Enzymes

scholarly journals RESPIRATORY ENZYMES IN OXIDATIVE PHOSPHORYLATION

1955 ◽  
Vol 217 (1) ◽  
pp. 395-407 ◽  
Author(s):  
Britton Chance ◽  
G.R. Williams
Keyword(s):  
Oxidative Phosphorylation ◽  
Respiratory Enzymes

Mitochondrial function in flying honeybees (Apis mellifera): respiratory chain enzymes and electron flow from complex III to oxygen

2000 ◽  
Vol 203 (5) ◽  
pp. 905-911 ◽  
Author(s):  
R.K. Suarez ◽  
J.F. Staples ◽  
J.R. Lighton ◽  
O. Mathieu-Costello
Keyword(s):  
Surface Area ◽  
Muscle Mass ◽  
Respiratory Chain ◽  
Mitochondrial Function ◽  
Electron Flow ◽  
Complex Iii ◽  
High Mass ◽  
Metabolic Rates ◽  
Turnover Rates ◽  
Respiratory Enzymes

The biochemical bases for the high mass-specific metabolic rates of flying insects remain poorly understood. To gain insights into mitochondrial function during flight, metabolic rates of individual flying honeybees were measured using respirometry, and their thoracic muscles were fixed for electron microscopy. Mitochondrial volume densities and cristae surface densities, combined with biochemical data concerning cytochrome content per unit mass, were used to estimate respiratory chain enzyme densities per unit cristae surface area. Despite the high content of respiratory enzymes per unit muscle mass, these are accommodated by abundant mitochondria and high cristae surface densities such that enzyme densities per unit cristae surface area are similar to those found in mammalian muscle and liver. These results support the idea that a unit area of mitochondrial inner membrane constitutes an invariant structural unit. Rates of O(2) consumption per unit cristae surface area are much higher than those estimated in mammals as a consequence of higher enzyme turnover rates (electron transfer rates per enzyme molecule) during flight. Cytochrome c oxidase, in particular, operates close to its maximum catalytic capacity (k(cat)). Thus, high flux rates are achieved via (i) high respiratory enzyme content per unit muscle mass and (ii) the operation of these enzymes at high fractional velocities.

Effects of hypercapnia on ECoG and oxidative metabolism in neonatal dog brain

1995 ◽  
Vol 78 (6) ◽  
pp. 2272-2278 ◽  
Author(s):  
H. Yoshioka ◽  
H. Miyake ◽  
D. S. Smith ◽  
B. Chance ◽  
T. Sawada ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Resonance Spectroscopy ◽  
Respiratory Enzymes ◽  
Arterial Pco2 ◽  
A Value ◽  
Electrocorticogram Ecog ◽  
The Brain ◽  
Mitochondrial Respiratory

The effects of hypercapnia on cerebral electrical activity and mitochondrial oxidative phosphorylation were studied in the anesthetized neonatal dog by using the electrocorticogram (ECoG) and 31P-magnetic resonance spectroscopy. Three levels of hypercapnia with arterial PCO2 values of approximately 70, 100, and 140 Torr reduced the intracellular pH of the brain from 7.11 to 6.99, 6.87, and 6.76, respectively. These levels of hypercapnia also reduced ADP concentration ([ADP]) from 21.5 to 18.1, 14.8, and 12.9 microM as well as the average ECoG power output by 20, 30, and 40%. A Michaelis-Menten relationship for the mitochondrial respiratory enzymes was fitted with [ADP] and the change in the average ECoG. The result suggests that mitochondrial respiration is regulated by [ADP] and that the in vivo Michaelis-Menten constant for ADP was 21 microM, a value close to the in vitro value. The mitochondrial maximal reaction velocity was reduced by only 10% during hypercapnia and showed no relationship with the degree of acidosis, suggesting that mitochondrial respiratory enzymes are not responsible for the inhibition of the brain electrical activity.

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