Protonophoric Activity of NADH Coenzyme Q Reductase and ATP Synthase in Coupled Submitochondrial Particles from Horse Platelets

1997 ◽  
Vol 235 (3) ◽  
pp. 469-473 ◽  
Author(s):  
Alessandra Baracca ◽  
Laura Bucchi ◽  
Anna Ghelli ◽  
Giorgio Lenaz
Keyword(s):  
Atp Synthase ◽  
Coenzyme Q ◽  
Submitochondrial Particles

Steady-State Kinetics of the Reduction of Coenzyme Q Analogs by Complex I (NADH:Ubiquinone Oxidoreductase) in Bovine Heart Mitochondria and Submitochondrial Particles†

Biochemistry ◽  
1996 ◽  
Vol 35 (8) ◽  
pp. 2705-2716 ◽  
Author(s):  
Romana Fato ◽  
Ernesto Estornell ◽  
Salvatore Di Bernardo ◽  
Francesco Pallotti ◽  
Giovanna Parenti Castelli ◽  
...  
Keyword(s):  
Steady State ◽  
Complex I ◽  
Coenzyme Q ◽  
Heart Mitochondria ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Submitochondrial Particles ◽  
Bovine Heart ◽  
Steady State Kinetics ◽  
Kinetics Of

Arabidopsis 4-COUMAROYL-COA LIGASE 8 contributes to the biosynthesis of the benzenoid ring of coenzyme Q in peroxisomes

2019 ◽  
Vol 476 (22) ◽  
pp. 3521-3532
Author(s):  
Eric Soubeyrand ◽  
Megan Kelly ◽  
Shea A. Keene ◽  
Ann C. Bernert ◽  
Scott Latimer ◽  
...  
Keyword(s):  
Oxidative Metabolism ◽  
Time Course ◽  
Reverse Genetics ◽  
De Novo ◽  
Coenzyme Q ◽  
Control Level ◽  
Wild Type ◽  
Fluorescent Reporters ◽  
Coa Ligase ◽  
Peroxisomal Targeting

Plants have evolved the ability to derive the benzenoid moiety of the respiratory cofactor and antioxidant, ubiquinone (coenzyme Q), either from the β-oxidative metabolism of p-coumarate or from the peroxidative cleavage of kaempferol. Here, isotopic feeding assays, gene co-expression analysis and reverse genetics identified Arabidopsis 4-COUMARATE-COA LIGASE 8 (4-CL8; At5g38120) as a contributor to the β-oxidation of p-coumarate for ubiquinone biosynthesis. The enzyme is part of the same clade (V) of acyl-activating enzymes than At4g19010, a p-coumarate CoA ligase known to play a central role in the conversion of p-coumarate into 4-hydroxybenzoate. A 4-cl8 T-DNA knockout displayed a 20% decrease in ubiquinone content compared with wild-type plants, while 4-CL8 overexpression boosted ubiquinone content up to 150% of the control level. Similarly, the isotopic enrichment of ubiquinone's ring was decreased by 28% in the 4-cl8 knockout as compared with wild-type controls when Phe-[Ring-13C6] was fed to the plants. This metabolic blockage could be bypassed via the exogenous supply of 4-hydroxybenzoate, the product of p-coumarate β-oxidation. Arabidopsis 4-CL8 displays a canonical peroxisomal targeting sequence type 1, and confocal microscopy experiments using fused fluorescent reporters demonstrated that this enzyme is imported into peroxisomes. Time course feeding assays using Phe-[Ring-13C6] in a series of Arabidopsis single and double knockouts blocked in the β-oxidative metabolism of p-coumarate (4-cl8; at4g19010; at4g19010 × 4-cl8), flavonol biosynthesis (flavanone-3-hydroxylase), or both (at4g19010 × flavanone-3-hydroxylase) indicated that continuous high light treatments (500 µE m−2 s−1; 24 h) markedly stimulated the de novo biosynthesis of ubiquinone independently of kaempferol catabolism.

The Effect of Dietary Glutathione and Coenzyme Q10 on the Prevention and Treatment of Inflammatory Bowel Disease in Mice

2004 ◽  
Vol 74 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Liu ◽  
Russell ◽  
Smith ◽  
Bronson ◽  
Milbury ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Coenzyme Q ◽  
Histological Evaluation ◽  
Therapeutic Effects ◽  
Prevention Study ◽  
Prevention And Treatment ◽  
Inflammatory Bowel ◽  
Pre Treatment

Because reactive oxygen species have been implicated as mediators of inflammatory bowel disease (IBD), we evaluated the potential preventive and therapeutic effects of two dietary antioxidants, glutathione (GSH) and coenzyme Q10 (CoQ10) on dextran sulfate sodium (DSS)-induced colitis in mice. Fifty female 8-wk old Swiss-Webster mice were randomly assigned to 4 groups for a pre-treatment 'prevention' study: (1) GSH (1% of diet); (2) CoQ10 (200 mg/kg/d); (3) DSS only (3% of drinking water); (4) control (no treatment). The mice in groups 1 and 2 were fed with GSH or CoQ10 for 21 wks, and the mice in groups 1, 2 and 3 were provided DSS from wk 7 for 4 cycles (1 cycle = 1 wk DSS followed by 2-wk water). Another 50 mice were randomly assigned to 4 groups for a 21-wk 'treatment' study where the mice in groups 1, 2, and 3 were administered DSS for 6 cycles (18 wks) to induce colitis. GSH and CoQ10 were added from wk 7 until the completion of the protocol. Loose stools and hemocult positivity were modestly but significantly reduced with GSH or CoQ10 at several periods during the intervention in both the prevention and treatment studies. In contrast, histological evaluation revealed increases in colonic dysplasia and ulceration with GSH or CoQ10. Thus, in this mouse model, GSH and CoQ10 appear to have a beneficial effect on acute signs of IBD, but may have an adverse impact on the chronic pathophysiology of the disease. Further studies using additional animal models are required to determine whether GSH or CoQ10 provide a favorable or unfavorable benefit:risk ratio in the prevention or treatment of IBD.

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.

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