Sentences with phrase «mitochondrial electron transport»

But when you have excessive iron, it catalyzes the formation of excessive hydroxyl free radicals from the peroxide, which decimate your mitochondrial DNA, mitochondrial electron transport proteins and cellular membranes.

• Coenzyme Q10: CoQ10 is a vital member of the mitochondrial electron transport system (and therefore generation of ATP) and also a potent antioxidant.

Coenzyme Q10 is an important nutrient that is a cofactor in the mitochondrial electron transport chain, the biochemical pathway in cellular respiration from which adenosine triphosphate (ATP) and metabolic energy is derived.

Chance, along with Henry Lardy and later Ron Williams, worked out methods to separate mitochondria from cells and preserve their metabolic activity in vitro and invented the dual wavelength spectrophotometer to analyze mitochondrial electron transport coupled to ATP synthesis.

This protein is one of the nuclear - coded polypeptide chains of cytochrome c oxidase, the terminal oxidase in mitochondrial electron transport.

Specific role of mitochondrial electron transport in blood - stage Plasmodium falciparum.

Flavoprotein (FP) subunit of succinate dehydrogenase (SDH) that is involved in complex II of the mitochondrial electron transport chain and is responsible for transferring electrons from succinate to ubiquinone (coenzyme Q).

Meanwhile, fish oil intensified oxidation associated with ageing, lowered mitochondrial electron transport chain activity and altered the relative telomere length.

These 10 sets encode proteins responsible for four related bioenergetic processes: nuclear - encoded mitochondrial electron transport (the key energy - extracting operation), mitochondrial biogenesis (by which new mitochondria are formed) as well as glucose utilization and glucose sensing (processes by which glucose levels are evaluated and modified).

Not exact matches

The mutations that underlie the mitochondriopathies Myoclonic Epilepsy with Ragged Red Fibers (MERRF) and some variants of Mitochondrial Encephalomyopathy, Lactic Acidosis, and Strokelike Episodes (MELAS) create defective versions of particular mitochondrial amino acid tRNAs, leading to inefficient translation of electron transport system (ETS) subuMitochondrial Encephalomyopathy, Lactic Acidosis, and Strokelike Episodes (MELAS) create defective versions of particular mitochondrial amino acid tRNAs, leading to inefficient translation of electron transport system (ETS) subumitochondrial amino acid tRNAs, leading to inefficient translation of electron transport system (ETS) subunit proteins.

A famous example from the superfamily is cytochrome c oxidase, the last enzyme in the respiratory electron transport chain located in the mitochondrial membrane (see graph).

Salicylic acid binding of mitochondrial alpha - ketoglutarate dehydrogenase E2 affects mitochondrial oxidative phosphorylation and electron transport chain components and plays a role in basal defense against tobacco mosaic virus in tomato

Mitochondrial membrane ATP synthase (F (1) F (0) ATP synthase or Complex V) produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain.

So when we deliver less electrons to the electron transport chain this lowers the voltage on the inner mitochondrial membrane and this gives us a lowered associate magnetic field with that electron current on this membrane.

Removing acidic processed foods, sugar, flour, high - glycemic foods, coffee, and alcohol can prevent alterations in membrane potential which compromises mitochondrial function by interfering with the electron transport chain integral to oxygen - based oxidative phosphorylation (55, 56).

Electron microscopy showed dose dependent mitochondrial changes following indomethacin administration consistent with uncoupling of oxidative phosphorylation (or inhibition of electron transport) which were indistinguishable from those seen with the uncoupler dinitrElectron microscopy showed dose dependent mitochondrial changes following indomethacin administration consistent with uncoupling of oxidative phosphorylation (or inhibition of electron transport) which were indistinguishable from those seen with the uncoupler dinitrelectron transport) which were indistinguishable from those seen with the uncoupler dinitrophenol.

Electron microscopy showed mitochondrial damage following NSAID (indomethacin) compatible with uncoupling of oxidative phosphorylation and inhibition of electron trElectron microscopy showed mitochondrial damage following NSAID (indomethacin) compatible with uncoupling of oxidative phosphorylation and inhibition of electron trelectron transport.

Electron microscopy shows dose dependent mitochondrial changes that are indicative of uncoupling of oxidative phosphorylation or inhibition of electron trElectron microscopy shows dose dependent mitochondrial changes that are indicative of uncoupling of oxidative phosphorylation or inhibition of electron trelectron transport.

This includes a detailed, yet a fully understandable description of the biochemistry of aerobic respiration versus anaerobic fermentation, glycolysis, the Krebs Cycle, the electron transport chain, lactic acid overproduction and how cancer cells develop as a result of mitochondrial metabolic dysfunction leading to genetic errors, resulting in metastasis.