Sentences with phrase «mitochondria cytochrome»

Not exact matches

Alpha - lac, the Lund and Karolinska teams have demonstrated, can persuade mitochondria torelease cytochrome c.

Because mitochondria are inherited from the mother, even breeding with parasites that don't have cytochrome b mutations won't help the parasite escape its fate.

More of both support cell suicide as now sick or injured cells signal mitochondria to release factors such as cytochrome c into the cell cytoplasm.

All of this damage damages extremely precious mitochondrial DNA, which make the mitochondrias dysfunctional, clogging lysosome for mitophagy, and being incapable of keeping mitochondrial membrane potential (leading to Cytochrome C loss through mitochondrial permeability pores) and mitochondrial ATP OXPHOS respiration.

Certain particle compounds may directly generate ROS in vivo because of their surface chemistry (eg, metals, organic compounds, and semiquinones) or after bioactivation by cytochrome P450 systems (eg, polycyclic aromatic hydrocarbon conversion to quinones).6, 290 a, 290 b A particle surface or anions present on otherwise more inert particles may disrupt iron homeostasis in the lung and thereby also generate ROS via Fenton reactions.291 Other PM constituents may do so indirectly by the upregulation of endogenous cellular sources (eg, nicotinamide adenine dinucleotide phosphate [NADPH]-RRB- oxidase) 292,293 or by perturbing organelle function (eg, mitochondria) by taken - up PM components.261 Particle stimulation of irritant and afferent ANS fibers may also play a role in local and systemic oxidative stress formation.294 Given the rich antioxidant defenses in the lung fluid, secondarily generated oxidization products of endogenous molecules (eg, oxidized phospholipids, proteins) or a reduction in endogenous antioxidants per se may be responsible at least in part for the state of oxidative stress in the lungs (along with instigating the subsequent cellular responses) rather than ROS derived directly from PM and its constituents.

In the body, free radicals are produced in the mitochondria during detoxification reactions (cytochrome 450), in peroxisomes, and during inflammation.

And the interesting thing if you look at the mitochondria, as it's laid out, Cytochrome 1 and Cytochrome 5 which is ATPase that redox potential is designed go from about -400 all the way to zero where oxygen is.

(8) Coenzyme Q10 serves in the mitochondria as an electron carrier to cytochrome oxidase, the major system for cellular energy production.

«By stimulating the cytochrome oxidase enzyme, we are utilizing that oxygen in the respiratory chain inside of the mitochondria, producing more ATP for that cell.

Finally, the treatment stimulates the cytochrome oxidase enzyme in your cells» mitochondria.

In your mitochondria, there's also a specific molecule called cytochrome c oxidase, which is involved in the energy production within the mitochondria.

This toxin stops the cell respiration as a non-competitive inhibitor for an enzyme in the mitochondria that is referred to as cytochrome c oxidase, causing asphyxiation in the cells.