Sentences with phrase «formation by mitochondria»

Not exact matches

Serine Hydrolase Inhibitors Block Necrotic Cell Death by Preventing Calcium Overload of the Mitochondria and Permeability Transition Pore Formation.
ApoE as a major causative factor and therapeutic target in Alzheimer's disease and other neurodegenerative disorders; small - molecule structure correctors to convert apoE4 to apoE3 and reverse the detrimental effects of apoE4 on mitochondria and the cytoskeleton; small - molecule protease inhibitors to block the formation of toxic fragments of apoE4; Plasma lipoprotein metabolism regulation involving apoE and apoB; cholesterol homeostasis modulation by lipoprotein receptors controlling lipoprotein clearance by the liver; Plasma HDL cholesterol (HDL - C) metabolism in the progression of atherosclerosis; the genetic epidemiology of the metabolic syndrome and low HDL - C levels established by the Turkish Heart Study.
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.
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