The first is prevention
with endogenous antioxidants — superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase work together to stabilize then break down the free radical so it can be used to regenerate glutathione, the body's most potent antioxidant.
Not exact matches
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.
It is one of the body's
endogenous antioxidants, along
with superoxide dismutase (SOD), CoEnzyme Q10 (CoQ10), alpha lipoic acid and Catalase.
All these substances can help prevent free radical damage, and together
with the body's natural
antioxidants (
endogenous), they are the main source of protection for muscles and other tissues.
Moreover, reactive nitrogen and oxygen species (RNOS) are used extensively in cellular signalling, and cells adaptively regulate
endogenous antioxidants on short time scales to respond to deletorious spikes of RNOS faster than we could ever achieve
with dietary
antioxidants.
A growing body of evidence indicates that consuming large quantities of
antioxidants like vitamin C, E, and β - carotene can interfere
with the body's
endogenous antioxidant system.
Our ancestors evolved to deal
with these exobiotic toxins
with robust
endogenous antioxidant and detoxification responses, and in their absence (eg, in a highly processed diet), our cells don't get the expected cues to ramp up defenses.