Oxygen alone, no. It is the understated "few items" in solution that treat/reverse acidosis both pulmonary and metabolic/systemic.
Principally the bicarbonate ions [HCO3-] draw protons/positively charged molecules/acids/*insert synonym* out of circulation upon direct contact in blood and through the renal walls along diffuse/osmotic/active transport chemogradients and directly interacts with the chemoreceptors as the yin to oxygen's yang (direct antagonist).
The Na/Mg/Ca/Cl ions added alongside help to regulate the basification occurring before aiding normal cellular processes.
Pfffft! Anything outside one's knowledge scope is simply something you haven't yet learned!
COPD prominently presents fibrotic and vacuolar physiology, the mechanical disruption from such screws up the concentration gradients within lung tissue due to inconsistent volumes of air inhaled with little regulation of frequency being physically prevented from passing efficiently. Flooding an obstructed airway with concentrated O2 would induce fairly significant oxidative stress and subsequent cellular death much more readily than in persons of non-clinical pulmonary physiology.
Haven't heard "paraquat" for a while, the nomenclature based name of Methyl Viologen is much more common IME.
Though you could call it "Dave" and it'd still bend your system over and fuck it like a remarkably libidinous two dollar whore.
The mimicry of polyamine(s) and subsequently becoming a concentrated slush in the lungs (alveolar vessels and sacs) is one thing, and akin to various cytotoxins a la Fluoroacetate in mitochondria. That its structure is highly reactive and most importantly reversibly so and thus the constant eternal metabolism of superoxide (less Marvel, more ubertoxin) radicals is quite the unique kick in the teeth though. The impact in the lungs also pales in comparison to that presented once deposition in the renal system occurs, obliterating any efficacy of filtration like that which exists as the entire purpose of a kidney and thus quickly inducing systemic signalling issues and associated cell death.
Doesn't it also have a habit of appearing inactive/in remission in pulmonary scans/imaging until getting bored and inducing massive tumour cascades a few years down the line?
If it isn't detailed in my to-hand tox. literature I may have to prod Google later on for reading material so... cheers, I guess.
