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Long-COVID patients presented with an even further drops in tryptophan, a significant association between MitSox (oxidative stress) and intracellular levels of a regulatory molecule called p16INK4a that tamps down oxidative stress was found, and so were elevated suPAR levels (associated with increased inflammation, tryptophan degradation) The drastic tryptophan decrease in the long-COVID patients got the authors attention

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