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Description
The mechanism of metabolic acidosis and 5-oxoprolinuria is the following: decreased levels of cellular glutathione lead to decreased feed-back inhibition of -glutamylcysteine synthetase
Nrf2 then accumulates in the cytoplasm and translocates to the nucleus [25], where the Nrf2-dependent self Neh1 attaches to sMAF transcription factors
Virol J
However, PGE2 is known to play a dual role, as it can both suppress the immune response against M.tb and protect the host from excessive inflammation, suggesting that NSAIDs should be exercised with caution for TB treatment [128]
10.3390/antiox10081198 132
