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Importantly, our cell culture observations were corroborated by our results obtained in animal studies, suggesting that increased hepatic protein S -glutathionylation contributes to NAFLD pathogenesis via suppression of the NF-B signaling pathway in hepatocytes

Lu proposes in [12] that the high glutathione concentration in hepatocytes is a storage mechanism for cysteine

This can cause a glutathione deficiency and a systemic immune reaction

Moreover, the hyperhomocysteinemia associated with an increased cardiovascular risk is stronger in non-insulin-dependent diabetes mellitus than in normal subjects (Hoogeveen et al, 1998)

In addition, we observed that inhibiting plant NADPH oxidase partially restored the virulence of the mutants