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In this review, the biochemical basis of oxidative stress in ASD is examined, the mechanistic understanding of antioxidant-based interventions is assessed, and the structureactivity relationships that dictate their therapeutic value are discussed

Enzyme replacement therapy for hypophosphatasia has shown promising results in human clinical trials, reducing mortality in hypophosphatasia and improving chondromalacia, lung function and exercise milestones in these patients [44]

Cytoplasmic p53 has been reported to inhibit G6PD protein directly through protein-protein interaction[40], so it is possible that acidosis may reduce the interaction by lowering cytoplasmic pools of p53 or pH-dependent conformational changes