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Sido et al, 1998), the increase in -GCS in mucosa from TNBS-treated rats can be interpreted as an adaptive response to control the consequences of the stress induced by TNBS as -GCS-HS is known to be upregulated in response to divergent stressful conditions including oxidative stress or GSH depletion (Morales et al, 1997, 1998

[25] More evidence of NAD+s significance in promoting mitochondrial and metabolic health may be seen in murine cells overexpressing the NADase CD38, which also had greater lactate levels, aberrant mitochondria, including missing or enlarged cristae, and lower oxygen consumption