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This AOP is constituted the MIE as sterol regulatory element binding transcription factor 2 (SREBF2) gene activation and repressions of glutathione synthetase (GSS) and glutathione S-transferases (GSTA1, GSTA2, GSTA3, GSTA5) genes and the KEs as perturbation of cholesterol, though up regulated unsaturated fatty acid concentration, and glutathione homeostasis leading to oxidative stress, DNA damage and AO as hepatotoxicity (HepG2 cell death)

TPP, sodium tripolyphosphate

In the early stages of AD, heightened immune responses facilitate the clearance of A [197, 198]

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After heat shock, a defect in cytosolic superoxide dismutase causes a rise in intracellular oxidation and rapid mortality in the stationary phase (Sunthonkun et al., 2019) (Table 1)