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Combining KRAS inhibitors with glutaminolysis inhibitors may create synthetic lethality by simultaneously blocking oncogenic signaling and metabolic support

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On the contrary, in adult male rats treated with 25 g/kg/week AFB1 for 8 weeks, AFB1 could trigger obvious neurotoxicity, inflammatory responses, oxidative stress and, anxiety and depression-like behaviors (241)

Matrix metalloproteinase-9 activation in hyperhomocysteinemic rats is triggered by the opening of the mitochondrial permeability transition pore and antagonism of the N-methyl-D-aspartate receptor-1 (NMDA-R1), resulting in myocyte dysfunction due to elevated calcium overload and oxidative stress [40]

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Available at: Accessed 9/28/18