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The SCC-61/rSCC-61 specific models were generated by estimating relative changes in metabolic gene transcriptomic data to populate upper flux constraints by the theoretical limit of Vmax values, as described in ( Figure 3A that are responsible for 84-90% of the cellular NAD(P)H production in the rSCC-61 and SCC-61 cells and thus will have the most significant impact on the suppression of ROS and response to radiation

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Despite GSTP1 inhibition, the cause of insignificance in overall GST activity may be due to other GST isoforms remaining uninhibited, and compensatory mechanisms may upregulate other GST isoforms, indicating the need for further investigations

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