Figure 4.

Suggested pathomechanism for G72 in the mitochondria. Mitochondrial LG72 attenuates the activity of the complex I of the respiratory chain, presumably through binding to the flavin-mononucleotide (FMN) group. Impaired complex I functions results in an increased production of superoxide (O₂^−.), which in turn leads to increased lipid/protein peroxidation and reduced aconitase activity. The detoxifying glutathione S-transferase (GST), which is upregulated in G72Tg mice, converts GSSH and lipid hydroperoxide (LO2H) into GSSG, water, and lipid alcohol (LOH). Augmented GST protein expression diminishes the glutathione pool in the cell.