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At subtoxic concentrations, H 2 S has been shown to stimulate ATP production at the level of oxidative phosphorylation, both as a source of electron equivalents for the mETC (via SQR-mediated quinone reduction, Table 1), and through per-sulphidation of ATPase, which maintains the enzyme in its activated state

The complex clinical response to selective serotonin reuptake inhibitors in depression: a network perspective