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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

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Previous three-phase study showed similar "mixed" results This follows a three-phase study performed by the same Baylor / Kyowa Hakko team (Sarah McKinley-Barnard, Tom Andre, Kyowa Hakko's Masahiko Morita, and Darryn S

however, one must not ignore the side effects