Alternative means to elevate of suppress biologic H2S levels

Elevating H2S LevelsSuppressing H2S Levels
Modulating H2S degradationInhibiting H2S metabolizing enzymesRhodanese deficiency (TST−/− systems); SQR silencing and ETHE1 deficiency boost H2S levels. Antioxidants reduce ROS-mediated H2S degradation and boost H2S levelsActivating H2S metabolizing enzymesSQR or rhodanese overexpression? No pharmacological approaches
Modulating semistable H2S “pools”Administering H2S metabolites or enhancing H2S regeneration from endogenous H2S “pools”Thiosulfate and sulfane sulfur administration can elevate H2S levels and produce biologic effects consistent with H2S generation. Aspirin has been shown to accelerate H2S release from sulfane sulfurInhibiting the clearance or excretion of H2S metabolites?No known pharmacological approaches
Regulating the expression of H2S-producing enzymesUpregulating CBS, CSE or 3-MST expressionUpregulation of enzyme expression (e.g. using taurine) Overexpression of H2S producing enzymes as as an experimental tool. Inhibition of CBS degradation (LON protease inhibitors)Downregulating CBS, CSE, or 3-MST expressionInhibiting enzyme expression? Enhancing CBS degradation by ubiquitination enhancers or protease activators?
Alternative ways of regulating the enzymatic production of H2SIncreasing CBS, CSE, or 3-MST-mediated H2S productionSupplementation of substrates (l-cysteine, homocysteine for CBS/CSE), 3-MP for 3-MST. Activating CBS by its cofactor SAM. Some of the H2S donors (garlic-derived polysulfides, S-propargly-cysteine) rely, in part on CSE-mediated conversion for H2S production in biologic systemsIncreasing CBS-, CSE-, or 3-MST-mediated H2S productionDepleting substrates (l-cysteine, homocysteine for CBS/CSE), 3-MP for 3-MST. Administering cysteinase (cancer therapy). Inhibiting CBS by blocking its cofactor binding