Biochemical Mechanism | Notes |
---|---|
radical scavenging antioxidant | • antioxidant inhibitor of peroxynitrite-mediated processes via activation of N-methly-D-aspartate (NMDA) receptors [82]. |
 | • shield cultured neurons from oxidative damage by increasing levels of glutathione [83]. |
 | • induce upregulation of HO-1, anti-inflammatory and cytoprotective genes [84, 85]. |
 | • inhibits myeloperoxidase and destroys H2O2 [86]. |
 | • mediates mitochondrial preservation in post hypoxic conditions that are ideal for mitochondrial permeability transition pore (MPTP) that would cause the mitochondria to break down and lead to cell death [56]. |
anti-apoptotic | • reduces IR induced apoptosis via reduction of cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP) [87]. |
 | • protection of isolated mitochondria by decreasing Ca2+ loading via vascular smooth muscle KATP channel-mediated hyperpolarization [23, 38, 56] or inhibition of L-type Ca2+ channels. |
 | • H2S activated STAT3 and Protein Kinase C (PKC) inhibits the pro-apoptotic factor Bad and upregulated the prosurvival proteins Bcl-2 and Bcl-xl by altering phosphorylation [56]. |
 | • H2S influences inactivation of pro-apoptotic pathways through survival pathway of extracellular-signal regulated kinase (ERK1/2)/mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI-3-kinase) [56]. |
anti-inflammatory | • inhibit leukocyte adherence in the rat mesenteric microcirculation during vascular inflammation [38]. |
decrease radiosensitivity | • transiently and reversibly inhibiting mitochondrial respiration [38]. |
metabolic alteration | • produces a "suspended animation-like" metabolic status with hypothermia and reduced oxygen demand in pigs (who received it intravenously) [88]. and mice (who received hydrogen sulfide via inhalation) [89, 90]. |
 | • mice breathing 80 ppm of H2S for 6 hr reduced heart rate, core body temperature, respiratory rate and physical activity where as blood pressure remained unchanged [56]. |