Such_Saturation
Member
- Joined
- Nov 26, 2013
- Messages
- 7,370
Rotten egg gas holds key to healthcare therapies
The synthesis and functional evaluation of a mitochondria-targeted hydrogen sulfide donor, (10-oxo-10-(4-(3-thioxo-3H-1,2-dithiol-5-yl)phenoxy)decyl)triphenylphosphonium bromide (AP39)
The neuroprotection of hydrogen sulfide against MPTP-induced dopaminergic neuron degeneration involves uncoupling protein 2 rather than ATP-sensitive potassium channels.
Attaches to iron AND modulates nitric oxide?
Hydrogen sulfide cytoprotective signaling is endothelial nitric oxide synthase-nitric oxide dependent
Hydrogen sulfide inhibits nitric oxide production and nuclear factor-κB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide
CO treatment also inhibited LPS-induced NO production and iNOS expression via its inactivation of NF-κB.
Even though CO is toxic to the cytochromes, this mechanism plays a minor role in clinical CO poisoning, since
the amount of CO required to poison cytochromes is 1000 times higher than the lethal dose. CO binds to intracellular myoglobin in the myocardium and impairs the oxygen supply to the mitochondria (Carbon monoxide intoxication: An updated review)
Superoxide generation by endothelial nitric oxide synthase: The influence of cofactors
Heme-iron ligands, cyanide, imidazole, and the phenyl(diazene)-derived radical inhibit superoxide generation.
The synthesis and functional evaluation of a mitochondria-targeted hydrogen sulfide donor, (10-oxo-10-(4-(3-thioxo-3H-1,2-dithiol-5-yl)phenoxy)decyl)triphenylphosphonium bromide (AP39)
The neuroprotection of hydrogen sulfide against MPTP-induced dopaminergic neuron degeneration involves uncoupling protein 2 rather than ATP-sensitive potassium channels.
Attaches to iron AND modulates nitric oxide?
Hydrogen sulfide cytoprotective signaling is endothelial nitric oxide synthase-nitric oxide dependent
Hydrogen sulfide inhibits nitric oxide production and nuclear factor-κB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide
CO treatment also inhibited LPS-induced NO production and iNOS expression via its inactivation of NF-κB.
Even though CO is toxic to the cytochromes, this mechanism plays a minor role in clinical CO poisoning, since
the amount of CO required to poison cytochromes is 1000 times higher than the lethal dose. CO binds to intracellular myoglobin in the myocardium and impairs the oxygen supply to the mitochondria (Carbon monoxide intoxication: An updated review)
Superoxide generation by endothelial nitric oxide synthase: The influence of cofactors
Heme-iron ligands, cyanide, imidazole, and the phenyl(diazene)-derived radical inhibit superoxide generation.
