The influence of sulfide and cyanide on axonal function

Hydrogen Sulfide and the Pathogenesis of Atherosclerosis

“…Disulfide bond rearrangement is essential for platelet function (25). H 2 S is known to reduce disulfide bonds in proteins (9, 10), which makes it a likely candidate to alter platelet activation. Zagli et al (110) showed that 30 μ M NaHS inhibited platelet aggregation in vitro induced by ADP, collagen, epinephrine, arachidonic acid, thromboxane mimetic, U46619 (a synthetic analog of PGH 2 ), and thrombin.…”

Hydrogen Sulfide and the Pathogenesis of Atherosclerosis

“…Disulfide bond rearrangement is essential for platelet function (25). H 2 S is known to reduce disulfide bonds in proteins (9, 10), which makes it a likely candidate to alter platelet activation. Zagli et al (110) showed that 30 μ M NaHS inhibited platelet aggregation in vitro induced by ADP, collagen, epinephrine, arachidonic acid, thromboxane mimetic, U46619 (a synthetic analog of PGH 2 ), and thrombin.…”

Review: Mitochondria and disease progression in multiple sclerosis

“…The terminal complex (cytochrome c oxidase or complex IV) is where over 90% of oxygen is consumed [45]. Complex IV is a target of NO, which is present in active MS lesions and is implicated in conduction block as well as axonal degeneration, and cyanide, a specific complex IV inhibitor, impairs nerve conduction [47–50]. In the case of severe oxidative phosphorylation defects, the ability of mitochondria to handle calcium is impaired [51,52].…”

“…By applying cyanide to sciatic nerves, Beck et al. showed a decrease in compound action potential and conduction velocity, which was partially reversible, as well as a time‐ and concentration‐dependent effect on conduction block [50]. The likely functional consequences of complex IV defects are also shown by the conduction block induced by NO [87].…”

Automated Polarographic Determination of Sulfide as Contaminant in Parenteral Amino Acid Solutions

“…1 Hydrogen sulfide and its toxic precursor salts, sodium sulfide (Na 2 S) and sodium hydrogensulfide (NaHS), cause a variety of effects within the central [2][3][4][5] and peripheral nervous systems. 6 Sulfide concentrations have been determined by a variety of methods in various sources, such as petroleum products, atmospheric gases, aqueous samples, 7 blood 8 and homogenates of brain, 9 but we have noted a lack of methods for determining sulfide at trace levels as a contaminant of medicaments.…”

Hydrogen Sulfide and the Pathogenesis of Atherosclerosis

“…Disulfide bond rearrangement is essential for platelet function (25). H 2 S is known to reduce disulfide bonds in proteins (9, 10), which makes it a likely candidate to alter platelet activation. Zagli et al (110) showed that 30 μ M NaHS inhibited platelet aggregation in vitro induced by ADP, collagen, epinephrine, arachidonic acid, thromboxane mimetic, U46619 (a synthetic analog of PGH 2 ), and thrombin.…”

Review: Mitochondria and disease progression in multiple sclerosis

“…The terminal complex (cytochrome c oxidase or complex IV) is where over 90% of oxygen is consumed [45]. Complex IV is a target of NO, which is present in active MS lesions and is implicated in conduction block as well as axonal degeneration, and cyanide, a specific complex IV inhibitor, impairs nerve conduction [47–50]. In the case of severe oxidative phosphorylation defects, the ability of mitochondria to handle calcium is impaired [51,52].…”

“…By applying cyanide to sciatic nerves, Beck et al. showed a decrease in compound action potential and conduction velocity, which was partially reversible, as well as a time‐ and concentration‐dependent effect on conduction block [50]. The likely functional consequences of complex IV defects are also shown by the conduction block induced by NO [87].…”

Automated Polarographic Determination of Sulfide as Contaminant in Parenteral Amino Acid Solutions

“…1 Hydrogen sulfide and its toxic precursor salts, sodium sulfide (Na 2 S) and sodium hydrogensulfide (NaHS), cause a variety of effects within the central [2][3][4][5] and peripheral nervous systems. 6 Sulfide concentrations have been determined by a variety of methods in various sources, such as petroleum products, atmospheric gases, aqueous samples, 7 blood 8 and homogenates of brain, 9 but we have noted a lack of methods for determining sulfide at trace levels as a contaminant of medicaments.…”

Hydrogen Sulfide and the Pathogenesis of Atherosclerosis

“…Disulfide bond rearrangement is essential for platelet function (25). H 2 S is known to reduce disulfide bonds in proteins (9, 10), which makes it a likely candidate to alter platelet activation. Zagli et al (110) showed that 30 μ M NaHS inhibited platelet aggregation in vitro induced by ADP, collagen, epinephrine, arachidonic acid, thromboxane mimetic, U46619 (a synthetic analog of PGH 2 ), and thrombin.…”

Review: Mitochondria and disease progression in multiple sclerosis

“…The terminal complex (cytochrome c oxidase or complex IV) is where over 90% of oxygen is consumed [45]. Complex IV is a target of NO, which is present in active MS lesions and is implicated in conduction block as well as axonal degeneration, and cyanide, a specific complex IV inhibitor, impairs nerve conduction [47–50]. In the case of severe oxidative phosphorylation defects, the ability of mitochondria to handle calcium is impaired [51,52].…”

“…By applying cyanide to sciatic nerves, Beck et al. showed a decrease in compound action potential and conduction velocity, which was partially reversible, as well as a time‐ and concentration‐dependent effect on conduction block [50]. The likely functional consequences of complex IV defects are also shown by the conduction block induced by NO [87].…”

Automated Polarographic Determination of Sulfide as Contaminant in Parenteral Amino Acid Solutions

“…1 Hydrogen sulfide and its toxic precursor salts, sodium sulfide (Na 2 S) and sodium hydrogensulfide (NaHS), cause a variety of effects within the central [2][3][4][5] and peripheral nervous systems. 6 Sulfide concentrations have been determined by a variety of methods in various sources, such as petroleum products, atmospheric gases, aqueous samples, 7 blood 8 and homogenates of brain, 9 but we have noted a lack of methods for determining sulfide at trace levels as a contaminant of medicaments.…”