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Studies:
Recent evidence indicates Down's Syndrome trisomy patients may
overproduce amyloid beta but are also protected from cardiovascular
disease. I think this may be due to the fact that Down's patients also
have an extra copy of the H2S-producing cystathionine beta synthase.
AND H2S is cardioprotective. Turns out, H2S can lower sympathetic tone.
I think this might be a reason the cardiovascular system appears
protected in Down's Syndrome. It's also suspicious that in colitis,
patients can't detox H2S *and* they have impaired sympathetic flow into
the gut.
Neurochem Res. 2009 Mar;34(3):400-6. Epub 2008 Jul 16
*
Effect of hydrogen sulfide on sympathetic neurotransmission and
catecholamine levels in isolated porcine iris-ciliary body.
Kulkarni KH, Monjok EM, Zeyssig R, Kouamou G, Bongmba ON, Opere CA, Njie
YF, Ohia SE.
Department of Pharmacological and Pharmaceutical Sciences, College of
Pharmacy, University of Houston, Houston, TX 77204, USA.
In the present study, we investigated the pharmacological action of
hydrogen sulfide (H2S, using sodium hydrosulfide, NaHS, and/or sodium
sulfide, Na2S as donors) on sympathetic neurotransmission from isolated,
superfused porcine iris-ciliary bodies. We also examined the effect of
H2S on norepinephrine (NE), dopamine and epinephrine concentrations in
isolated porcine anterior uvea. Release of [3H]NE was triggered by
electrical field stimulation and basal catecholamine concentrations was
measured by high performance liquid chromatography (HPLC). Both NaHS and
Na2S caused a concentration-dependent inhibition of electrically evoked
[3H]NE release from porcine iris-ciliary body without affecting basal
[3H]NE efflux. The inhibitory action of H2S donors on NE release was
attenuated by aminooxyacetic acid (AOA) and propargyglycine (PAG),
inhibitors of cystathionine beta-synthase (CBS) and cystathionine
gamma-lyase (CSE), respectively. With the exception of dopamine, NaHS
caused a concentration-dependent reduction in endogenous NE and
epinephrine concentrations in isolated iris-ciliary bodies. We conclude
that H2S can inhibit sympathetic neurotransmission from isolated porcine
anterior uvea, an effect that is dependent, at least in part, on
intramural biosynthesis of this gas. Furthermore, the observed action of
H2S donors on sympathetic transmission may be due to a direct action of
this gas on neurotransmitter pools.
Publication Types:
* In Vitro
PMID: 18629636
The formation of H2S from cyst(e)ine is catalyzed by three enzymes,
cystathionine beta synthase, cystathionase, and 3-mercaptopyruvate
sulfurtransferase. In the liver, kidney, enterocytes and vascular smooth
muscle cells, H2S is principally synthesized by cystathionase. In
contrast, it is synthesized by cystathionine beta synthase in the brain
and partially by 3-mercaptopyruvate sulfurtransferase in cardiac tissue.
H2S is catabolized, essentially in mitochondria by thiosulfate
reductase. The sulfite generated is then oxidized to sulfate by sulfite
oxidase. The amount of thiosulfate excreted in the urine is the best
indicator of H2S biosynthesis, together with sulfhemoglobin
determination in erythrocytes. H2S acts as a neuromodulator in the
brain, increasing responses mediated by NMDA receptors, facilitating the
induction of long-term potentialization in the hippocampus. H2S also
acts as a vasodilator, acting directly on ATP-dependent potassium
channels in vascular smooth muscle cells. The concentration of H2S is
abnormally low in the brains of subjects with Alzheimer's disease, due
to changes in the concentration of the physiological activator of
cystathionine beta synthase. The overproduction of H2S described in
subjects with Down's syndrome probably results from the overproduction
of cystathionine beta synthase, as the gene encoding this protein is
located on chromosome 21 [PMID 15329822]
Recent evidence indicates Down's Syndrome trisomy patients may
overproduce amyloid beta but are also protected from cardiovascular
disease. I think this may be due to the fact that Down's patients also
have an extra copy of the H2S-producing cystathionine beta synthase.
AND H2S is cardioprotective. Turns out, H2S can lower sympathetic tone.
I think this might be a reason the cardiovascular system appears
protected in Down's Syndrome. It's also suspicious that in colitis,
patients can't detox H2S *and* they have impaired sympathetic flow into
the gut.
Neurochem Res. 2009 Mar;34(3):400-6. Epub 2008 Jul 16
*
Effect of hydrogen sulfide on sympathetic neurotransmission and
catecholamine levels in isolated porcine iris-ciliary body.
Kulkarni KH, Monjok EM, Zeyssig R, Kouamou G, Bongmba ON, Opere CA, Njie
YF, Ohia SE.
Department of Pharmacological and Pharmaceutical Sciences, College of
Pharmacy, University of Houston, Houston, TX 77204, USA.
In the present study, we investigated the pharmacological action of
hydrogen sulfide (H2S, using sodium hydrosulfide, NaHS, and/or sodium
sulfide, Na2S as donors) on sympathetic neurotransmission from isolated,
superfused porcine iris-ciliary bodies. We also examined the effect of
H2S on norepinephrine (NE), dopamine and epinephrine concentrations in
isolated porcine anterior uvea. Release of [3H]NE was triggered by
electrical field stimulation and basal catecholamine concentrations was
measured by high performance liquid chromatography (HPLC). Both NaHS and
Na2S caused a concentration-dependent inhibition of electrically evoked
[3H]NE release from porcine iris-ciliary body without affecting basal
[3H]NE efflux. The inhibitory action of H2S donors on NE release was
attenuated by aminooxyacetic acid (AOA) and propargyglycine (PAG),
inhibitors of cystathionine beta-synthase (CBS) and cystathionine
gamma-lyase (CSE), respectively. With the exception of dopamine, NaHS
caused a concentration-dependent reduction in endogenous NE and
epinephrine concentrations in isolated iris-ciliary bodies. We conclude
that H2S can inhibit sympathetic neurotransmission from isolated porcine
anterior uvea, an effect that is dependent, at least in part, on
intramural biosynthesis of this gas. Furthermore, the observed action of
H2S donors on sympathetic transmission may be due to a direct action of
this gas on neurotransmitter pools.
Publication Types:
* In Vitro
PMID: 18629636
The formation of H2S from cyst(e)ine is catalyzed by three enzymes,
cystathionine beta synthase, cystathionase, and 3-mercaptopyruvate
sulfurtransferase. In the liver, kidney, enterocytes and vascular smooth
muscle cells, H2S is principally synthesized by cystathionase. In
contrast, it is synthesized by cystathionine beta synthase in the brain
and partially by 3-mercaptopyruvate sulfurtransferase in cardiac tissue.
H2S is catabolized, essentially in mitochondria by thiosulfate
reductase. The sulfite generated is then oxidized to sulfate by sulfite
oxidase. The amount of thiosulfate excreted in the urine is the best
indicator of H2S biosynthesis, together with sulfhemoglobin
determination in erythrocytes. H2S acts as a neuromodulator in the
brain, increasing responses mediated by NMDA receptors, facilitating the
induction of long-term potentialization in the hippocampus. H2S also
acts as a vasodilator, acting directly on ATP-dependent potassium
channels in vascular smooth muscle cells. The concentration of H2S is
abnormally low in the brains of subjects with Alzheimer's disease, due
to changes in the concentration of the physiological activator of
cystathionine beta synthase. The overproduction of H2S described in
subjects with Down's syndrome probably results from the overproduction
of cystathionine beta synthase, as the gene encoding this protein is
located on chromosome 21 [PMID 15329822]
