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In flor, than de. In fuxico legitimation id kort polisen siku amazon esthetician jobs in. They incubated rat aortic tissue homogenate with a NO donor for 90 min, which significantly increased H2S generation in a concentration-dependent manner. Mammalian CSE protein is made up of 12 cysteines. The specific cysteine residues that interact with NO have not been determined.

Patel et al. CSE can be upregulated by bacterial endotoxin as well as during liver regeneration The apparent repression of CSE as a consequence of human immunodeficiency due to virus infection and the significant upregula-tion of CSE during lactation in rats have also been reported CSE transcription and protein turnover rates are also affected by vitamin B6 availability Testosterone is another endogenous CSE stimulator.

This would also explain testosterone-induced relaxation of rat aortic rings in vitro, which again was inhibited by PPG and BCA. The mechanism for the transcriptional regulation of CSE is not clear, but there is evidence for the involvement of my-eloid zinc finger 1 and specificity protein 1 SP1; also known as Sp1 transcription factor Like many other transcription factors, Sp1 can bind to specific cis-acting sequences of the selective genes to regulate their transcription by assisting RNA polymerase binding.

CSE is one of those Sp1 regulated genes. The mutation of these two sites significantly decreased luciferase reporter gene activity. The binding of Sp1 to the human CSE promoter was increased in differentiated human aorta SMCs compared with that in the proliferative SMCs, unmasked with the chromatin immunoprecipitation assay Knockdown Sp1 expression largely abolished CSE expression MicroRNA miR is an oncogenic miRNA that inhibits apoptosis in various carcinomas and affects cell-cell proliferation and migration.

The overexpression of MiR was abundant in rat carotid arteries after angioplasty and in proliferative human aorta SMCs as well as injured mouse carotid arteries Two miR complementary regions in the human Sp1 3'-UTR and have been identified, and mutation of these two regions abolished the suppressive effect of miR precursor on the luciferase reporter activity of the human Sp1 gene Transfection of human aorta SMCs with miR precursor for 48 h led to a dose-dependent increase in miR expression and simultaneous decrease in CSE and Sp1 protein expressions.

Since Sp1 was not knocked down or inhibited in this study before the mir precursor transfection, a direct effect of miR on CSE expression cannot be excluded yet CSE expression in both yeast and mammals appears to be induced by oxidative stresswhereas transcription of the human CBS gene is clearly repressed by reactive oxygen species. The temporal and spatial expression patterns of CSE differ significantly from those of CBS during embryogenesis through to early neonatal life.

Insulin downregulates the expression of CBS in liver tissues Insulin also has the potential to downregulate the expression of the CSE gene PPG has been used in different cell culture studies at concentrations of 10 mM, and it does not have direct cytotoxic effect at this concentration range on human aortic smooth muscle cells PPG has been used to inject animals. The injection also significantly suppressed H2S production in vascular and ileum tissues Administration of PPG 3.

The level of gastric H2S was increased after ethanol-induced gastric damage, and they were reverted by PPG. The whole treatment lasted for 4 days. PPG reduced renal H2S formation rate and CSE expression and inhibited cisplatin-induced tubulointerstitial lesions in the outer medulla. Increased expression of tumor necrosis factor TNF -a, macrophages, neutrophils, and T lymphocytes, associated with cisplatin treatment, were also reduced by PPG.

The search for true selective inhibitors for CSE has been ongoing for decades, but not much progress can be spotlighted. The relative selective-ness and effectiveness of PPG on CSE activity are largely decided by the concentration range of this agent used PPG may have nonspecific effects at high concentrations on other proteins, such as aspartate aminotransferase and alanine aminotransferase Its molecular weight is BCA blocks H2S synthesis activity in rat liver preparations with.

Tang et al. However, the nonspecific effect of BCA on other molecular targets cannot be excluded. It is soluble in cold water and in alcohol. HA has been used both as a reducing agent and an antioxidant.

It inhibits many heme-containing enzymes. Some non-heme molecular targets are also affected by HA For example, HA may be converted to NO in vivo. In fact, AOA can be better used as a general inhibitor for aminotransferase AOA can also form a carboxymethoxamate by trapping pyruvate to exert different biological functions At 2 mM, AOA completely inhibited the sulfate and thio-sulfate formation from L-cysteine and the sulfate formation from L-cysteinesulfinate in rat liver mitochondrial preparations This suggests the inhibition of CAT.

Methylglyoxal MG inhibits the activity of partially purified rat liver L-glutamine: D-fluctosephosphate aminotransferase ED 2. This MG effect can be reversed by cysteine It was found that, in in vitro enzyme kinetic studies of MST, 3-mercaptopropionic acid acted as a non-competitive inhibitor and 2-mercaptopropionic acid acted as an uncompetitive inhibitor of MST with respect to 3-MP Based on their capability of being cyanide antidotes in vivo, three a-keto acids a-ketobutyrate, a-ketoglutarate, and.

Their IC50 values were between 9. A minor endogenous source of H2S is the nonenzymatic reduction of elemental sulfur to H2S using reducing equivalents obtained from the oxidation of glucose, which has been described in erythrocytes Human erythrocytes produce H2S when provided with elemental sulfur or inorganic polysulfides 43, Increased oxidative stress and hyperglycemia will promote H2S production from this path.

All essential components of this nonenzymatic path are present in vivo, including the supply of reducible sulfur. The presence of millimolar concentration of sulfur in blood circulation has been reported in humans or mice. Sulfide, via nonenzymatic oxidation, yields thiosulfate. The latter can be converted to sulfite by thiosulfate reductase in liver, kidney, or brain tissues or by thiosulfate sulfurtrans-ferase in the liver. H2S can also be released from thiosulfate and persulfides.

Garlic and garlic-derived organic polysulfides induce H2S production in a thiol-dependent manner. A significant amount of exhaled H2S has been measured after intravenous administration of sodium sulfide An increased amount of exhaled H2S has also been reported after inhibition of endogenous NO synthesis.

Given the fact that the endogenous production of H2S can be altered in various pathophysiological conditions, it may be useful to evaluate the possibility of using exhaled H2S as a diagnostic measurement. H2S is also excreted in the urine primarily as sulfate either free sulfate or thiosulfate and in feces and flatus unchanged as free sulfide. Hydrogen sulfide in mitochondria is first oxidized to thio-sulfate and then to sulfite and sulfate To be clear, two molecules of H2S form one molecule of thiosulfate.

Thio-sulfate formation had been previously demonstrated in isolated and perfused rat livers and kidneys Rhodanese is reported as a sul-fide-detoxifying enzyme Between the two isoforms of rhodanese, thiosulfate cyanide sulfurtransferase TST ac. The sulfite that is produced through this reaction is quickly oxidized to sulfate.

Therefore, sulfate ends up being the major end-product of H2S catabolism under physiological conditions, which is also the reason why urinary thiosulfate is determined by many to be a nonspecific marker of entire-body H2S production.

In the cecal mucosa and liver homogenates of Sprague-Dawley rats, H2S is metabolized to thiosulfate and sulfate The oxidation of H2S to thiosulfate in the rat liver is under the impact of heme compounds, metal-protein complexes, and ferritin The conversion of H2S to sulfate has been observed for a long time The rate and the extent of sulfide oxidation were seen to be variable from one organ to another. Methylation is another catabolic pathway for H2S.

While the oxidation of H2S occurs mainly in mitochondria, meth-ylation mainly takes place in the cytosol. Interestingly, meth-anethiol is also a colorless gas with a smell like rotten cabbage. Methanethiol can be further methylated, although much more slowly, to dimethylsulfide CH3SCH3a relatively nontoxic compound. H2S has been reported to be methylated to methanethiol in vitro by the intestinal mucosa of Sprague-Dawley rats TSMT is a ubiquitous enzyme with the highest activity in the colonic and cecal mucosabut its activity has also been reported in the liver, lung, and kidney.

Compared with sulfide oxidation, sulfide methylation is slow. In one study, it was shown that sulfide methylyation is — 10, times slower than the oxidation rate of H2S in colonic mucosa The half-life of NO in blood is counted in seconds, and it can be scavenged by oxyhemoglobin H2S seems to be more stable in protein-free solution. However, H2S can also be scavenged by methemoglobin to form sulfhemoglobin. Therefore, the half-life of free H2S in blood may also be short. Decreased H2S production in CSE-overexpressed cells by methemoglobin also provided evidence that methemoglobin scavenged the endogenous H2S.

Since hemoglobin can scavenge NO, CO. H2S can also be scavenged by metallo- or disulfide-contain-ing molecules such as horseradish peroxidise, catalase, and oxidized glutathione 39, The reports on the effects of H2S on heart rates have been inconsistent.

Some studies claimed a negative chronotropic effect of H2S due to the inhibition of pacemaker cells in SA nodes. Xu et al. On the other hand, administration of H2S intravenously at 2. Administration of PPG to inhibit endogenous H2S production also did not alter it action potentials in the pacemaker cells of rabbits It is possible that at low concentration H2S would not have significant chronotropic effect.

On this note, some earlier studies using H2S at toxic levels indeed show the impact of H2S on heart rate. Acute exposure of rabbits to ppm of NaHS for 1.

Kohno et al. In contrast, another study found an increase in heart rates in rats exposed to ppm H2S for 1 h It should also be attended that baroreflex is quite different between humans and other mammals, which has to be. A negative inotropic effect means the decreased contract force or the required energy of muscular contractions, which is beneficial for lowering cardiac work load in conditions such as angina.

Not all studies support a negative inotropic effect of H2S. Surprisingly, both the negative and positive inotropic effects of NO and iso-proterenol were reversed by NaHS The inhibition of cAMP pathway by H2S was believed to be responsible for the reversal of the isoproterenol effect Increased intracellular calcium level by NaHS after it was first lowered by NO was accounted for as the molecular mechanism for the neutralization of the contractility in the presence of both H2S and NO The physiological meaning of this intriguing role of NaHS in counteracting both positive and negative inotropic influences in the heart is not clear.

The extrapolation of these observations from the isolated cardiomyocytes in vitro to the contractile dynamics of the heart in vivo under more physiological conditions should be carefully evaluated. This is consistent with the negative inotropic effects of other KATP channel activators, which induce cell membrane hyperpolarization.

NaHS-in-duced cardiac protection effect was also suppressed by 5-hydroxydecanoate 5-HD KATP activation can result in the closing of L-type calcium channels, reducing calcium entry, and inhibiting muscule contractility As the first identified gasotransmitter, NO relaxes smooth muscle of various vasculatures. Substances other than NO, including low-molecular-weight S-nitrosothiol intermediates, also contribute to the relaxation of smooth muscle CO has been found to dilate different vascular. H2S-induced vasorelaxation has been demonstrated in numerous types of blood vessels such as aorta, portal vein, mesenteric artery, cerebral arteries, and vas deferens from different species such as rats, mice, cows, guinea pigs, sheep, and humans.

The EC50 of H2S in inducing vasore-laxation is quite close to the reported endogenous level of H2S in plasma, which suggests that under physiological in vivo conditions the vascular tone of resistance arteries is likely regulated by endogenous H2S.

In addition, low concentrations of H2S enhance smooth muscle relaxation induced by NO in the helical tissue strips of the thoracic aorta Teague et al. The enhancing effect of H2S on NO-induced vasorelaxation is still controversial. Ali et al. It is likely that the interaction of NO and H2S may alter the vasorelaxant properties of these two gasotransmitters. Also, the common molecular target for NO and H2S may become desensitized after firstly encountering one of them.

The production of H2S in the presence of NO is a different story. CSE contains 12 cysteine residues that are potential targets for S-nitrosylation.

S-nitrosylation of CSE has the potential to increase the enzymatic activities The vasorelaxant effects of H2S-gassed solution or NaHS solution have been studied on preconstricted vascular tissues. The potency of vasorelaxant effect of H2S is affected by the preparations of H2S At the same concentration level, H2S-gassed solution has much stronger vasore-laxant effects than NaHS solution does. The stimulus used to precontract vascular tissues also significantly affects the effect of H2S.

Finally, different vascular tissues manifest different sensitivities to H2S. H2S relaxes small mesenteric arteries much more potent than aortic tissues Although rat aortic and mesenteric artery tissues produce similar levels of H2S, H2S is nearly sixfold more potent in relaxing rat mesenteric artery beds than relaxing rat aortic tissues. The higher sensitivity of mesenteric arteries to H2S speaks for the importance of H2S in regulating peripheral resistance.

The mechanisms for differential vasorelax-ant effects of H2S are not clear yet, but several possibilities. One explanation is the tissue-type specific distribution of the molecular targets of H2S. For example, the expression of KATP channels possibly differs in various vascular tissues with different isoforms. The second explanation is that sensitivities of contractile proteins to H2S and to intracellular calcium level may vary between conduit and resistant arteries Also, different types of blood vessels face different sheer stress levels, possess different cellular components smooth muscle cells, endothelial cells, and connective tissues, etc.

Finally, oxygen-dependent sensitivity of blood vessels to H2S should also be considered. It has been reported that H2S induced vasorelaxation at physiological O2 levels, and this vasorelaxation occurred much faster at below physiological O2 levels. With higher than physiological O2 levels, H2S has the tendency to induce vasoconstriction This could result from the product of H2S oxidation, which may mediate vasoconstriction.

Blood in small peripheral vessels has lower oxygen partial pressure, and these small vessels consume oxygen at higher rate due to the high content of smooth muscle cells and low collagen. The situation is just opposite in large conduit arteries. The difference in tissue oxygen level may explain different vascular effects of H2S. Another note worth taking is that the release of NO from S-nitrosoglutathione by H2S is oxygen dependent H2S functions as a vasodilator in cerebral circulation. Topical application of H2S to the newborn pigs induces dilation of pial arterioles Leffler et al.

Second, CSE proteins were detected in cerebral microvessels. While CBS proteins were detected in brain parenchyma, it was not detectable in cerebral microvessels. Whether this vasodilatory effect of H2S is unique to newborn animal or ubiquitous to cerebral circulation at other stages of development is not known.

The involvement of various signal transduction pathways in the vascular effects of H2S has been examined. H2S does not affect the production of cGMP, which leads to the inference that there is a different mechanism for the effect of H2S. Earlier studies also demonstrated that the vasorelaxant effects of H2S on rat vascular tissues are unlikely mediated by prostaglandin, protein kinase C, or cAMP pathways, Superoxide dismutase and catalase in the bath solution also did not alter the vasorelaxant effect of H2S, indicating that.

Therefore, under this experimental condition, the vasore-laxant effect of H2S was not mediated by the cGMP pathway KATP channel is the major molecular target of H2S for its vasorelaxant effect and smooth muscle hyperpolarization In the ileum, gliben-clamide did not interfere with the relaxation induced by H2S This finding may be seen as different membrane excitation-contraction coupling mechanisms in different muscle preparations.

In effect, though H2S inhibits KCl 20 mM -induced contractions of aortic tissues, it does not change the contraction of ileum induced by the same concentration of KCl The proliferation of vascular SMCs plays a critical role in the maintenance of vascular structure and functions, and its alteration leads to vascular remodeling and various prolif-erative vascular diseases.

However, cellular and molecular mechanisms that regulate SMC proliferation and differentiation are not fully understood.

H2S is an important endogenous modulator of cell proliferation and apoptosis The endogenous level of H2S affects the effect of exogenous H2S on cell apoptosis. Another study reported that exogenously applied. Treatment of the rats with NaHS significantly weakened balloon injury-induced neointimal hyperplasia and reduced vascular smooth muscle cell proliferation in the lesions in vivo. Similar observations were made in the mouse where carotid artery ligation resulted in enhanced neointima formation and downregulation of CSE expression The phos-phorylation of ERK transduces the apoptotic signal to its downstream enzyme cascades and eventually activates caspase Therefore, the activation ofERK and its downstream factor caspase-3 likely mediates H2S-induced cell apoptosis Whether activation of ERK could reverse NaHS-induced proliferation inhibition was not conducted by the same researchers The pro-apoptotic effect of H2S may also be related to the cell cycle due to the stimulation o f cyclin-dependent ki-nases.

S-diclofenac induces a dose-dependent decrease in the survival of primary and immortalized rat aortic vascular SMCs. The cells in G1 phase were not affected by S-diclofe-nac but asynchronized SMCs manifested with an increase in apoptotic cell death. S-diclofenac stabilized p53 and induced p21, p53AlP1, and Bax. But the anti-apoptotic factor Bcl-2 was not affected The same physiological stimuli do not necessarily elicit the same functional responses from different types of cells.

While H2S inhibits vascular SMC proliferation, the gaso-transmitter stimulates Der Sexyschneider - Various - Die Schleifer Von Paris (Cassette) proliferation and migration of vascular endothelial cells either in culture or in the whole blood vessel walls. It should be noticed that the pro-proliferative effect of H2S donors on ECs could not be detected if the concentrations of H2S donors were higher than physiologically relevant levels. The signaling pathways underlying the stimulatory effect of H2S on EC proliferation are complex and inconclusive.

H2S also protects ECs from different stress damages. This hyperglyce-mia stress results in impaired endothelium-dependent vas-orelaxation. In cultured microvascular ECs, the hypergly-cemia-induced EC damage was suppressed by supplementation of exogenous H2S to the culture media. Extending their observations from cultured endothelial cells, Suzuki et al. This in vitro transfec-tion reserved the endothelium-dependent vasorelaxant properties of the vascular rings in the presence of hypergly-cemia The isolated thoracic aorta rings from CSE KO mice were manifested with much more severely damaged endothelium-dependent relaxations than that from WT mice when incubated with the same hyperglycemic conditions in vitro An earlier study claimed that the relaxation of rat aortic tissues induced by NaHS was not altered by the removal of the endothelium Unfortunately, the concentrations of NaHS used to study the endothelium-dependent vasore-laxation were not specified in this study.

The expression of CSE protein was shown in endothelial layer of mouse vascular tissues The activation of muscarinic cholinergic receptor increases intracellular calcium level in endothelial cells, and the calcium-calmodulin complex activates CSE and produces H2S. Several lines of evidence support this conclusion.

Another potential source of endothelium-generated H2S is MST and CAT-catalyzed reactions, the two enzymes being located in aorta endothelium and using cysteine and a-ke. Once released from the en-dothelium, H2S relaxes beneath the vascular smooth muscles This mode of action of H2S is very familiar to that of NO. Considering that eliminating or limiting nitric oxide synthase NOS activity in various vascular beds does not completely remove endothelium-dependent vasorelax-ation, additional EDRF must fill the gap.

Future studies are expected to examine NO-mediated endothelium-dependent relaxation of large arteries from CSE knockout mice so that the relative contribution of NO and H2S to endothelium-dependent vasorelax-ation can be deciphered.

The vasore-laxant effect of EDHF is mainly mediated by small-conductance KCa channels and aided by intermediate-conductance KCa channels, which can be blocked by the coapplication of apamin and charybdotoxin. It is still up for debate as to whether EDHF is a diffusible EDRF or a simple electronic phenomenon that relays membrane potential change in endothelium to the underneath SMCs through low-electrical resistance myoendothelial gap junctions The coapplication of apamin 50 nM and charybdotoxin 50 nM significantly weakened H2S-induced relaxation of en-dothelium-intact rat aortic tissues The endothelium-dependent vasorelaxing effect of H2S becomes even more significant in small resistance arteries, such as isolated and perfused rat mesenteric artery bed MAB.

The removal of endothelium significantly reduced the H2S-induced dilation of MAB by approximately sevenfold. The smaller the size of the arteries such as mesenteric and coronary arteriesthe greater the contribution of EDHF to the endothelium-dependent vasorelaxation As such, EDHF would play a minor role in regulating the tone of conduit arteries, but a major role the coronary, mesenteric, and carotid arteries.

H2S also exerts a long-term effect on the proliferation of vascular endothelial cells as aforementioned. H2S might be released from vascular SMCs and then stimulate endothelium of small peripheral resistant arteries.

This hypothesis still waits to be ratified. The latter is the target of EDHF. Activation of these two types of channels by H2S jointly hyperpolarizes smooth muscle cells, leading to vasorelaxation. Mustafa et al.

Compared with the mesenteric artery tissues from WT mice, the same tissues from CSE KO mice had much lower hyperpolarization response to acetylcholine stimulation. Direct application of NaHS to the culture medium also hyperpolarized the cultured human aortic endothelial cells. Furthermore, H2S induced S-sulfhydration of Kir6. It is suggested that these ion channel sulfhydration could be the molecular mechanism underlying H2S-induced vascular hyperpolar-ization.

Although promising, the role of H2S as an EDHF cannot be firmly determined without several critical lines of evidence. H2O2 has been argued to be. H2S has significant effect on H2O2 metabolism. Whether the endothelium-depen-dent vasorelaxant effect of H2S is mediated by altered H2O2 production or altered redox status in endothelial cells is still not clear.

Some studies have addressed the action of H2S on nonmam-malian vertebrates, and phylogenetic surveys of H2S responses among the nonmammalian vertebrates have been provided, These studies demonstrated that nonmammalian vertebrates exhibit complex patterns of vascular responses to H2S, ranging from relaxation to constriction to triphasic response This complexity is linked to the blood oxygen level, the unique relationship of H2S with other gasotransmitters, and a wide spectrum of signaling pathways involved from KATP channels to calcium homeostasis in these animals The shared profiles of endogenous production of H2S and various vasoac-tive reactions to H2S between mammalian and nonmammalian vascular system further speak of an ancestral gasotrans-mitter role of H2S in cardiovascular system.

There has been little information about potential signaling actions of H2S in invertebrate tissues. Urechis caupo Echiuridae is a large 60 g or more marine echiuran worm found along the California coast. NaHS at 0. SNP at 0. H2S at 0. NaHS alone had no effect on the contractility of brachial muscles of the clam M.

This is similar to the action of NO on 5-hydroxytrypta-mine-induced contractions of the same muscle. These studies, although limited in the number of invertebrate species or tissue types, nevertheless indicate that H2S may act as an endogenous signaling transmitter in invertebrates, and that H2S, whether by itself or in combination with other signaling molecules, has the capacity to stimulate muscle contraction, rather than H2S-induced muscle relaxation in mammals.

It is also important to note that both U. Whether other invertebrates respond in a similar way to endogenous H2S as these sulfide-adapted invertebrates remains to be seen.

In mammalian central nervous system CNSCBS was found highly expressed in the hippocampus and the cerebellum CBS is mainly localised to astrocytesand microglial cells Immunohistological study showed that CBS is expressed both in brain neurons and astrocytes Additionally, in the adult brain CBS is highly expressed in some neurons, such as Purkinje cell neurons and hippocampal neurons H2S exerts multifaceted and important effects in CNS through modulation of neurotransmission and neuromodulation.

Glutamate is an important excitatory amino acid that functions as a neurotransmitter. Glutamate in mammalian brain is best known for its role in learning and memory, such as induction of long-term potentiated potential LTP and perception of pain. Abnormal glutamate metabolism can lead to excitatory neuronal injury. The neurological effects of glutamate are mediated by N-methyl-D-aspar-tate NMDA receptors in both central and peripheral nervous systems, with exceptions in the bone and pancreatic islet On the other hand, high concentration of H2S would damage brain and lead to decreased learning and memory function.

The acquisition of a new spatial task by the animals was largely not affected by H2S daily treatment. However, these animals showed impaired ability in finding all of the reinforcers prior to the end of a trial. Moreover, a new reversed contingency maze task demonstrated that H2S-treated animals made more overall arm entries than controls with a arm radial arm maze, showing an impaired learning ability.

H2S-in-duced increase in cAMP production and activation of PKA had also been previously reported in primary cultures of brain cellsas well as neuronal and glial cell lines. Garcia-Bereguiain et al. Considering the concentrations of NaHS and its application frequency, the increased glutamate release and cell death may reflect a toxi-cological situation The interaction of H2S and NMDA receptors has the potential to affect other neuronal activities, such as epilepsy, neuropathic pain, stroke, and Parkinson's diseases.

Prolonged activation of NMDA receptors causes calcium overload in cells and eventually leads to cell death. NMDA receptors have important roles in conditions such as stroke, neuropathic pain, epilepsy, and Parkinson's disease Deficiency in GABAergic inhibition leads to febrile seizures and neuronal hyperexcitability H2S has been shown.

Glial cells possess neurotransmitter receptors and respond to transmitters Reciprocal interactions between neurons and glia coordinate neuronal functions. It has been proposed that the reciprocal interactions between neurons and astrocytes are mediated by H2S, resulting in the regulation of synaptic activity. As-trocytes, a type of glia, respond to a neurotransmitter released from neurons.

This effect of NaHS was mimicked by neuronal excitation. The effects of H2S on catecholaminergic and amino acid neurotransmission have been noticed.

Sublethal or lethal concentrations of H2S inhibit monoamine oxidase and result in an increase in norepinephrine NE and epinephrine contents in the hippocampus, striatum, Der Sexyschneider - Various - Die Schleifer Von Paris (Cassette) brain stem, but not in the cortex and cerebellum Kulkarni et al.

It is not clear how the decreased endogenous H2S level would inhibit the effects of exogenous H2S. Some insights on the role of H2S in catecholamine metabolism have been revealed in rainbow trout chromaffin cells.

H2S increased intracellular calcium in cultured cerebellar granule. Chronic exposure to low concentrations of H2S increases serotonin and NE concentrations in the cerebellum and frontal cortex of neonatal rats In recent years, evidence for the role of H2S in the regulation of hypothalamo-pituitary system has been obtained.

KCl-evoked release of corticotrophin-releasing hormone CRH from rat hypothalamic explants was inhibited by NaHS in a concentration-dependent manner Suppression of oxidative stress is another action H2S takes in the brain. H2S inhibited HOCl-mediated inactivation of a1-antiproteinase and protein oxidation, HOCl-induced cytotoxicity, intracellular protein oxidation, and lipid per-oxidation H2S also protects brain endothelial cells against methionine-induced oxidative stress Both pronociceptive and antinociceptive effects of H2S have been reported.

The use of different preclinical models of pain may also cause the inconsistence of H2S effects. In a rat model of visceral pain induced by colorectal distension, H2S induced antinociceptive effect on the perception of painful sensation The administration routes of H2S would be another explanation for different roles of H2S in pain control.

Intraco-lonic application of NaHS increased visceral nociceptive behavior in mice that was accompanied by referred abdominal hyperalgesia and allodynia However, visceral sensitivity was not affected when NaHS was delivered in-traperitoneally rather than into the colon. Endogenous H2S plays a pro-nociceptive. This conclusion is based on two lines of evidence. Neutrophil recruitment to the plantar tissue was also prevented by PPG treatment.

PPG also had no effect on hypernociception induced by PGE2, a directly acting hypernociceptive mediator. Quite opposite to a pro-nociceptive role of endogenous H2S, exogenous NaHS plays an antinociceptive role once administered to the mice systemically by inhibiting both LPS- and PGE2-induced mechanical hypernociception. In this regard, exogenous H2S functions as a direct hyperno-ciceptive factor with its target on nociceptive neurons.

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