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Zoznam článkov

General Physiology and Biophysics


Volume 32, 2013, No. 3

Content:


  Nicotine interferes with purinergic signaling in smooth muscle cells isolated from urinary bladders of patients with lower urinary tract symptoms
Agnes Jenes 1), Gyula Szigeti, Ferenc Ruzsnavszky, Attila Varga, Laszlo Lorincz, Laszlo Csernoch

1)Department of Physiology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary. csl@edu.unideb.hu.


In patients with outlet obstruction, the contraction of the base is reduced compared to that of healthy individuals, while the contraction of the dome is not affected. Here, we investigated the cellular mechanisms that might be responsible for cholinergic effects blocking non-adrenergic non-cholinergic contractions in the base of the urinary bladder. Smooth muscle cells either from the base or from the dome of human urinary bladders were cultured to determine the contribution of cholinergic and purinergic mechanisms to their Ca2+ homeostasis. While ATP evoked Ca2+ transients in all the cells, nicotine and carbachol induced Ca2+ transients only in 56% and 44% of the cells, respectively. When ATP was administered together with nicotine or carbachol, the amplitudes of the Ca2+ transients recorded from cells prepared from the base of bladders were significantly smaller (42 ± 6% with nicotine and 56 ± 9% with carbachol) than those evoked by ATP alone. This inhibition was much less apparent in the dome of bladders. The inhibition between the cholinergic and purinergic signaling pathways reported in this work may decrease the strength of the contraction of the base of the urinary bladder in patients with outlet obstruction during voiding.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 295-302.

 
  Apolipoprotein E genotype may influence urinary gammacarboxyglutamate (Gla) concentrations in young individuals
Alexandra Crăciun 1), Cees Vermeer

1)Department of Biochemistry, University of Medicine and Pharmacy “Iuliu Hatieganu” Cluj-Napoca, Romania. acraciun@umfcluj.ro.


Upon degradation of vitamin K-dependent proteins (known as Gla-proteins) the free aminoacid Gla cannot be re-utilized and is excreted in the urine, where it can be used as an overall marker for vitamin K status. We report the urinary Gla excretion values in first morning void urine for healthy young Romanian subjects from birth, childhood and young adulthood. In these subjects we have evaluated age, gender and apo E genotype as potential confounders. The urinary free Gla/creat ratio (Gla/creat, mg/g) was highest in newborns (34.8 ± 19.5; p < 0.001), than fell in the group 4 to 48 months old (13.1 ± 11.1) to levels that were not significantly different from the young adult group (18.3 ± 5.5). No gender-related differences were observed in Gla/creat in newborns and young children, but Gla excretion in women was higher than in men (28.6%; p < 0.029). Remarkably, Gla excretion in subjects bearing the apo ε2+ allele was significantly lower (11.9 ± 4.2) than in those bearing combinations of the ε3+ and ε4+ alleles (20.3 ± 4.1). The novelty of this study resides in the evaluation of urinary Gla excretion in relation with apo E genotype, suggesting that apo ε2 allele is a risk factor for developing vitamin K insufficiency.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 303-310.

 
  Isoproterenol accelerates apoptosis through the over-expression of the sodium/calcium exchanger in HeLa cells
Sona Hudecova 1), Lubomira Lencesova, Lucia Csaderova, Jan Sedlak, Viera Bohacova, Marcela Laukova, Olga Krizanova

1)Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Bratislava, Slovak Republic.


Apoptosis induction causes over-expression of the Na+/Ca2+ exchanger of type 1 (NCX1) in the HeLa cell line. During induction of apoptosis and in the presence of isoproterenol hydrochloride (I; β-adrenergic agonist), increase in the NCX1 is even more pronounced. Anti-apoptotic Bcl-2 mRNA and protein is markedly reduced during apoptosis and in the presence of I, which causes a rapid increase in the Bax/Bcl-2 ratio. During apoptosis induction by apoptosis inducing kit (A), both with and without I, the active form of caspase-3, which is the executive enzyme in apoptosis, becomes visible on Western blots. Silencing NCX1 resulted in the reversal of the Bax/Bcl-2 ratio, it prevented a decrease in mitochondrial membrane potential compared to the AI group and it decreased the level of AI-induced apoptosis in HeLa cells. Based on the experiments with single apoptotic inducers camptothecin, cycloheximide and dexamethasone, it might be proposed that potentiated apoptotic effect in I-treated cells is due to the inhibition of nuclear topoisomerase. As illustrated in immunofluorescence and Western blot analysis, calnexin increased significantly during induction of the apoptosis in the presence of I. In addition, further decrease in sarco/endoplasmic ATPase 2 (SERCA2), decrease in reticular calcium and mitochondrial membrane potential was observed, which suggests development of the endoplasmic reticulum (ER) stress. Based on these results, we propose that I further enhanced NCX1 expression in apoptotic cells through the development of ER stress.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 311-323.

 
  The guinea pig atrial A1 adenosine receptor reserve for the direct negative inotropic effect of adenosine
Zsuzsanna Kiss 1), Krisztian Pak, Judit Zsuga, Bela Juhasz, Balazs Varga, Andras Szentmiklosi, David Haines, Arpad Tosaki, Rudolf Gesztelyi

1)Department of Pharmacology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.


Although the A1 adenosine receptor (A1 receptor), the main adenosine receptor type in cardiac muscle, is involved in powerful cardioprotective processes such as ischemic preconditioning, the atrial A1 receptor reserve has not yet been quantified for the direct negative inotropic effect of adenosine. In the present study, adenosine concentration-effect (E/c) curves were constructed before and after pretreatment with FSCPX (8-cyclopentyl-N3-[3-(4-(fluorosulfonyl)benzoyloxy)propyl]-N1-propylxanthine), an irreversible A1 receptor antagonist, in isolated guinea pig atria. To prevent the intracellular elimination of the administered adenosine, NBTI (S-(2-hydroxy-5-nitrobenzyl)-6-thioinosine), a nucleoside transport inhibitor, was used. As expected, NBTI alone and FSCPX-pretreatment alone shifted the adenosine E/c curve to the left and right, respectively. However, in the presence of NBTI, FSCPX-pretreatment appeared to increase the maximal response to adenosine. By means of the receptorial responsiveness method (RRM), our recently developed procedure, adenosine E/c curves generated in the presence of NBTI were corrected for the bias caused by the endogenous adenosine accumulated by NBTI. The corrected curves indicate a substantial A1 receptor reserve for the direct negative inotropy evoked by adenosine. In addition, our results suggest that accumulation of an endogenous agonist may bias the E/c curve constructed with the same or similar agonist that can lead to seemingly paradoxical results.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 325-335.

 
  The effect of photodynamic treatment on the morphological and mechanical properties of the HeLa cell line
Petr Kolar 1), Katerina Tomankova, Jakub Malohlava, Jana Zapletalova, Milan Vujtek, Klara Safarova, Dalibor Jancik, Hana Kolarova

1)Department of Medical Biophysics, Faculty of Medicine and Dentistry, Institute of Molecular and Translational Medicine, Palacky University, Hnevotinska 3, 775 15 Olomouc, Czech Republic.


High resolution imaging of biological structures and changes induced by various agents such as drugs and toxins is commonly performed by fluorescence and electron microscopy (EM). Although high-resolution imaging is possible with EM, the requirements for fixation and staining of samples for image contrast severely limits the study of living organisms. Atomic force microscopy (AFM), on the other hand, is capable of simultaneous nanometer spatial resolution and piconewton force detection, allowing detailed study of cell surface morphology and monitoring cytomechanical information. We present a method that images and studies mechanically characterized cells using AFM. We used a HeLa cell line (cervix carcinoma cell), which is sensitive to photodynamic treatment (PDT); growth media as a scanning surrounding; atomic force microscopy NT-MDT Aura for cytomechanical measurement; and scanning electron microscope Hitachi Su 6600 for control images of the cells. The modulus of elasticity for intact and photodynamically damaged cells can indicate mechanical changes to the main properties of cells. Cell elasticity changes can provide information on the degree or value of cell damage, for example after PDT. Measurements were carried out on approximately sixty cells, including three independent experiments on a control group and on sixty cells in a photodamaged group. Cells before PDT show higher elasticity: the median of Young´s modulus on the nucleus was 35.283 kPa and outside of the nucleus 107.442 kPa. After PDT, the median of Young’s modulus on the nucleus was 61.144 kPa and outside of the nucleus was 193.605 kPa.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 337-346.

 
  Epilobium angustifolium extract demonstrates multiple effects on dermal fibroblasts in vitro and skin photo-protection in vivo
Ema Ruszová 1), José Cheel, Stanislav Pávek, Martina Moravcová, Martina Hermannová, Ilona Matějková, Jiřina Spilková, Vladimír Velebný, Lukáš Kubala

1)Contipro Biotech s.r.o., Dolni Dobrouc, Czech Republic. ema.ruszova@fnhk.cz.


Stress-induced fibroblast senescence is thought to contribute to skin aging. Ultraviolet light (UV) radiation is the most potent environmental risk factor in these processes. An Epilobium angustifolium (EA) extract was evaluated for its capacity to reverse the senescent response of normal human dermal fibroblasts (NHDF) in vitro and to exhibit skin photo-protection in vivo. The HPLC-UV-MS analysis of the EA preparation identified three major polyphenol groups: tannins (oenothein B), phenolic acids (gallic and chlorogenic acids) and flavonoids. EA extract increased the cell viability of senescent NHDF induced by serum deprivation. It diminished connective tissue growth factor and fibronectin gene expressions in senescent NHDF. Down-regulation of the UV-induced release of both matrix metalloproteinase-1 and -3 and the tissue inhibitor of matrix metalloproteinases-1 and -2, and also down-regulation of the gene expression of hyaluronidase 2 were observed in repeatedly UV-irradiated NHDF after EA extract treatment. Interestingly, EA extract diminished the down-regulation of sirtuin 1 dampened by UV-irradiation. The application of EA extract using a sub-irritating dose protected skin against UV-induced erythema formation in vivo. In summary, EA extract diminished stress-induced effects on NHDF, particularly on connective tissue growth factor, fibronectin and matrix metalloproteinases. These results collectively suggest that EA extract may possess anti-aging properties and that the EA polyphenols might account for these benefits.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 347-359.

 
  Transintestinal transport mechanisms of 5-aminosalicylic acid (in situ rat intestine perfusion, Caco-2 cells) and Biopharmaceutics Classification System
Libuše Smetanová 1), Věra Štětinová, Dagmar Kholová, Martin Kuneš, Milan Nobilis, Zbyněk Svoboda, Jaroslav Květina

1)Institute of Experimental Biopharmaceutics, Joint Research Centre of the Academy of Sciences of the Czech Republic and PRO.MED.CS Praha a.s., Hradec Králové, Czech Republic. liba.smetanova@seznam.cz.


The aim of the study was 1) to estimate permeability of 5-aminosalicylic acid (5-ASA), 2) to categorize 5-ASA according to BCS (Biopharmaceutics Classification System), and 3) to contribute to determination of 5-ASA transintestinal transport and biotransformation mechanisms. The in situ rat intestine perfusion was used as an initial method to study 5-ASA transport. The amount of 5-ASA (released from tablet) transferred into portal circulation reached 5.79 ± 0.24%. During this transport, the intestinal formation of 5-ASA main metabolite (N-ac-5-ASA) occurred. N-ac-5-ASA was found in perfusate both from intestinal lumen and from v. portae. In in vitro Caco-2 monolayers, transport of 5-ASA (10–1000 µmol/l) was studied in apical-basolateral and basolateral-apical direction (iso-pH 7.4 conditions). The transport of total 5-ASA (parent drug plus intracellularly formed N-ac-5-ASA) was linear with time, concentration- and direction-dependent. Higher basolateral-apical (secretory) transport was mainly caused by higher transport of the metabolite (suggesting metabolite efflux transport). Transport of 5-ASA (only parent drug) was saturable (transepithelial carrier-mediated) at low doses, dominated by passive, paracellular process in higher doses which was confirmed by increased 5-ASA transport using Ca2+-free transport medium. The estimated low 5-ASA permeability and its low solubility enable to classify 5-ASA as BCS class IV.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 361-369.

 
  The effect of probiotic Escherichia coli strain Nissle 1917 lipopolysaccharide on the 5-aminosalicylic acid transepithelial transport across Caco-2 cell monolayers
Věra Štětinová 1), Libuše Smetanová, Dagmar Kholová, Jaroslav Květina, Zbyněk Svoboda, Zdeněk Zídek, Helena Tlaskalová-Hogenová

1)Institute of Experimental Biopharmaceutics, Joint Research Centre of PRO.MED.CS Praha a.s. and the Academy of Sciences of the Czech Republic, Hradec Králové, Czech Republic. stetinovaulmanova@seznam.cz.


The object of this study was to investigate the effect of probiotic Escherichia coli strain Nissle 1917 (EcN) (i) EcN lipopolysaccharide (EcN LPS) and (ii) bacteria-free supernatant of EcN suspension (EcN supernatant) on in vitro transepithelial transport of mesalazine (5-aminosalicylic acid, 5-ASA), the most commonly prescribed anti-inflammatory drug in inflammatory bowel disease (IBD). Effect of co-administered EcN LPS (100 µg/ml) or EcN supernatant (50 µg/ml) on the 5-ASA transport (300 µmol/l) was studied using the Caco-2 monolayer (a human colon carcinoma cell line) as a model of human intestinal absorption. Permeability characteristics for absorptive and secretory transport of parent drug and its intracellularly-formed metabolite were determined. The quantification of 5-ASA and its main metabolite N-acetyl-5-amino-salicylic acid (N-Ac-5-ASA) was performed by high performance liquid chromatography. Obtained results suggest that neither EcN LPS nor EcN supernatant had effect on the total 5-ASA transport (secretory flux greater than absorptive flux) and on the transport of intracellularly formed N-Ac-5-ASA (preferentially transported in the secretory direction). The percent cumulative transport of the total 5-ASA alone or in combination with EcN LPS or EcN supernatant did not exceed 1%.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 371-380.

 
  A miniature microdrive for recording auditory evoked potentials from awake anurans
Haitham Mohammed 1), Nasr Radwan, Wolfgang Walkowiak, Anwar Elsayed

1)Biophysics Department, Faculty of Science, Cairo University, Giza, Egypt. haitham_sharaf@yahoo.com.


Electrical activity recording from the brains of awake animals is a corner stone in the study of the neurophysiological basis of behavior. To meet this need, a microelectrode driver suitable for the animal of interest has to be developed. In the present study a miniature microdrive was developed specifically for the leopard toad, Bufo regularis, however, it can be used for other small animals. The microdrive was designed to meet the following requirements: small size, light weight, simple and easy way of attaching and removing, advancing and withdrawing of microelectrode in the animal brain without rotation, can be reused and made from inexpensive materials. To assess the performance of the developed microdrive, we recorded auditory evoked potentials from different auditory centers in the toad’s brain. The potentials were obtained from mesencephalic, diencephalic and telencephalic auditory sensitive areas in response to simple and complex acoustic stimuli. The synthetic acoustical tones introduced to the toad were carrying the dominant frequencies of their mating calls.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 381-388.

 
  TRPA1 ion channels in vagal afferent nerves contribute to ventilator-induced lung injury in a rat model
Shenhui Wang 1), Pengcai Shi, Yuelan Wang

1)Department of Anesthesiology, Shandong provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong province, 250012, China. wyl2003shr@163.com.


In order to investigate the effects of transient receptor potential channel A1 (TRPA1)-mediated neurogenic inflammatory reaction on the process of ventilator-induced lung injury (VILI). A rat VILI model was created, and the TRPA1 selective antagonist, HC-030031, was used to investigate the role of TRPA1 in the process of VILI. 50 rats were randomly divided into five groups: vehicle group, low tidal volume group, high tidal volume group, low tidal volume group with TRPA1 inhibitor, high tidal volume group with TRPA1 inhibitor. Biochemical index of lung injury in each group were determined, including the W/D ratio, total protein, count of WBC, content of MDA, activities of MPO and SOD, content of IL-8, TNF-α and substance P. Results showed that TRPA1 inhibitor could significantly reduce the inflammatory response and generation of reactive oxygen species, improve SOD activity and inhibit the production of inflammatory factors in lung tissues. TRPA1 was expressed in vagal nerve afferents, and the TRPA1 antagonist significantly inhibited the expression of substance P, indicating the involvement of TRPA1 in neurogenic inflammation. In conclusion, TRPA1 might be involved in the pathophysiological process of VILI by inducing the neurogenic inflammation, and TRPA1 inhibitor could inhibit inflammatory response of VILI.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 389-394.

 
  Increased production of IL-6 and IL-17 in lipopolysaccharide-stimulated peripheral mononuclears from patients with rheumatoid arthritis
Lucia Chovanova 1), Miroslav Vlcek, Katarina Krskova, Adela Penesova, Zofia Radikova, Jozef Rovensky, Dana Cholujova, Jan Sedlak, Richard Imrich

1)Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic.


TLR4-mediated inflammatory responses are important for innate immune functions, thus their alterations may participate in the pathogenesis of rheumatoid arthritis (RA). Cortisol is one of the most potent immunomodulatory hormones involved in control of inflammation. In this study, we analyzed TLR4-mediated responses and cortisol effects on the process in peripheral blood mononuclear cells (PBMC) from RA patients. Lipopolysaccharide-stimulated PBMC from 23 female patients and 15 healthy controls were cultured in the presence or absence of cortisol (1 μM) for 24 h. A panel of 17 inflammatory cytokines was analyzed in the cell culture supernatants. Higher (p < 0.05) concentrations of IL-6, IL-17 and MCP-1 were found in lipopolysaccharide-stimulated PBMC from RA patients compared to controls. After normalization of stimulated cytokine secretion to unstimulated cells, a significantly higher (p < 0.05) IL-6 and G-CSF production was found in RA PBMC. Cortisol induced stronger (p < 0.05) suppression of lipopolysaccharide-stimulated secretion of IL-1β, IL-6, IL-17 and G-CSF in RA group compared to controls. The observed higher production of the key inflammatory cytokines by RA PBMC to lipopolysaccharide stimulation supports involvement of TLR4-mediated processes in RA pathogenesis. The higher sensitivity of LPS-stimulated RA PBMC to immunosuppressive effects of cortisol may reflect adaptive processes to chronic inflammation.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 395-404.

 
  The apoptosis pathway of photodynamic therapy using 9-HpbD-a in AMC-HN3 human head and neck cancer cell line and in vivo
Jin-Chul Ahn 1)

1)Medical Laser Research Center, Dankook University, 29-1, Anseo-dong, Cheonan, Chungnam, Korea. jcahn@dankook.ac.kr.


9-Hydroxypheophorbide-a (9-HpbD-a), a new photosensitizer was extracted from the green alga Spirulina platensis. The anticancer effects of photodynamic therapy (PDT) treatment using 9-HpbD-a against human head and neck cancer cell HN3 and in vivo mice model were investigated. Cells were incubated with 9-HpbD-a for at least 6 hours or more followed by the laser irradiation. Cytotoxicity of 9-HpbD-a against HN3 cell was determined using the MTT assay, propidium iodide and Hoechst 33342 staining and transmission electron microscopy (TEM). To determine the mechanism of cell death, Western blot analysis was performed. The antitumor effect was confirmed in a cancer cell xenograft nude mouse model by photodynamic therapy (PDT) using 9-HpbD-a. For normal control and the 9-HpbD-a only treated group, tumor tissues showed continuous tumor growth (100%). For laser only treated experimental group, 3 treatments showed no remission (75.0%), and was one recurrence (25.0%). Out of 16 tumors in the fourth group of photodynamic treatment, 10 cured (62.5%), 4 recurrence (25.0%), and 2 did not heal (12.5%) were confirmed. PDT using a 9-HpbD-a and 665 nm diode laser showed significant antitumor effects. Thus PDT using 9-HpbD-a can be a useful new treatment method in the treatment of cancer in the future.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 405-413.

 
  Effect of aging on formation of reactive oxygen species by mitochondria of rat heart
Stanislav Kuka 1), Zuzana Tatarkova, Peter Racay, Ján Lehotský, Dušan Dobrota, Peter Kaplan

1)Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University, Martin, Slovak Republic.


Mitochondrial electron transport chain is thought to be a major source of reactive oxygen species (ROS) during aging. However, this view is supported mainly by accumulation of mitochondrial oxidative damage with age and the exact sites of ROS formation remains unknown. In the present study, we measured rate of ROS formation using 2',7'-dichlorofluorescein (DCF) probe in cardiac mitochondria from adult (6-month-old), old (15-month-old) and senescent (26-month-old) rats. In mitochondria oxidizing complex II substrate, succinate, the rate of ROS formation progressively increased with age. In the presence of complex I inhibitor rotenone or complex III inhibitor antimycin A, the rate ROS formation significantly decreased, but even the combination of inhibitors could not fully prevent generation of ROS. Age-dependent increase of ROS formation was accompanied by a loss of thiol groups, tryptophan degradation and increased lipid peroxidation. These data suggest that in addition to complex I and complex II other mitochondrial sites can contribute to accelerated ROS generation and oxidative damage during aging.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 415-420.

 
  Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats
Ibrahim Ibrahim 1), Eman Elbassuoni, Merhan Ragy, Wagdy Habeeb

1)Physiology Department, Minia University School of Medicine, Minia, Egypt. emanelbassuoni@yahoo.com.


Renal ischemia-reperfusion (I/R) is the major cause of acute renal failure. Renal I/R have distant effects on other organs, especially the heart. The purpose of this study was to investigate cardiac lesion following bilateral renal ischemia (50 minutes) and reperfusion (48 hours) in adult rats, to test sex differences in the development of cardiac lesions after acute renal I/R and to investigate the effect of estrogen on this type of cardiac lesions. 70 adult albino rats were divided into 7 groups: control male, I/R male, control female, I/R female, female with bilateral ovariectomy, I/R female with bilateral ovariectomy and I/R female with bilateral ovariectomy treated with estrogen. Renal and cardiac functions in both sexes were deteriorated following acute renal I/R injury proved by the increase in serum urea, creatinine, lactate dehydrogenase and creatine kinase levels. These cardiac lesions are mainly due to the oxidative stress response in the form of the increase in cardiac tissue lipid peroxide, and the decrease in cardiac tissue glutathione reductase, superoxide dismutase and catalase levels. In conclusion, female rats are more protected from the renal and cardiac lesions following acute renal I/R injury than male, since estrogen significantly decreases these lesions mainly by inhibiting the oxidative stress response.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 421-428.

 
  Low molecular thiols, pH and O2 modulate H2S-induced S-nitrosoglutathione decomposition – •NO release
Marian Grman 1), Anton Misak, Claus Jacob, Zuzana Tomaskova, Anna Bertova, Torsten Burkholz, Peter Docolomansky, Ladislav Habala, Karol Ondrias

1)Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, 833 34 Bratislava, Slovak Republic.


We studied the involvement of O2, pH and low molecular thiols in H2S-induced decomposition of S-nitrosoglutathione (GSNO). The GSNO decomposition – •NO release was evaluated by UV-VIS spectroscopy and Griess assay. The H2S donor Na2S was used. O2 slightly increased, but was not necessary for the H2S-induced GSNO decomposition. The rate of GSNO decomposition depended on pH; the maximum rate was observed at pH 7.4–8.0, and this decreased with lowering pH (6.4–4.5) as well as with increasing pH at 9.0–12.0. H2S-induced GSNO decomposition was slowed by the presence of other thiols, such as L-cysteine (Cys), N-acetyl-L-cysteine (NAC) and L-glutathione (GSH), but not in the presence of L-methionine (Met) or oxidized glutathione (GSSG). In sharp contrast, at pH 6.0, H2S-induced GSNO decomposition was negligible, yet the presence of Cys, NAC and GSH induced the H2S-driven GSNO decomposition (whilst Met and GSSG were inactive). In conclusion we postulate an involvement of low molecular thiols and pH in •NO signaling, by modulating the interactions of H2S with nitroso compounds, and hence in part they also appear to control H2S-triggered •NO release. The interaction of H2S and/or its derivatives with the thiol group may be responsible for the observed effects.

General Physiology and Biophysics. Volume 32, 2013, No. 3: 429-441.