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PubMed1997

Measurement of upregulation of inducible nitric oxide synthase in the experimental autoimmune encephalomyelitis model using a positron emitting radiopharmaceutical.

Excess nitric oxide has been implicated in the pathogenosis of experimental autoimmune encephalomyelitis (EAE) which is an animal model for multiple sclerosis. Positron emission tomography (PET) is an imaging technique that has shown utility for studying enzyme systems in vivo. A positron-labeled inducible nitric oxide synthetase (iNOS) inhibitor has been studied in EAE-affected mice as well as controls. Greater uptake of the radiolabeled inhibitor was observed in the spinal cord of the affected mice than of control mice. Increased uptake was also observed in other organs not previously implicated in this experimental model. The increased uptake of the radiopharmaceutical in this model suggests that this tracer may have the potential for measuring increased levels of iNOS in humans by PET.

Animals↗
PubMed1998

Certain S-substituted isothioureas not only inhibit NO synthase catalytic activity but also decrease translation and stability of inducible NO synthase protein.

In an attempt to identify potent inhibitors of inducible (type II) NO synthase (iNOS) for use in cell culture systems, we found that two S-substituted isothioureas were very potent in cell culture but one such compound also interfered with the induction of NO synthase. S-Ethylisothiourea (EITU) and S-aminoethylisothiourea (AEITU) were found to be much more potent than NG-methylarginine, NG-nitroarginine methy lester, or aminoguanidine as inhibitors of NO production by cultured RAW 264.7 cell macrophages activated by lipopolysaccharide (LPS). The approximate EC50 values as inhibitors of NO production, assessed by 24-h accumulation in cell culture media, were 10 microM (EITU), 30 microM (AEITU), 300 microM (NG-methylarginine), and 1000 microM (aminoguanidine). EITU was found to inhibit NO production by activated macrophages without interfering with the induction of iNOS. More specifically, EITU failed to influence transcription of iNOS mRNA (Northern blot analysis), translation of iNOS protein (pulse experiments), or degradation of translated iNOS protein (pulse-chase experiments). In contrast, however, AEITU interfered markedly with the induction of iNOS by mechanisms attributed to inhibition of translation of iNOS mRNA into functional protein as well as acceleration of degradation of already translated iNOS protein. These observations indicate that AEITU should not be used in cell culture experiments where the intent is solely to assess the consequences of inhibition of iNOS catalytic activity.

Animals↗
PubMed2000

Effects of inducible nitric oxide synthase inhibition on cerebral edema in severe hypertension.

In order to clarify the causative role of cytotoxic nitric oxide (NO) in hypertensive cerebral injury, the effects of inducible nitric oxide synthase (iNOS) inhibition on leukocytes and endothelial function were examined using stroke-prone spontaneously hypertensive rats (SHRSP). For the iNOS inhibition, S-methylisothiourea (SMT) was administered to 12-week-old male SHRSP for 3 weeks. Immunohistochemical examination were carried out for the expression of intercellular adhesion molecule-1 (ICAM-1), glucose transporter-1 (GLUT-1), fibrinogen and glial fibrillary acidic protein (GFAP) in cerebral cortex. The effects of iNOS inhibition was also examined for Mac-1 expression by flow cytometric analysis. Plasma NO metabolites level was significantly lower in the SMT group than in the control group. Mac-1 expression was inhibited by SMT. In the SMT group, brain weight was significantly lower than in the control. By SMT administration, ICAM-1 expression was suppressed, GLUT-1 was enhanced, fibrinogen was decreased and GFAP was decreased as compared to those in control group. In hypertensive cerebral injury in SHRSP, iNOS-derived NO, mainly in activated leukocytes, could be an important causative factor for endothelial injury.

Animals↗
PubMedDate not supplied

Myocardial infarction and nitric oxide.

The report deals with the induction of the inducible form of nitric oxide synthase (iNOS) in infarcted heart muscle of rabbit and man. In the rabbit, nitric oxide synthase was significantly increased in the infarcted area beginning on the third day following ligation of a coronary artery. iNOS induction occurred primarily in macrophages. In man, iNOS immunoreactivity was also primarily localized in macrophages on the seventh day following death from myocardial infarction. Of the specific inhibitors of iNOS in infarcted heart muscle, S-methylisothiourea (SMT) was the most potent. Its greatest effect occurred in the normal non-affected area of the heart. Dexamethasone and cyclosporin A failed to inhibit iNOS. Apoptosis of macrophages commenced two days following ligation of a coronary artery.

Animals↗
PubMed1997

Influence of different classes of NO synthase inhibitors in the pig gastric fundus.

The inhibitory potency of different classes of nitric oxide synthase (NOS) inhibitors (amino acid-based substances, guanidines, isothioureas, imidazoles and indazoles) versus peripheral neuronal NOS in the pig gastric fundus was investigated by studying their influence on electrically induced relaxations in non-adrenergic noncholinergic conditions. Circular muscle strips were mounted for isotonic registration in the presence of atropine and guanethidine, and tone was raised with 5-hydroxytryptamine. Electrical field stimulation (40 V, 0.1 ms, 4 Hz, 10 s) induced short-lasting relaxations. The inhibitory effect of 1-phenylimidazole could not be evaluated because it nearly abolished the 5-hydroxytryptamine-induced tone of the tissues. 7-Nitroindazole, imidazole, 2-iminobiotin and aminoguanidine did not inhibit the electrically induced relaxations, while the other 9 substances tested were able to do so. The influence of the incubation period was tested by studying the inhibitory effect after incubation for 10 up to 60 min. For N(G)-nitro-L-arginine methyl ester (L-NAME), N(G)-nitro-L-arginine (L-NNA), L-N5-(1-iminoethyl)-ornithine (L-NIO), L-N6-(1-iminoethyl)-lysine (L-NIL), S-methyl-L-thiocitrulline and S-isopropyl isothiourea there was a moderate increase in the inhibitory effect up to 30 min of incubation so that they were incubated for 30 min to study their inhibitory potency. For L-thiocitrulline, S-methyl isothiourea and S-ethyl isothiourea, an incubation period of 60 min was used. The 9 substances concentration-dependently inhibited the electrically induced relaxations with a maximal inhibitory effect of approximately 80% except for S-methyl isothiourea (Emax of 53%). The overall order of potency was: S-isopropyl isothiourea > S-ethyl isothiourea > or = S-methylL-thiocitrulline > or = L-NNA > L-NIO > L-NAME > S-methyl isothiourea > L-thiocitrulline > L-NIL. While the potency for S-isopropyl isothiourea (EC50: 3.1 x 10(-5) M, n = 6) to S-methyl isothiourea (EC50: 11.5 x 10(-5) M, n = 5) was in the same range, the potency of L-thiocitrulline and L-NIL was clearly lower. This study showed several compounds to be potent inhibitors of peripheral neuronal NOS in the pig gastric fundus while some compounds, that were reported to inhibit brain neuronal NOS were not effective. The EC50 values found for the effective substrates in this functional study may be a guideline for the concentrations required to evaluate the role of NO in NANC neurotransmission in gastrointestinal smooth muscle preparations.

Animals↗
PubMed1999

High blood levels of nitric oxide in rats subjected to prolonged respiratory arrest and their modulation during adrenocorticotropin-induced resuscitation.

Anaesthetized rats, endotracheally intubated and mechanically ventilated with room air, were subjected to a 5-min period of asphyxia by turning off the ventilator. The ventilator was then turned back on and, simultaneously, the animals were treated with either the adrenocorticotropin fragment 1-24 [ACTH-(1-24), 160 microg/kg in a volume of 1 ml/kg i.v.] or an equivalent volume of saline. Nitric oxide (NO)-haemoglobin formation was detected ex vivo in arterial blood by electron spin resonance spectrometry; arterial blood pressure, electrocardiogram (ECG) and electroencephalogram (EEG) were monitored for a 60-min observation period, or until prior death. During asphyxia, there was massive formation of NO (red cell concentrations 40-80 microM), associated with a dramatic fall in mean arterial pressure and pulse pressure, marked bradycardia and ECG signs of ischaemic damage, as well as an isoelectric EEG. Treatment with ACTH-(1-24) produced a prompt (within 15 min) and long-lasting drop in NO blood levels, associated with an almost immediate (within 1 min) restoration of cardiovascular function and with a more gradual recovery of EEG, which became normal after 3040 min; all parameters remained stable throughout the 60-min observation period. In saline-treated rats, on the other hand, there was a further increase in NO blood levels, as detected 3 min after treatment, and all died within 5-8 min. Moreover, pretreatment and treatment with S-methylisothiourea sulphate (SMT, 3 mg/kg i.v.), a relatively specific inhibitor of inducible NO synthase, inhibited NO formation, but did not affect the mortality rate (100% within 5-8 min). The present results provide the first evidence that prolonged asphyxia is associated with high blood concentrations of NO, and that the life-saving effect of melanocortin peptides in severe hypoxic conditions is associated with a complete normalization of NO blood levels. However, the lack of SMT protection in this experimental model seems to rule out the possibility that the ACTH-(1-24)-induced resuscitation is due to an effect on NO overproduction.

Adrenocorticotropic Hormone↗
PubMed2000

S-Methylisothiourea sulfate improves renal, but not hepatic dysfunction in canine endotoxic shock model.

OBJECTIVE: Excess production of nitric oxide (NO) by inducible NO synthase (iNOS) has been implicated in the pathophysiology of septic shock. This study was designed to see whether S-methylisothiourea sulfate (SMT), a selective inhibitor for iNOS, prevents cardiovascular changes and multiple organ damage in the canine endotoxic shock model. DESIGN: Prospective, comparable, experimental study. SETTING: Laboratory at a university hospital. SUBJECTS: Twenty male mongrel dogs were studied under pentobarbital anesthesia. INTERVENTIONS: Dogs were divided into three groups: bacterial lipopolysaccharide (LPS) group (n = 7) receiving continuous infusion of LPS (2 mg/kg/h for 1 h); LPS plus SMT group (n = 7) receiving LPS and SMT (1 mg/kg, bolus i. v., followed by continuous infusion of 1 mg/kg/h for 1 h); and vehicle plus SMT group (n = 6). MEASUREMENTS AND RESULTS: Hemodynamics, blood gas parameters, and urine output were measured during 6 h observation periods. Serum levels of lactate, transaminases, and bilirubin were measured at baseline, 1 and 6 h. Creatinine and free water clearance, urine sodium excretion and fractional excretion of sodium were calculated. LPS caused a profound hypotension associated with decreases in cardiac output and oxygen delivery, lactic acidosis, renal and liver dysfunction, and thrombocytopenia. SMT prevented the LPS-induced hypotension and renal dysfunction, whereas it did not affect the LPS-induced decreases in cardiac output or oxygen delivery, hyperlactatemia, liver dysfunction, or thrombocytopenia. SMT alone had no appreciable effects on hemodynamics, blood gases, liver or renal functions. CONCLUSIONS: These findings show that SMT improves renal, but not hepatic dysfunction, in dogs with endotoxic shock, suggesting that iNOS-derived NO plays differential roles in sepsis-associated multiple organ dysfunction.

Animals↗
PubMed2000

Characterization of histamine H3 receptors in mouse brain using the H3 antagonist [125I]iodophenpropit.

We have characterized the binding of the histamine H3 receptor antagonist [125I]iodophenpropit to mouse brain. [125I]Iodophenpropit saturably bound to mouse brain membranes with a pKd-value of 9.31+/-0.04 nM and a receptor binding density of 290+/-8 fmol per mg protein. Saturation binding analysis revealed binding of [125I]iodophenpropit to a single class of sites, showing linear Scatchard plots and Hill coefficients not different from unity (nH=0.98+/-0.02). At a concentration of 0.25 nM [125I]iodophenpropit, specific binding represented about 75% of the total binding. Competition binding curves for H3 receptor antagonists were fitted best to a one-site model, showing pKi-values in general accordance with the pA2-values obtained in mouse cerebral cortex. Displacement of [125I]iodophenpropit by the H3 receptor agonists (R)-alpha-methylhistamine, immepip, imetit and histamine were fitted best to a two-site model. Competition binding curves of (R)-alpha-methylhistamine showed a rightward shift upon incubation with GTPgammaS (10 microM), indicating the involvement of G-proteins in H3 agonist binding. In contrast, competition binding curves of the antagonists iodophenpropit, thioperamide and burimamide were not affected by GTPgammaS (10 microM). Autoradiographic experiments showed that [125I]iodophenpropit binding sites were heterogeneously distributed, similarly to the distribution of histamine H3 receptors reported in rat brain. Highest densities were observed in the cerebral cortex, the striatum, the nucleus accumbens, the globus pallidus and the substantia nigra. In conclusion, we have demonstrated that in mouse brain, [125I]iodophenpropit selectively binds to histamine H3 receptors. We also observed that the mouse brain H3 receptors labelled by [125I]iodophenpropit displayed binding characteristics and a distribution similar to rat brain.

Animals↗
PubMed2001

Ion selectivity of the cytoplasmic binding sites of the Na,K-ATPase: II. Competition of various cations.

In the E1 state of the Na,K-ATPase all cations present in the cytoplasm compete for the ion binding sites. The mutual effects of mono-, di- and trivalent cations were investigated by experiments with the electrochromic fluorescent dye RH421. Three sites with significantly different properties could be identified. The most unspecific binding site is able to bind all cations, independent of their valence and size. The large organic cation Br2-Titu3+ is bound with the highest affinity ( Na+ > Cs+ > Li+. The second type of binding site is specific for monovalent cations. its binding affinity is higher than that of the first type, for Na+ ions the equilibrium dissociation constant is < 0.01 mM. Since binding to that site is not electrogenic it has to be close to the cytoplasmic surface. The third site is specific for Na+, no other ions were found to bind, the binding is electrogenic and the equilibrium dissociation constant is 0.2 mM.

Animals↗
PubMed2004

Inducible nitric oxide synthase inhibition in cyclophosphamide induced hemorrhagic cystitis in rats.

Cyclophosphamide (CP) is an antineoplastic agent used alone or in combination with other chemotherapeutic agents for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) is a major potential toxicity and dose limiting side effect of CP. Recently, it has been shown that endogenous inflammatory mediators are involved in cystitis by increasing nitric oxide (NO) production in target tissue. The aim of this study was to evaluate the relationship between NO and CP induced hemorrhagic cystitis HC in rats. A total of 30 female Spraque-Dawley rats were divided into 4 groups. Group 1 served as control, three groups received single dose of CP (100 mg/kg) intraperitoneally (i.p.): group 2 received CP only. Group 3 received the NO precursor L-arginine (80 mg/kg/day), and group 4 received the selective inducible NO synthase (iNOS) inhibitor S-methylisothiourea (SMT; 20 mg/kg/day) before and the day after cyclophosphamide injection. CP injection resulted in severe cystitis. SMT but not L-arginine produced marked inhibition of CP induced bladder damage. We concluded that NO produced by iNOS, is an important mediator in the pathogenesis of CP induced cystitis.

Animals↗
PubMed2004

Inhibition of NOS2 ameliorates cardiac remodeling, improves heart function after myocardial infarction in rats.

OBJECTIVE: Previous studies have shown increased expression of nitric oxide synthase 2 (NOS2) in rat heart several weeks after myocardial infarction (MI). The aim of this study was to examine the effect of chronic administration of S-methylisothiourea (SMT), a selective NOS2 inhibitor, commenced one week after MI on hemodynamic parameters and left ventricular (LV) remodeling in rats. METHODS: Rats with MI induced by left coronary ligation were given SMT (0.5 mg/kg/d) or saline by gavage starting one week after MI. After chronic administration for five weeks, hemodynamic and cardiac morphologic studies were performed, and lung water content, plasma NO(x) concentration, NOS2 protein level, myocyte size and collagen volume fraction of noninfarct LV area were quantified. RESULTS: The NO(x) concentration in plasma and the NOS2 protein level in noninfarct myocardium in MI rats were higher than controls. When compared with the MI rats receiving saline, chronic administration of SMT reduced myocyte size (15.1 +/- 1.6 microm vs 16.9 +/- 2.3 microm, P < 0.05), collagen volume fraction of noninfarct LV area (4.4% +/- 1.1% vs 5.7% +/- 1.2%, P < 0.01) and lung water content (77.4% +/- 1.4% vs 79.3% +/- 0.9%, P < 0.01), without affecting infarct size. Administration of SMT had no significant effect on heart rate and mean arterial pressure, but decreased LV end-diastolic pressure (8.7 +/- 2.1 mmHg vs 13.4 +/- 3.1 mmHg, P < 0.01), central venous pressure (0.9 +/- 0.3 mmHg vs 1.5 +/- 0.5 mmHg, P < 0.01) and inner LV diameter (6.9 +/- 0.3 mm vs 7.2 +/- 0.3 mm, P < 0.05) in the MI rats. Plasma level of NO(x) in the MI rats receiving SMT was reduced to control level. CONCLUSIONS: Chronic administration of SMT had beneficial effects on LV remodeling and cardiac dysfunction in MI rats, suggesting the possibility that inhibition of NOS2 could be a therapeutic tool for cardiac dysfunction after MI.

Animals↗
PubMed2003

Deferoxamine reduces and nitric oxide synthase inhibition increases neutrophil-mediated myotube injury.

We tested the contribution of reactive oxygen species (ROS), reactive nitrogen species (RNS) and the beta 2 integrin CD18 to neutrophil-mediated myotube injury. Human myotubes were cultured with human neutrophils in the presence or absence of inhibitors directed against ROS, RNS, and CD18. Muscle injury was assessed by a (51)Cr release assay. The inclusion of superoxide dismutase (50-500 U/ml) in the culture medium did not affect myotube injury. A significant protective effect was provided by including catalase (600-2400 U/ml), deferoxamine (1-2 mM), or anti-CD18 antibody (10 microg/ml) in the culture medium. S-Ethylisothiourea (500-1000 microM), an inhibitor of nitric oxide synthase (NOS), significantly increased myotube injury and reduced nitric oxide (NO) in cultures consisting of only myotubes. In conclusion, neutrophil-mediated skeletal muscle injury appears to be largely dependent on CD18-mediated neutrophil adhesion and iron-dependent hydroxyl radical production. In addition, skeletal muscle NOS activity may protect skeletal muscle against the injury caused by neutrophils.

CD18 Antigens↗
PubMed2006

Reinforcement therapy using nitric oxide synthase inhibitors against endotoxin shock in dogs.

PURPOSE: Nitric oxide synthase (NOS) inhibitors were confirmed to correct the hypotension associated with septic shock, but the overall prognosis is often pessimistic. The histological findings failed to show any improvement. In fact, some patients even exhibited signs of exacerbation. The purpose of this study was to investigate the therapeutic effects of NOS inhibitors and catecholamines in dogs suffering from endotoxin shock. The histological changes produced by these agents were also evaluated. METHODS: Mongrel dogs were used under midazolam anesthesia. A PiCCO continuous cardiac output monitoring catheter was placed in the femoral artery, and a central venous monitoring catheter was placed in the external carotid artery. RESULTS: Endotoxin (0.5 mg/kg, i.v.) was administered to cause shock. After this shock state was observed, the NOS inhibitors and catecholamines raised the blood pressure, and norepinephrine (NA, 2 microg/kg/h) was found to be more potent than S-methylisothiourea (SMT, 20 microg/kg/h). The combined effects of SMT-NA or SMT-DOB were greater than those of NA or dobutamine (DOB) alone. The histological changes induced by endotoxin shock were not ameliorated by the administration of NOS inhibitors but instead appeared to be exacerbated to some degree. CONCLUSION: NOS inhibitors combined with cathecholamines were thus suggested to be able to reduce the cathecolamine dosage in patients suffering from septic shock; They are thus considered to be hemodynamically effective agents.

Animals↗
PubMed1986

The lactam of alpha-guanidinoglutaric acid (1-amidino-2-pyrrolidone-5-carboxylic acid).

alpha-Guanidinoglutaric acid (alpha-GGA) has been reported to occur in the cerebral cortex after epileptic seizures. No physical characteristics of alpha-GGA have been given. A practical procedure for the preparation of alpha-GGA is reported here. alpha-GGA forms a lactam in aqueous solution at 80 degrees C. It is proposed to substitute this lactam, 1-amidino-2-pyrrolidone-5-carboxylic acid (pAGlu), for pyroglutamic acid (pGlu) at the N-terminal position in neuropeptides to modify their biological characteristics. L(+)-Glutamic acid was reacted with S-methylisothiourea (I) at pH 10 in aqueous solution to form L(-)-alpha-guanidinoglutaric acid: mp 165-168 degrees C, [alpha]22D = -22.7 (C = 4, 2 M HCl). alpha-GGA reacted promptly with excess reagent to form a salt, S-methylisothiourea-alpha-guanidinoglutarate: mp 209-210 degrees C, [alpha]22D = -13.0 (C = 4, 2 M HCl). I was removed from the salt with aqueous picric acid, since I readily formed an insoluble picrate, S-methylisothiourea picrate (mp 225-228 degrees C). Alternatively, the salt was added to a cation exchange column, and the alpha-GGA was eluted with molar ammonium acetate buffer, pH 9.5. Its lactam, 1-amidino-2-pyrrolidone-5-carboxylic acid, mp 248-249 degrees C, [alpha]22D = +2.1 (C = 4, 2 M HCl), formed a picrate (mp 196-199 degrees C).

Chemical Phenomena↗
PubMed1994

Reduction of DNA synthesis, pigment synthesis, pigmentation gene mRNA and resistance to UVB in human melanoma cells treated with analogues of a histamine (H2) agonist.

Two groups of S-[2-(N,N-dialkylamino)ethyl]isothiourea derivates which depigmented melanoma cells either with inhibition of tyrosinase (group 1, R = methyl, isopropyl) or without inhibition of tyrosinase (group 2, R = benzyl, phenyl) were studied. Treatment of human melanoma cells with non-lethal doses of group 1 drugs led to a reduction in the levels of mRNA for the pigmentation genes tyrosinase, tyrosinase-related protein-1 and Pmel 17. The group 1 drug S-[2-N,N-diisopropylamino)ethyl[isothiourea] (DINOR) (R = isopropyl) produced only moderate inhibition of DNA, RNA and protein synthesis in three cell lines during the first 24 hr of treatment, and there was no correlation between the extent of inhibition and long-term toxicity. A group 2 drug (R = benzyl) rapidly inhibited DNA synthesis in an amelanotic melanoma cell line (MM96E) sensitive to killing by the drug; association of the latter with inhibition of RNA or protein synthesis was less clear. MM96E cells were also sensitive to killing by reactive oxygen species. In pigmented melanoma cells (MM418), incorporation of [125I]thiouracil, a false precursor of melanin, increased during the first 24 hr of treatment with DINOR whereas a group 2 drug (R = phenyl) inhibited incorporation of [125I]thiouracil. Cells depigmented by treatment with drugs from either group suffered the same amount of DNA damage as pigmented cells after UVB irradiation, as judged by inhibition of DNA synthesis, but did not recover as well as pigmented cells, whether or not drug was present during recovery. The results suggested that (1) group 1 agents down-regulated message for several pigmentation genes, possibly at the transcriptional level; (2) the toxicity of group 2 drugs was related to reactive oxygen species; and (3) melanin protected cells from UVB by enhancing cellular recovery.

Blotting, Northern↗
PubMed1978

Comparative effect of a family of substituted thiopseudoureas on protein synthesis by rat liver and Walker carcinoma ribosomes.

In order to assess the role played respectively by the pseudothiourea group and the alkylic chain in the inhibition of protein synthesis and tumour growth caused by compound AHR-1911, a series of eight related substances were studied. The blockade of protein synthesis on liver and Walker carcinoma ribosomes and on suspensions of Walker carcinoma cells, depended essentially on the length of the alkylic chain and the substitution in C-1. The minimum chain was 9 carbons and a plateau in the activity was reached at 11 carbons. Replacement of the thiourea group in C-1 by an NH2 group did not change the pattern. A double bond in the distal section of the chain (AHR-1911) increased inhibition on intact cells with a parallel decrease in cytotoxicity, and reduced the aggregation of ribosomes, protein synthesis factors and other proteins. The antitumor effect depends on the pseudothiourea group and is not caused primarily by interference with protein synthesis. Aminoacyl tRNA binding and transfer appeared to be targets of AH4-1911, but this did not affect significantly tRNA change or nascent peptide release. Drug binding to ribosomes and their subsequent aggregation can be regulated by K+ concentration and temperature. It is assumed that the inhibition of protein synthesis is caused by AHR-1911 effects on elongation factors, impairing their interaction with ribosomes.

Animals↗