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PubMed2004

Evaluation of radioprotective action of compounds using Saccharomyces cerevisiae.

The yeast Saccharomyces cerevisiae serves as a model eukaryotic system to screen radioprotectors that can be used primarily in radiotherapy as well as in occupational workers in nuclear and allied industries. A number of antioxidants are suggested to be radioprotectors by virtue of their ability to quench reactive oxygen species, but their radioprotective action has not been investigated so far. In this study, a number of antioxidants were tested for their efficacy in radioprotection using yeast cells. Sulfhydryl compounds (disulfiram at 100 and 200 microM) and reduced glutathione (10 and 100 mM), purified compounds of plant origin, such as curcumin (1 mM, 10 mM, and 100 mM), quercetin (100 and 500 microM), rutin (100 and 200 microM), ellagic acid (100,200, and 500 microM) and gallic acid (100 and 500 microM)-were studied. The results revealed that all compounds, except gallic acid, specifically protected normal yeast cells from gamma-radiation damage. Using rad 52 mutants, which lack recombinational DNA repair pathway, it has been found that protection was solely brought about by reducing DNA damage rather than by interfering with DNA repair. Results with DNA repair polymerase further substantiated this contention. We conclude that simple eukaryotic yeast cells can serve as a test system not only for rapid screening of radiomodifiers but also to study their mode of action.

Curcumin↗
PubMed1994

The role of gastric muscle relaxation in cytoprotection induced by san-huang-xie-xin-tang in rats.

We examined the mechanism of the protective effect of San-huang-xie-xin-tang (SHXT), a traditional oriental drug, on the gastric mucosa. SHXT, given intraduodenally, inhibited the gastric secretion in pylorus-ligated rats. SHXT, given orally 30 min before the administration of aspirin, HCl-aspirin and ethanol, protected the gastric mucosa from these agent-induced gastric lesions, although it had no effect on the gastric lesions induced by indomethacin and water immersion stress. Oral administration of SHXT increased gastric contents (muscle relaxation) when they were measured 30 min after SHXT administration. SHXT also inhibited carbachol-contracted gastric muscle in vitro. Neither increased gastric contents nor inhibited ethanol lesions of SHXT were observed when these were tested 4 h after SHXT administration. Pretreatment with indomethacin which is a prostaglandin synthesis inhibitor, and N-ethylmaleimide which is a sulfhydryl blocker did not influence either the increased gastric contents or inhibited ethanol lesions of SHXT. These results indicate that gastric muscle relaxation plays an important role in the gastric protective mechanisms of SHXT, and the endogenous prostaglandins and the sulfhydryl compounds are not necessary for the action of SHXT.

Administration, Oral↗
PubMedDate not supplied

Gastroprotective effects of pantoprazole against experimental mucosal damage.

The present study investigated the gastroprotective effects of the proton pump inhibitor pantoprazole on gastric mucosal damage induced by ethanol-HCl in rats. Omeprazole was used as reference drug. The morphometric analysis of gastric histological sections revealed that pantoprazole and omeprazole dose-dependently prevented the necrotic mucosal injury evoked by ethanol-HCl (ED50 = 14.1 and 21.6 micromol/kg, respectively). These effects were associated with a marked increment of Alcian blue recovery from gastric bound mucus (ED50 = 18.8 and 29.3 micromol/kg, respectively). In addition, both pantoprazole and omeprazole inhibited gastric acid secretion in pylorus-ligated rats (ED50 = 1.5 and 3.3 micromol/kg, respectively). Further experiments indicated that the protective effects of pantoprazole were not modified by L-365,260 (a gastrin receptor antagonist), suramin (a drug able to interfere with endogenous growth factors), N(G)-nitro-L-arginine (an inhibitor of nitric oxide synthase) or systemic ablation of capsaicin-sensitive sensory nerves, whereas they were partly blocked by indomethacin (an inhibitor of prostaglandin synthesis) and fully prevented by N-ethylmaleimide (a potent blocker of sulfhydryl compounds). The present data provide histomorphometric evidence that: 1) pantoprazole is endowed with gastroprotective properties and is more active than omeprazole in preventing the necrotic mucosal damage induced by ethanol-HCl; 2) according to the rank order of ED50 values, the protective effects of both drugs appear to depend mainly on the enhancement of the gastric mucosal barrier rather than on the inhibition of acid secretion; 3) an increased production of prostaglandins, as well as an increased availability of sulfhydryl radicals at the level of the gastric mucosa may account for the gastroprotective effects of pantoprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1972

Auxin activity of 3-methyleneoxindole in wheat.

A product of the enzymatic oxidation of indole-3-acetic acid, 3-methyleneoxindole, is at least 50-fold more effective than indole-3-acetic acid in stimulating the growth of wheat (Triticum vulgare, red variety) coleoptiles. Ethylenediaminetetra-acetic acid can antagonize the growth-stimulating properties of the parent compound, indole-3-acetic acid, presumably by chelating Mn(2+), which is required for the enzymatic oxidation of indole-3-acetic acid. The growth stimulating effect of 3-methyleneoxindole, a product of the blocked reaction, on the other hand, is still evident in the presence of ethylenedia-minetetraacetic acid. In the presence of 2-mercaptoethanol, indole-3-acetic acid fails to stimulate the elongation of wheat coleoptiles. The property of binding to sulfhydryl compounds including 2-mercaptoethanol is unique to 3-methyleneoxindole among indole-3-acetic acid and its oxidation products. These findings suggest that 3-methyleneoxindole is an obligatory intermediate in indole-3-acetic acid induced elongation of wheat coleoptiles.

Journal Article↗
PubMed2003

Gastroprotective effects of phenylpropanoids from the rhizomes of Alpinia galanga in rats: structural requirements and mode of action.

The effects of 1'S-1'-acetoxychavicol acetate and related phenylpropanoids isolated from the rhizomes of Alpinia galanga on ethanol-induced gastric lesions in rats were examined. Among them, 1'S-1'-acetoxychavicol acetate and 1'S-1'-acetoxyeugenol acetate markedly inhibited the ethanol-induced gastric mucosal lesions (ED(50)=0.61 and ca. 0.90 mg/kg). In addition, 1'S-1'-acetoxychavicol acetate inhibited the lesions induced by 0.6 M HCl (ED(50)=0.73 mg/kg) and aspirin (ED(50)=0.69 mg/kg) but it did not show a significant effect on indomethacin-induced gastric lesions and acid output in pylorus-ligated rats at doses of 0.5-5.0 mg/kg. From the gastroprotective effects of various related compounds, the 1'-acetoxyl group of 1'S-1'-acetoxychavicol acetate and 1'S-1'-acetoxyeugenol acetate was found to be essential for their strong activity. With regard to the mode of action, the gastroprotective effects of 1'S-1'-acetoxychavicol acetate were attenuated by pretreatment with indomethacin and N-ethylmaleimide, and 1'S-1'-acetoxychavicol acetate significantly increased the glutathione levels of gastric mucosa in rats. These findings suggest that endogenous prostaglandins and sulfhydryl compounds are involved in the protective effect of 1'S-1'-acetoxychavicol acetate.

Administration, Oral↗
PubMed1980

Effects of sulfhydryl reagents on phagocytosis and exocytosis in rabbit polymorphonuclear leukocytes.

The effect of sulfhydryl reagents on phagocytosis and concomitant enzyme release and on ionophore A 23187 + Ca2+-induced exocytosis in rabbit polymorphonuclear leukocytes (PMN's) was studied. Membrane-penetrating sulfhydryl reagents such as cytochalasin A and N-naphthylmaleimide in micromolar concentrations inhibit both phagocytosis and exocytosis. Poorly penetrating reagents such as p-chloromercuribenzene sulfonate (pCMBS) and 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB), inhibit only in high concentrations (pCMBS), or they are ineffective as inhibitors (DTNB). Inhibition by pCMBS is not reversed by glutathione or dithiothreitol; this suggests that some pCMBS probably enters the cell. Specific intracellular sulfhydryl compounds appear to be essential in the cellular apparatus involved in phagocytosis and exocytosis; various possibilities are considered. A concentration of N-naphthylmaleimide which completely inhibits phagocytosis and exocytosis leaves cellular ATPase activity intact.

4-Chloromercuribenzenesulfonate↗
PubMed1994

Sequential methylation of 2-mercaptoethanol to the dimethyl sulfonium ion, 2-(dimethylthio)ethanol, in vivo and in vitro.

Thioether methyltransferase (S-adenosyl-L-methionine: thioether S-methyltransferase; EC 2.1.1.96) catalyzes the methylation of X in compounds of the type R-X-R'(X = S, Se, Te), yielding a methyl onium ion. Previous results using mice have demonstrated a role for thioether methyltransferase in the conversion and clearance of thioethers by methylation to more water-soluble methyl sulfonium ions suitable for excretion in the urine. A potential major physiological source of thiethers is reactions catalyzed by microsomal thiol methyltransferase (S-adenosyl-L-methionine: thiol S-methyltransferase; EC 2.1.1.9), which has been shown to methylate a diverse range of aliphatic sulfhydryl compounds. This study provides evidence for the sequential methylation of the aliphatic thiol, 2-mercaptoethanol, first to the methyl thioether, 2-(methylthio)ethanol, by thiol methyltransferase followed by methylation of this methyl thioeter to the dimethyl sulfonium ion, 2-(-dimethylthio)ethanol, by thioether methyltransferase. This sequence of reactions was demonstrated in vivo by injecting mice i.p. with radioactive 2-mercaptoethanol and analyzing the labeled methylated products, 2-(methylthio)ethanol and 2(dimethylthio)ethanol, in the urine by HPLC. In addition, the system converting 2-mercaptoethanol to 2-(dimethylthio)ethanol was reconstituted in vitro using solubilized mouse liver microsomes as a source of thiol methyltransferase and purified thioether methyltransferase from mouse lung. The results of these in vivo and in vitro studies established the sequential methylation of 2-mercaptoethanol by these two enzymes.

Animals↗
PubMed1979

Inhibition of the enzymatic activity of ligandin by organogermanium, organolead or organotin compounds and the biliary excretion of sulfobromophthalein by the rat.

Ligandin binds several classes of compounds, has glutathione-S-transferase activity and is postulated to function in the intracellular transport of substances which bind to it and/or are substrates for its enzymatic activity. The effects of a group of organometals reported to inhibit the enzymatic activity of ligandin on the biliary excretion of sulfobromophthalein have been investigated to determine what role the enzymatic activity of ligandin has with respect to the biliary excretion of the dye. Triethyllead reduced the rate of dye excretion into the bile without affecting blood pressure, blood or liver sulfhydryl compounds or the volume of bile flow. The organometal had no effect on the initial rate of plasma dye clearance. Inhibited biliary sulfobromophthalein excretion by triethylead-treated rats correlated with relative increases in liver and bile unconjugated dye, decreases in liver and bile conjugated dye and reduced glutathione-S-aryltransferase activity in supernatant fractions isolated from the liver. The results clearly demonstrated that the tested organometals can inhibit the enzymatic activity of ligandin in vivo and suggested that, if ligandin has a role in the translocation of the dye from the blood to the liver, the enzymatic activity of the protein may not be involved.

Animals↗
PubMed2002

Protective effects of polygodial and related compounds on ethanol-induced gastric mucosal lesions in rats: structural requirements and mode of action.

The methanolic extract from the leaves of Tasmannia lanceolata was found to potently inhibit ethanol-induced gastric lesions in rats. Through bioassay-guided separation, three known sesquiterpenes, polygodial, polygodial 12 alpha-acetal, and polygodial 12 beta-acetal, and a new sesquiterpene, methyl isodrimeninol, were isolated as the active constituents. Among them, polygodial showed very potent gastroprotective effects (ED(50)=0.028 mg/kg, po). From the gastroprotective effects of various reduction and oxidation derivatives of polygodial, the dialdehyde or diacetal structure was found to be essential for the strong activity. Since the gastroprotection of polygodial was attenuated by pretreatment with indomethacin, N-ethylmaleimide, N(G)-nitro-L-arginine methyl ester and ruthenium red, endogenous prostaglandins, sulfhydryl compounds, nitric oxide and vanilloid receptors may be involved in the protective activity.

Animals↗
PubMed1993

Oxidation of alpha-tocopherol in subcellular fractions from rat brain and its possible involvement in nerve function.

The turnover rate of vitamin E is slow in nerve tissue. Therefore, we have developed in vitro techniques to study the biochemical reactions of this nutrient in brain. Subcellular fractions were isolated from the cerebral hemispheres of 4-month-old, male, Fisher 344 rats. Aliquots of fractions (500 micrograms protein) were suspended in 50 mM phosphate buffer at pH 7.4 and incubated at room temperature (20-22 degrees) or 37 degrees for 2 hr in the presence or absence of the following oxidizing agents: 1 mM tertiary butyl hydroperoxide, 10 microM linoleic acid hydroperoxide, 0.5 to 50 mM 2,2'-azobis (2-amidinopropane) dihydrochloride (ABAPH) or 0.1 to 2 mM 2,2'-azobis (2,4-dimethyl) valeronitrile (ABDVN). The latter two compounds generate free radicals upon heating. After oxidation, the subcellular fractions were sedimented, saponified and assayed for tocopherol by liquid chromatography. Linoleic acid hydroperoxide was the most potent oxidizing agent, suggesting that endogenous fatty acid peroxides (e.g. eicosanoid intermediates) are very powerful oxidizing agents. Vitamin E may play an important role in providing antioxidant protection for membranes against excessive oxidation induced by these peroxides. Tocopherol in mitochondria and microsomes was much more susceptible to oxidation than synaptosomal tocopherol. The possible reasons for this observation are: (a) mitochondria and microsomes may contain less of the other reducing agents such as sulfhydryl compounds than synaptosomes, and/or (b) the electron transport structures in the former two subcellular fractions may be facilitating oxidation of tocopherol induced by free radicals. A portion of tocopherol remained unoxidized in all subcellular fractions even at high concentrations of ABAPH, suggesting that tocopherol exists in labile and nonlabile biochemical compartments or complexes.

Amidines↗
PubMed1993

Depletion of circulating cyst(e)ine by oral and intravenous mesna.

The sulfhydryl status of normal and tumour cells is critically important in determining their susceptibility to various cytostatic agents. As a sulfhydryl compound, mesna (sodium 2-mercaptoethane-sulfonate) which is used in large doses to prevent haemorrhagic cystitis associated with certain chemotherapeutic regimens might derange cellular thiol homeostasis. In order to investigate the effects of mesna on the concentrations of thiols in plasma, cysteine, glutathione and their disulfides were measured by HPLC following the oral and intravenous administration of mesna to healthy volunteers. After 7.3 mmol mesna i.v. free cysteine rose from 8.2 (95% CI 7.0-9.4) nmol ml-1 to 53.6 (47.4-59.8) nmol ml-1 at 5 min, most likely due to reduction of circulating cystine by the sulfhydryl drug. This initial rise was followed by a marked decrease of total cyst(e)ine in plasma from 276 (215-337) nmol ml-1 to a nadir of 102 (89-115) nmol ml-1 between 30-120 min after infusion, most likely due to an increased uptake of cysteine into cells and an increased urinary excretion of cyst(e)ine. Qualitatively similar changes were seen after oral mesna. The present data indicate that mesna depletes circulating cyst(e)ine and may thereby markedly alter the sulfhydryl status of cells in vivo although the drug itself is not taken up by most cells.

Administration, Oral↗
PubMed1987

Interception of some direct-acting mutagens by ergothioneine.

Ergothioneine, a novel imidazole sulfhydryl/thione compound formed in millimolar amounts by fungi, is a potentially important defense against electrophiles and free radicals. Protection may well occur both in organisms that synthesize ergothioneine and in animals including man that ingest and store ergothioneine in red blood cells, the liver, seminal fluid, and central nervous system. Ergothioneine blocks the mutagenicity for Salmonella strain TA1950 (hisG46 uvrB) of the nitrosation products of spermidine to an extent that is approximately proportional to the ergothioneine concentration. Ergothioneine also alleviates mutagenicity of cumene and t-butyl hydroperoxides but does not react with N-methyl-N'nitro-N-nitrosoguanidine as does the cysteinyl sulfhydryl compound, glutathione.

4-Nitroquinoline-1-oxide↗
PubMed1976

Purification and properties of an enzyme catalyzing the splitting of carbon-mercury linkages from mercury-resistant Pseudomonas K-62 strain. I. Splitting enzyme 1.

An enzyme (S-1) which catalyzes the splitting of carbon-mercury linkages of organomercury compounds was purified about 24-fold from the cell-free extract of mercury-resistant Pseudomonas K-62 strain by treatment with streptomycin, precipitation with ammonium sulfate, and successive chromatography on Sephadex G-150, DEAE-Sephadex, and DEAE-cellulose. A purified preparation of the enzyme showed a single band on polyacrylamide gel electrophoresis, and was colorless. The molecular weight of the enzyme was estimated to be 19,000, and Km was 5.3 X 10(-5) M for p-chloromercuribenzoic acid (PCMB). The temperature and pH optimum for the reaction were 50degrees and 7.0, respectively. The enzyme was capable of catalyzing the decomposition of methylmercuric chloride (MMC), ethylmercuric chloride (EMC), phenylmercuric acetate (PMA), and PCMB in the presence of a sulfhydryl compound to form a mercuric ion plus methane, ethane, benzene, or benzoic acid, respectively. The mercuric ion thus formed was reduced to metallic mercury by metallic mercury-releasing enzyme (MMR-enzyme).

Chloromercuribenzoates↗
PubMed1995

Intragastric polyethylene glycol-400 protects against ethanol-induced gastric mucosal lesions despite pretreatment with indomethacin or iodoacetamide.

It has been shown that intragastric administration of polyethylene glycol-400 (PEG-400) by gavage needle protected the rat gastric mucosa from 96% ethanol-induced lesions in a dose-dependent fashion. The inhibitions of the lesions were 10.5, 53.5, 94.6, and 99.2% at doses of 275, 1375, 2750, and 5500 mg/kg, respectively. The duration of the protective effect was approximately 12 hr. The gastroprotection offered by PEG-400 was not modified by pretreatment with either subcutaneous indomethacin (25 mg/kg) or iodoacetamide (100 mg/kg). Gastric motility, measured by a balloon method, was dose-dependently inhibited by intragastric administration of PEG-400. The inhibited gastric motility (amplitude gastric contraction) induced by PEG-400 was not modified by pretreatment with either indomethacin or iodoacetamide. The gastric emptying rate, investigated by measuring the disappearance of intragastrically administered [99mTc]DTPA from the stomach of rats treated with PEG-400 (5500 mg/kg) was markedly retarded. There was an increase in both the fluid volume and the mucus volume retained in the gastric lumen only for PEG-400 (5500 mg/kg) at 1, 2, and 4 hr after administration. The rats treated with 0.7 ml of vehicle plus 96% ethanol had significantly less damage than those treated with 0.2 ml of vehicle plus 96% ethanol. These results indicate that intragastric PEG-400-protective effect was not mediated by endogenous prostaglandins, sulfhydryl compounds of the gastric mucosa, or changes in gastric contractile patterns. We conclude that the protective effect of intragastric PEG-400 may be the result of retarded gastric emptying together with an osmotic pull of fluid into the stomach and the increase in gastric mucus volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Gastroprotective effect of intragastric clarithromycin against damage induced by ethanol in rats.

Intragastric administration of clarithromycin, a macrolide antibiotic, macroscopically protected the rat gastric mucosa from 96% ethanol-induced lesions. This protective effect was dose-dependent, the reduction being 92.3, 81.4, 52.2, and 5.4% at doses of 400, 200, 100, and 50 mg/kg, respectively. Clarithromycin protection was not significantly modified by pretreatment with either subcutaneous indomethacin (5 mg/kg), a selective cyclooxygenase inhibitor, or iodoacetamide (100 mg/kg), a specific sulfhydryl blocker. Gastric motor activity, measured by the balloon method, was inhibited by clarithromycin in a dose-dependent fashion. The inhibited gastric motor activity induced by clarithromycin was not modified by pretreatment with either indomethacin or iodoacetamide. Ethanol (1 ml/rat, gavage needle) induced hemorrhagic bandlike lesions in the mucosa of the glandular stomach along the long axis of the greater curvature with the occurrence of a complete inhibition of gastric motor activity. This inhibition was not modified by pretreatment with clarithromycin, indomethacin, or iodoacetamide. There was an increase in the fluid volume for clarithromycin at 100, 200, and 400 mg/kg at 30 min and in the mucus volume only for clarithromycin at 400 mg/kg at 30 min. Gastric mucosal blood flow was absent in the ethanol-induced lesions but in the nonlesion areas was the same in clarithromycin-pretreated and vehicle-pretreated rats as in control (no ethanol) rats. Clarithromycin protection was significantly diminished, although not completely abolished by subcutaneous yohimbine (5 mg/kg), a selective alpha2-adrenoceptor antagonist. Yohimbine also significantly reduced both basal and clarithromycin-stimulated gastric mucus secretion. Our data support the conclusion that the protective effect of intragastric clarithromycin was not mediated by endogenous prostaglandins, sulfhydryl compounds of the gastric mucosa, or changes in the gastric contractile patterns. The protection may be the result of an increase in both the fluid volume and the mucus volume retained in the gastric lumen. alpha2-Adrenoceptors possibly are involved by the mucus-dependent mechanism.

Adrenergic alpha-Antagonists↗
PubMed2006

Evidence for covalent lipoyl adduction with dopaquinone following tyrosinase-catalyzed oxidation.

Previous studies have examined the conjugation of sulfhydryl compounds such as L-cysteine and glutathione with DOPA-quinone following the oxidation of tyrosine and DOPA by tyrosinase. These covalent reactions play a key role in the regulation and metabolism of pigment cells. We report on the first direct evidence for the formation of lipoyl adducts in reactions of thiol groups with DOPA-quinone in dihydrolipoic acid (6,8-dimercaptooctanoic acid [DHLA]). Incubating DHLA with DOPA-quinone followed by tyrosinase-catalyzed oxidation resulted in the three products predicted by HPLC-UV and LC-ESI(-)-MS analyses for DHLA DOPA conjugates. In the current study, we identified 5-S-lipoyl-DOPA among the principal products isolated by HPLC and characterized by FAB(-)-MS, ESI(-)-MS/MS, and 1H NMR, 2D-COSY studies. Collectively, these results suggest that DHLA undergoes sulfhydryl conjugation with DOPA-quinone, pointing to the involvement of thiol-reactive metabolites.

Benzoquinones↗
PubMed1989

Selective killing of human T cell lymphotropic virus type I-transformed cell lines by a damavaricin Fc derivative.

n-Pentyl ether of damavaricin Fc (n-pentyl DvFc) preferentially killed human T-cell lymphotropic virus type I (HTLV-I)-transformed cell lines. The mechanism of action of the drug was investigated using MT-4 cells. Cytotoxic action was diminished by the removal of n-pentyl DvFc from the culture or by the addition of sulfhydryl compounds such as 2-mercaptoethanol and dithiothreitol. The killing activity of n-pentyl DvFc was also diminished by membrane-acting agents including quinidine and diphenylhydantoin. Influx and subsequent efflux of Ca2+ were observed when either HTLV-I infected (MT-4 cells) or uninfected cells were treated with n-pentyl DvFc. An efflux of K+ was observed in HTLV-I infected MT-4 cells immediately after the exposure of the cells to n-pentyl DvFc. The K+ efflux, however, was not observed in the uninfected T cells. n-Pentyl DvFc seems to act primarily on the cell surface of MT-4 cells, leading to the perturbation of membrane function. The restoration of cell growth, however, is critically dependent on the presence of dithiothreitol and 2-mercaptoethanol, implying a role for a free sulfhydryl group in the killing activity.

Anti-Bacterial Agents↗