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PubMed2000

Bile acid sulfonate and 7-alkylated bile acid analogs: effect on intestinal absorption of taurocholate and cholesterol 7alpha-hydroxylase activity in cultured rat hepatocytes.

The effects of sulfonate analogs of cholic (C), chenodeoxycholic (CDC), and ursodeoxycholic acid (UDC) and three 7-alkylated CDCs--7-methyl-, 7-ethyl-, and 7-propyl-CDCs--on taurocholate absorption from rat terminal ileum in situ and on cholesterol 7alpha-hydroxylase activity in primary culture of the rat liver were investigated. The sulfonate analogs of two dihydroxy bile acids CDC and UDC, but not C, significantly decreased the absorption of taurocholate. Taurine conjugates of 7-alkylated CDC slightly decreased the taurocholate absorption, and tauro-7-propyl-CDC significantly suppressed the absorption. Although the sulfonate analogs of C and CDC reduced cholesterol 7alpha-hydroxylase activity by 40% and 60% compared to control, UDC-sulfonate analog did not affect enzymatic activity. These results were consistent with those of the lead compounds, C, CDC, and UDC. The introduction of methyl group at C-7 position of CDC attenuated the reduction in cholesterol 7alpha-hydroxylase activity by CDC. However, elongation of the alkyl group resulted in an inhibitory effect. The present study revealed the following: 1) bile acid sulfonates act on cholesterol and bile acid metabolism in a similar manner as taurine conjugated bile acids; and 2) the biologic properties of CDC could be altered by the introduction of alkyl group at C-7 position.

Animals↗
PubMed2002

Antifungal activity of substituted 8-quinolinol-5- and 7-sulfonic acids: a mechanism of action is suggested based on intramolecular synergism.

8-Quinolinol-5-sulfonic acid was nearly devoid of antimicrobial activity, due to what was believed to be an unfavorable partition coefficient. Since twenty six 8-quinolinol-5- and 7-sulfonic acids were available from our previous work, they were tested against six fungi. The 7-chloro and 7-bromo-5-sulfonic acids and the 5-chloro and 5-bromo-7-sulfonic acids showed fungal inhibition within one order of magnitude of that of 8-quinolinol. It is suggested that a nonchelating mechanism is in part responsible for this fungitoxicity. Five additional 5-sulfonic acids with chlorine in positions 3-, 6-, 3,6-, 3,7-, and 6,7- that were suitable for studies in synergism became available more recently. The enhanced activities of the dichlorosulfonic acids over the correspondingly substituted monochlorosulfonic acids is attributed to intramolecular synergism.

Antifungal Agents↗
PubMed1997

The sulfonic acid polymers PAMPS [poly(2-acrylamido-2-methyl-1-propanesulfonic acid)] and related analogues are highly potent inhibitors of angiogenesis.

The sulfonic acid polymers poly(2-acrylamido-2-methyl-1-propanesulfonic acid) (PAMPS), poly(4-styrenesulfonic acid) (PSS), and poly(anetholesulfonic acid) (PAS) proved to be highly potent inhibitors of angiogenesis in the chick chorioallantoic membrane (CAM) assay. PAMPS was found to achieve a dose-dependent inhibition of microvessel formation in the CAM assay ranging from 57 +/- 16% inhibition at 10 micrograms/disc to 72 +/- 15% at 150 micrograms/ disc. Also, PSS and PAS caused a strong inhibition of angiogenesis (55 +/- 19% and 48 +/- 16%, respectively, at 50 micrograms/disc), whereas poly(vinylsulfonic acid) (PVS) was found to be inactive at this dose. The compounds proved to be nontoxic for the developing chick embryo at these doses. Suramin, which was included as a reference compound, caused only a slight inhibition of vascular density, at a dose of 150 micrograms/disc, whereas pentosan polysulfate (PPS) was found to be toxic. PAMPS, PAS, and PSS, but not PVS, inhibited microvessel formation in the rat aorta-ring assay. In addition, the increased [3H-methyl]dThd uptake in endothelial cells in vitro upon stimulation with basic fibroblast growth factor (bFGF) was inhibited by PAMPS, PAS, and PSS at 20 micrograms/ml. A strong correlation (r = 0.95) was found between the antiangiogenic effect of the sulfonic acid polymers in the CAM assay and their inhibition of the bFGF-induced mitogenic response, indicating that bFGF is the target for these sulfonic acid polymers. These results suggest that sulfonic acid polymers, and in particular PAMPS, may be considered as specific, nontoxic angiogenesis inhibitors.

Animals↗
PubMed1985

Sulfonic acid enkephalin: binding specificity to rat brain opiate receptors.

We tested sulfonic-acid enkephalin, a SO3H-Tyr derivative of the Leu-enkephalin, for its binding capacity to rat brain opiate receptors, by competition against several tritiated enkephalins. Using [3H]DADLE as the competitor, we demonstrated that sulfonic-acid enkephalin binds to rat brain opiate receptors, and using [3H]DSLET and [3H]DAGO as the competitors, we demonstrated that sulfonic-acid enkephalin binds preferentially to delta-opiate receptors. The affinity ratio of sulfonic-acid enkephalin for delta-opiate receptors versus mu-opiate receptors, is considerably higher than that of the parent compound, Leu-enkephalin, and of DADLE and is similar to the affinity ratio of DSLET for the same receptors.

Animals↗
PubMed1994

In vitro and in vivo inhibition of ortho- and paramyxovirus infections by a new class of sulfonic acid polymers interacting with virus-cell binding and/or fusion.

A series of sulfonic acid polymers were shown to be potent and selective inhibitors of respiratory syncytial virus (RSV) and influenza A virus. The compounds inhibit the replication of RSV and influenza A virus in HeLa and MDCK cells, at concentrations of 0.16 and 4.0 micrograms/ml, respectively, and are nontoxic to growing cells at concentrations of > 100 micrograms/ml. The mode of antiviral action of the sulfonic acid polymers can be ascribed to inhibition of virus-cell fusion (for influenza A virus) or inhibition of both virus-cell binding and fusion (for RSV). The sulfonic acid prototype PAMPS [poly(2-acrylamido-2-methyl-1-propanesulfonic acid)], when administered intranasally to mice as a single dose of 10 or 50 mg per kg of body weight at the time of infection, completely inhibited influenza A virus replication (in lungs) and virus-associated lung consolidation in immunocompetent mice and completely protected NMRI and SCID (severe combined immune deficiency) mice against influenza A virus-associated mortality. When administered 1 h before or after virus inoculation, no protective effect was observed at a dose of 10 or 100 mg/kg. Sulfonic acid polymers exert selective inhibitory effects on RSV and influenza A virus replication.

Animals↗
PubMed2006

The suramin analog 4,4',4'',4'''-(carbonylbis(imino-5,1,3-benzenetriylbis (carbonylimino)))tetra-kis-benzenesulfonic acid (NF110) potently blocks P2X3 receptors: subtype selectivity is determined by location of sulfonic acid groups.

We have previously identified the suramin analog 4,4',4'',4'''-(carbonylbis(imino-5,1,3-benzenetriylbis(carbonylimino)))tetrakis-benzene-1,3-disulfonic acid (NF449) as a low nanomolar potency antagonist of recombinant P2X(1) receptors. Here, we characterize, by two-electrode voltage-clamp electrophysiology, three isomeric suramin analogs designated para-4,4',4'',4''''-(carbonylbis(imino-5,1,3-benzenetriylbis (carbonylimino)))tetrakis-benzenesulfonic acid (NF110), meta-(3,3',3'',3''''-(carbonylbis(imino-5,1,3-benzenetriylbis (carbonylimino)))tetra-kis-benzenesulfonic acid (NF448), and ortho-(2,2',2'',2''''-(carbonylbis(imino-5,1,3-benzenetriylbis (carbonylimino)))tetra-kis-benzenesulfonic acid (MK3) with respect to their potency in antagonizing rat P2X receptor-mediated inward currents in Xenopus laevis oocytes. Meta, para, and ortho refer to the position of the single sulfonic acid group relative to the amide bond linking the four symmetrically oriented benzenesulfonic acid moieties to the central, invariant suramin core. NF448, NF110, and MK3 were >200-fold less potent in blocking P2X(1) receptors than NF449, from which they differ structurally only by having one instead of two sulfonic acid residues per benzene ring. Although the meta- and ortho-isomers retained P2X(1) receptor selectivity, the para-isomer NF110 exhibited a significantly increased activity at P2X(3) receptors (K(i) approximately 36 nM) and displayed the following unique selectivity profile among suramin derivatives: P2X(2+3) = P2X(3) > P2X(1) > P2X(2) >> P2X(4) > P2X(7). The usefulness of NF110 as a P2X(3) receptor antagonist in native tissues could be demonstrated by showing that NF110 blocks alphabeta-methylene-ATP-induced currents in rat dorsal root ganglia neurons with similar potency as recombinant rat P2X(3) receptors. Together, these data highlight the importance of both the number and exact location of negatively charged groups for P2X subtype potency and selectivity.

Adenosine Triphosphate↗
PubMed1995

Evaluation of urinary mercury excretion after administration of 2,3-dimercapto-1-propane sulfonic acid to occupationally exposed men.

The purpose of this study was to determine the clinical efficacy of 2,3-dimercapto-1-propane sulfonic acid, Na salt, on the urinary excretion of mercury as well as its possible adverse effects. Ten men with occupational mercury exposure (urinary level of 50 micrograms/g creatinine or more) were assigned to receive 2,3-dimercapto-1-propane sulfonic acid p.o. (DIMAVAL capsules, 100 mg) 300 mg/d for five days. Informed written consent was obtained from each subject. Hematology analyses, blood, chemistry, and urinalysis were obtained at the start of the study, at the end of the 2,3-dimercapto-1-propane sulfonic acid treatment and 72 hours after the administration of the final dose of 2,3-dimercapto-1-propane sulfonic acid. Twenty-four-hour urine mercury levels were closely monitored throughout therapy. All data and measurements before and during drug doses were evaluated by analyses of variance. In all subjects mean urine mercury was significantly increased (p < .05) after pre-2,3-dimercapto-1-propane sulfonic acid treatment. One subject had a moderate hypersensitivity reaction (rash) to 2,3-dimercapto-1-propane sulfonic acid but no other toxic effects were observed.

Adult↗
PubMed2004

Beneficial effects of GW274150 treatment on the development of experimental colitis induced by dinitrobenzene sulfonic acid.

Inflammatory bowel disease is associated with inducible nitric oxide synthase (iNOS) expression, oxidative and nitrosative stress, and leukocyte infiltration in the colon. Here, we investigate the effects of the selective iNOS-inhibitor (S)-2-amino-(1-iminoethylamino)-5-thiopentanoic acid (GW274150) on the development of experimental colitis induced by dinitrobenzene sulfonic acid. When compared to dinitrobenzene sulfonic acid-treated mice, GW274150 (5 mg/kg i.p.)-treated mice subjected to dinitrobenzene sulfonic ACID-induced colitis experienced a significantly lower rate of the extent and severity of the histological signs of colon injury. Dinitrobenzene sulfonic acid-treated mice experienced hemorrhagic diarrhoea and weight loss. At 4 days after the administration of dinitrobenzene sulfonic acid, the mucosa of the colon exhibited large areas of necrosis. Immunohistochemistry for nitrotyrosine and poly (ADP-ribose) (PAR) showed an intense staining in the inflamed colon. Treatment of dinitrobenzene sulfonic acid-treated mice with GW274150 significantly reduced the degree of hemorrhagic diarrhoea and weight loss caused by administration of dinitrobenzene sulfonic acid. GW274150 also caused a substantial reduction of (i) the degree of colon injury, (ii) the rise in myeloperoxidase (MPO) activity (mucosa), (iii) the increase in staining (immunohistochemistry) for nitrotyrosine, as well as (iv) PARP activation caused by dinitrobenzene sulfonic acid in the colon. Thus, GW274150 treatment reduced the degree of colitis caused by dinitrobenzene sulfonic acid. We propose that selective inhibition of iNOS activity with GW274150 may be useful in the treatment of inflammatory bowel disease.

Animals↗
PubMed1998

Dietary monounsaturated n-3 and n-6 long-chain polyunsaturated fatty acids affect cellular antioxidant defense system in rats with experimental ulcerative colitis induced by trinitrobenzene sulfonic acid.

The intrarectal administration of trinitrobenzene sulfonic acid in rats induces ulcerative colitis, which results in histological alterations of colonic mucosa, severe modification of the cellular antioxidant defense system, and enhanced production of inflammatory eicosanoids. This study evaluated the influence of different dietary fatty acids, i.e., monounsaturated, n-3, and n-3 + n-6 polyunsaturated fatty acids, on the recovery of the colonic mucosa histological pattern, the cellular antioxidant defense system of colon, and PGE2 and LTB4 colonic mucosa contents in a model of ulcerative colitis induced by intrarectal administration of trinitrobenzene sulfonic acid. Administration of dietary n-3 polyunsaturated fatty acids led to a minimum stenosis score, a higher histological recovery, lower colon alkaline phosphatase and gamma-glutamyltranspeptidase activities, and lower mucosal levels of PGE2 and LTB4 compared with the other two experimental groups. However, glutathione transferase, glutathione reductase, glutathione peroxidase, and catalase activities were lower in the group treated with n-3 polyunsaturated fatty acids than in the groups fed with either the monounsaturated or the n-6 + n-3 polyunsaturated enriched diet. We conclude that n-3 polyunsaturated fatty acids can be administered to prevent inflammation in ulcerative colitis, but they cause a decrease in the colonic antioxidant defense system, promoting oxidative injury at the site of inflammation.

Animals↗
PubMed1998

Comparison of enhanced elimination of bismuth in humans after treatment with meso-2,3-dimercaptosuccinic acid and D,L-2,3-dimercaptopropane-1-sulfonic acid.

Two groups of 12 human volunteers, who had been treated with colloidal bismuth subcitrate, because of Helicobacter pylori-associated gastritis, participated in the study. The patients received a single dose of meso-2,3-dimercaptosuccinic acid (DMSA) or D,L-2,3-dimercaptopropane-1-sulfonic acid (DMPS) at a dose of 30 mg kg-1 in a randomized single blind study. In contrast to DMPS, increasing concentrations of bismuth in blood were observed during the first 4 h after intake of DMSA. In urine, both chelators induced a 50-fold increase in urinary bismuth excretion compared with the control urines. The treatment was well tolerated. The results indicate that both DMSA and DMPS effectively increase the elimination of bismuth in human urine. Consequently, both chelators may be of benefit in the treatment of patients with bismuth intoxication.

Adult↗
PubMed2003

Cholinergic pathways modulate experimental dinitrobenzene sulfonic acid colitis in rats.

Recent studies have suggested that neuroimmune interactions modulate intestinal mucosal immune responses. In the current study, we examined the role of cholinergic pathways in modulating the severity of acute dinitrobenzene sulfonic acid colitis, using pharmacological agents to suppress acetylcholinesterase in Sprague-Dawley rats, and evaluating the colitis in the cholinergic hyperresponsive Flinder's sensitive line rats and their control counterparts, the Flinder's resistant line. Colitis was induced by intrarectal dinitrobenzene sulfonic acid (80 mg x ml(-1) in 50% ethanol); controls received intrarectal saline. Sprague-Dawley rats received an acetylcholinesterase inhibitor, physostigmine (50 microg x kg(-1) s.c.) or neostigmine (50 microg x kg(-1) s.c.), 30 min prior to intrarectal dinitrobenzene sulfonic acid; controls received saline vehicle. On day 5, the macroscopic damage score, myeloperoxidase activity (an estimate of granulocyte infiltration) and smooth muscle thickness were evaluated in the inflamed colonic segment. Significant increases in macroscopic damage score and colonic smooth muscle thickness were observed in Sprague-Dawley and Flinder's Resistant Line rats on day 5 following intrarectal dinitrobenzene sulfonic acid compared to saline controls. Increased myeloperoxidase activity was also observed in dinitrobenzene sulfonic acid-treated Sprague-Dawley rats and Flinder's Resistant Line rats. In contrast, Flinder's Sensitive Line rats failed to demonstrate a significant rise in macroscopic damage, smooth muscle layer thickness, or myeloperoxidase activity on day 5 following intrarectal dinitrobenzene sulfonic acid when compared to saline-treated Flinder's Sensitive Line controls. Neostigmine and physostigmine treatment prior to intrarectal dinitrobenzene sulfonic acid significantly attenuated macroscopic damage score, myeloperoxidase activity and smooth muscle thickness on day 5 compared to colitic Sprague-Dawley controls. Significantly greater reductions in myeloperoxidase activity were observed with physostigmine vs. neostigmine pretreatment. These data suggest that cholinergic pathways modulate the acute colonic inflammatory response associated with the dinitrobenzene sulfonic acid model, with central pathways exerting a greater protective effect relative to peripheral pathways. Further studies are required to determine the contributions of sites in the nervous system and neuro-effector junctions.

Animals↗
PubMed1993

Perfluorooctane sulfonic acid is a potent inducer of peroxisomal fatty acid beta-oxidation and other activities known to be affected by peroxisome proliferators in mouse liver.

Perfluorooctane sulfonic acid is almost as potent as perfluorooctanoic acid in causing increases in peroxisomal fatty acid beta-oxidation, peroxisomal catalase activity, omega-hydroxylation of lauric acid, cytosolic epoxide hydrolase activity and cytosolic DT-diaphorase activity. Octane sulfonic acid was ineffective at doses used for perfluorooctane sulfonic acid and perfluorooctanoic acid. The results support the theory of co-regulation of these parameters and peroxisome proliferation. The fact that perfluorooctane sulfonic acid causes peroxisome proliferation challenges the hypothesis that the first step in this process is formation of a thioester between the proliferator (the carboxylic group) and coenzyme A.

Acyl Coenzyme A↗
PubMed2001

Capillary electrochromatography with polyacrylamide monolithic stationary phases having bonded dodecyl ligands and sulfonic acid groups: evaluation of column performance with alkyl phenyl ketones and neutral moderately polar pesticides.

In this report, we describe the preparation of porous polyacrylamide-based monolithic columns via vinyl polymerization. These monoliths possess in their structures bonded dodecyl ligands and sulfonic acid groups. While the sulfonic acid groups are meant to support the electroosmotic flow (EOF) necessary for moving the mobile phase through the monolithic capillary, the dodecyl ligands are introduced to provide the nonpolar sites for chromatographic retention. However, incorporating the sulfonic acid groups in the monoliths does not only support the EOF but also exhibit hydrophilic interaction with moderately polar compounds such as urea herbicides and carbamates insecticides. Consequently, mixed-mode (reversed-phase/normal phase) retention behavior is observed with neutral and moderately polar pesticides. The amount of sulfonic acid group in the monolith can be conveniently adjusted by changing the amount of vinylsulfonic acid added to the polymerization reaction. Optimum EOF velocity and adequate chromatographic retention are obtained when 15% vinylsulfonic acid is added to the reaction mixture. Under these conditions, rapid separation and high plate counts reaching greater than 400000 plates/m are readily obtained.

Acrylic Resins↗
PubMed1992

Sulfonic acid polymers as a new class of human immunodeficiency virus inhibitors.

Four sulfonic acid polymers [poly(4-styrenesulfonic acid)(PSS), poly(anetholesulfonic acid)(PAS), poly(vinylsulfonic acid)(PVS), poly(2-acrylamido-2-methyl-1-propanesulfonic acid)(PAMPS)] have been found to inhibit the cytopathicity of HIV-1 and HIV-2 in MT-4 cells at concentrations that are not toxic to the host cells. The sulfonic acid polymers also inhibited syncytium formation in co-cultures of MOLT-4 cells with HIV-1- or HIV-2-infected HUT-78 cells. They also inhibited binding of anti-gp120 mAb to HIV-1 gp120 and blocked adsorption of HIV-1 virions to MT-4 cells. PSS and PAS, but not PVS and PAMPS, interfered with the binding of OKT4A/Leu3a to the CD4 receptor. The anti-HIV activity of these polyanionic compounds can be ascribed to inhibition of the gp120-CD4 interaction. Sulfonic acid polymers represent a lead of anti-HIV compounds that warrant further evaluation of their therapeutic potential.

Antiviral Agents↗