Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SULFONES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed1986

Synthesis and properties of adenosine-5'-triphosphoro-gamma-1-(5-sulfonic acid)naphthyl ethylamidate: a fluorescent nucleotide substrate for DNA-dependent RNA polymerase from Escherichia coli.

A new fluorescent ATP analog, adenosine-5'-triphosphoro-gamma-1-(5-sulfonic acid)naphthyl ethylamidate (gamma-1,5-EDANS)ATP, containing the fluorophore N-(aminoethyl)-5-naphthylamine-1-sulfonic acid attached via a gamma-phosphoamidate bond was synthesized in good yield. It has absorption maxima at 255 and 344 nm and a fluorescence emission maximum at 490 nm. These spectral characteristics permit its uses as an energy acceptor for energy transfer from the intrinsic protein fluorophores and as an energy donor for the energy transfer to the intrinsic Co of Co-substituted RNA polymerases. This analog is a good substrate for Escherichia coli RNA polymerase and can be used to initiate the RNA chain. Incorporation of this analog into the total RNA synthesized was about 60% of that observed for ATP, independent of the templates used. Its Km values (22 and 118 microM) are twofold higher and its Vmax values (45 and 59 nmol/min/mg of enzyme) are 40% lower than those for ATP using calf thymus DNA and poly[d(A-T)], respectively, as template. For abortive initiation reaction using pAR1435 plasmid DNA as template, the Km and Vmax values of this analog are 2.7 times higher and 7 times lower, respectively, than those of ATP. With its desirable spectroscopic properties, (gamma-1,5-EDANS)ATP is a good probe for the studies of nucleotide-protein interactions, active site mapping of RNA polymerase, and other ATP-utilizing biological systems.

Adenosine Triphosphate↗
PubMed1991

Disulfiram may mediate erythrocyte hemolysis induced by diethyldithiocarbamate and 1,4-naphthoquinone-2-sulfonate.

The increase in 1,4-naphthoquinone-2-sulfonate (NQS)-induced hemolysis by the superoxide dismutase inhibitor diethyldithiocarbamate (DEDC) was formerly attributed to increased superoxide anion levels in the erythrocyte. Our results show that removal of DEDC after preincubation and prior to the addition of NQS did not produce a significant increase in hemolysis, which suggests that hemolysis is primarily caused by the reaction products of DEDC with NQS and not to the inactivation of superoxide dismutase. Disulfiram, the oxidized product of DEDC, was found to be the main product formed when excess DEDC was reacted with NQS. Oxygen uptake also occurred and hydrogen peroxide was formed. The latter caused the oxidation of DEDC to disulfiram as catalase prevented disulfiram formation. Disulfiram was found to readily hemolyze erythrocytes at low concentrations as well as to crosslink the proteins in the erythrocyte membrane. Furthermore, disulfiram-induced hemolysis was markedly enhanced in glutathione-depleted erythrocytes. Disulfiram was subsequently found to readily oxidize glutathione in red blood cells. When equimolar concentrations of DEDC and NQS were reacted, the major product formed was the diethyldithiocarbamate:1,4-naphthoquinone (DEDC:NQS) conjugate. However, the principal mediator of erythrocyte hemolysis when excess DEDC is reacted with 1,4-naphthoquinone-2-sulfonate is disulfiram, whose mode of action may be to modify membrane protein sulfhydryls.

Animals↗
PubMed1980

Cyclic photophosphorylation reactions catalyzed by ferredoxin, methyl viologen and anthraquinone sulfonate. Use of photochemical reactions to optimize redox poising.

The flavin analogue 5-deazariboflavin is a convenient catalyst for the photoreduction of low-potential redox compounds. In an anaerobic medium with Tricine buffer as the electron donor, 5-deazariboflavin is capable of photo-reducing both ferredoxin and methyl viologen. We have used this method to conduct a comparative study of the Photosystem I photophosphorylation activities supported by the reduced forms of ferredoxin, methyl viologen and anthraquinone sulfonate. All of these catalysts are capable of generating high rates (200-500 mumol ATP/h per mg chlorophyll) of cyclic photophosphorylation, but only the activity dependent on ferredoxin exhibits sensitivity to antimycin A. This finding suggests that the size of the catalyst and its ability to approach the thylakoid membrane, rather than low-redox potential, governs antimycin A sensitivity. Ferredoxin-catalyzed activity is, however, less sensitive to inhibition by dibromothymoquinone than are the activities supported by methyl viologen and anthraquinone sulfonate. This discrepancy is due to binding of the inhibitor by ferredoxin.

Anthraquinones↗
PubMed1976

Stimulation of Na+ transport across the toad urinary bladder by p-chloromercuribenzene sulfonate.

The sulfhydryl reagent p-chloromercuribenzene sulfonate increased the ISC across substrate-replete toad urinary bladder when applied to the mucosal (apical) surface. This increase was accounted for by an increased mucosal to serosal net flux of Na+. In the absence of substrate, the rise in ISC was accompanied by an irreversible increase in tissue conductance which was not apparent in the replete preparation. These findings suggest that p-chloromercuribenzene sulfonate may be useful in marking mucosal functions associated with the Na+ transport apparatus.

4-Chloromercuribenzenesulfonate↗
PubMed1977

Studies on the amino groups of myosin ATPase. III. Effect of nucleotides on the fluorescence of beta-naphthoquinone-4-sulfonate bound to amino groups of myosin.

beta-Naphthoquinone-4-sulfonate was used for chemical modification of amino groups of myosin. The reagent was found to affect also the sulfhydryl groups if the reaction was not prevented by previous disulfide exchange with cystamine. When cystamine protection was employed the ATPase (ATP phosphohydrolase, EC3.6.1.3) activity was enhanced in the presence of Mg2+ and decreased in the presence of K+ or Ca2+, a pattern typical of myosin with blocked essential amino groups. On addition of ATP or ADP a blueshift was observed in the fluorescent emission spectrum of beta-naphthoquinone-4-sulfonate bound by myosin, presumably owing to conformational changes in the environment of essential amino groups induced by the binding of nucleotides.

Adenine Nucleotides↗
PubMed1980

Heat denaturation of serum albumin monitored by 1-anilino-naphthalene-8-sulfonate.

The process of heat denaturation of serum albumin, and the properties of several denatured components of albumin were studied using 1-anilino-naphthalene-8-sulfonate as a probe dye. Like native albumin, these protein species all induce fluorescence of the dye with maximum emission at 470 nm when excited at 380 nm. However, the affinity of albumin for the dye decreased on denaturation. This fluorescent dye bound competitively to both native and denatured albumin with another probe dye, 2-(4'-hydroxyphenylazo)benzoic acid, has a specific absorption band at about 480 nm on binding with native albumin. Fatty acids, such as lauric acid, inhibited the interaction of 1-anilinonaphthalene-8-sulfonate with native albumin, but had little effect on its binding with denatured albumin.

Anilino Naphthalenesulfonates↗
PubMed1996

Effects of taurine and guanidinoethane sulfonate on toxicity of the pyrrolizidine alkaloid monocrotaline.

Monocrotaline (MONO), a pyrrolizidine alkaloid, causes pulmonary arterial hypertension and right ventricular hypertrophy due to hepatic metabolism to the alkylating pyrrole dehydromonocrotaline. Taurine a sulfonic amino acid, is hepato- and cardioprotective in a variety of conditions. We have examined the effects of taurine and its amidino analog, guanidinoethane sulfonate (GES), in rats injected i.p. with MONO (65 mg/kg). Taurine and GES were given as 1% solutions in drinking water beginning 14 days before administration of MONO and continuing for 14 days therafter, when the rats were killed. The MONO group had right ventricular hypertrophy and pulmonary hyperplasia. Compared with control, no significant changes in the right ventricle/left ventricle weight ratio, or the right ventricle/body weight ratio occurred in rats also given taurine of GES. Lung weights in these two groups were higher than in the control group, but below that of the MONO-alone group. The lethality of MONO over 14 days was decreased by taurine (LD50 for MONO alone 80 mg/kg; for MONO + taurine 121 mg/kg). Rats given only MONO had lower hepatic concentrations of GSH and cysteine (Cys), and higher activities of microsomal GSH transferase activity were no different from control. Gamma-Glutamylcysteine (Glu-Cys) synthetase and gamma-glutamyl transpeptidase activities were elevated. In MONO-injected rats given GES, hepatic GSH levels were higher and Cys levels were lower than in either the MONO alone or MONO + taurine groups. Gamma-Glu-Cys synthetase activity was depressed. Microsomal GSH transferase, GSH peroxidase and gamma-glutamyl transpeptidase activities were elevated. Livers of MONO-injected animals showed higher levels of serine (reversed by both taurine and GES) and glycine (Gly; reversed by GES) and lower levels of glutamine. Compared with control rats, the following changes occurred in serum amino acids: MONO alone: increased aspartate, taurine and lysine; taurine-supplemented: increased taurine, methionine (Met) and lysine, and decreased Gly; GES-supplemented: decreased asparagine, serine, Gly, arginine, taurine, and valine. Compared with the MONO-alone group, the taurine-supplemented group had higher glutamate (Glu), Met and alanine, and the GES-supplemented group higher alanine and lower serine, Gly, arginine and valine. We conclude that taurine protects against MONO-induced lethality and right ventricular hypertrophy. GES also protects against right ventricular hypertrophy. However, these agents act by different mechanisms, taurine preventing many of the biochemical changes induced by MONO, with GES inducing additional changes.

Amino Acids↗
PubMed1984

Receptor specificity of Ia-restricted T lymphoblasts activated against trinitrobenzene sulfonate-coupled spleen cells: recognition of distinct trinitrophenyl and Ia moieties.

The receptor specificity of H-2-restricted T lymphoblasts activated against trinitrobenzene sulfonate (TNBS)-coupled spleen cells was examined using an antigen binding assay. A population of Lyt-1+,2-T lymphoblasts acquired syngeneic Ia determinants during 4 days of primary culture with hapten-coupled stimulator cells. Syngeneic Ia was not reexpressed after trypsin treatment of the T cells, but was found after incubation with soluble Ia shed from lipopolysaccharide-activated blasts. Self-Ia binding was specific in that Lyt-1+,2- but not Lyt-1-,2+ cells acquired the antigen, and in that self-Ia bound more effectively than allogeneic Ia material. To determine the relationship of self-Ia binding to the recognition of foreign antigen, the binding of trinitrophenyl (TNP)-coupled plasma membrane vesicles by TNP-specific T cells was studied. TNP-vesicle binding occurred via TNP and H-2(Ia) molecules on the vesicles in that binding was inhibited with antibodies against TNP or H-2(Ia) molecules but not non-major histocompatibility complex (e.g., Ly-6.2) molecules on the vesicles. Complete inhibition of TNP-vesicle binding by an Iak-restricted TNP-specific T-cell line occurred with soluble TNP-lysine, but not an unrelated hapten, N-iodoacetyl-N-(5-sulfonic-1-naphthyl)ethylenediamine (I-AED)-cysteine. Conversely, I-AED-cysteine, but not TNP-lysine, inhibited binding of I-AED-coupled B6 vesicles by B6 anti-I-AED T cells. Significant, but weak inhibition of TNP-vesicle binding by the anti-TNP line was observed with glycoprotein preparations containing partially purified self-Ia molecules. However, inhibition was specific for I-Ak molecules, in that inhibition was lost after removal of I-Ak molecules from the glycoprotein preparation, and very little inhibition occurred with soluble glycoproteins prepared from thymocytes which contained very little Ia material or from LPS blasts of an unrelated H-2 haplotype. These results suggest a recognition model in which TNP and Ia determinants are recognized by neighboring receptor combining sites.

Animals↗
PubMed1990

Detection of five different human papillomavirus types in cervical lesions by in situ hybridization. A study of 110 cases using sulfonated probes.

Several findings suggest an etiologic relationship between genital tract squamous cell carcinoma and certain types of human papillomavirus (HPV). Detection of these HPV types in cervical lesions considered as preneoplastic states (ie, cervical intraepithelial neoplasia or CIN) is extremely important but difficult because the morphology of these states is highly heterogeneous and clinical course is rarely predictable. In situ hybridization (ISH) is the only technique allowing correlation between HPV type and tissue or cell morphology. In this report, 110 biopsy specimens from uterine cervix lesions were studied: 66 CIN, 10 invasive carcinoma, 28 metaplasia, and six condyloma acuminata. A new ISH technique based on direct modification of DNA probes by sulfonation was used. The hybridized DNA was revealed first by a specific monoclonal antibody against sulfonated DNA, and then by an alkaline phosphatase system. In order to determine the sensitivity level of this method, 14 biopsy specimens were also submitted to Southern blot hybridization. Five probes were used separately (HPV 6, 11, 16, 18, and 33) for each biopsy specimen. Results of ISH were correlated with morphologic criteria such as number of koilocytes and mitoses. Oncogenic HPV was found exclusively in CIN. The number of labeled cells varied with CIN grade. These data suggest that, whatever the grade, CIN represents a unique preneoplastic process, and that HPV replication depends on the squamous maturation of the pathologic epithelium.

Blotting, Southern↗
PubMed1996

FGF protection and inhibition of human neutrophil elastase by carboxymethyl benzylamide sulfonate dextran derivatives.

Several derivatized dextrans (DxD) containing defined percentage of carboxymethyl, carboxymethyl benzylamide and carboxymethyl benzylamide sulfonate groups have been shown to stimulate tissue repair in various in vivo models including skin, bone, muscle and cornea. These selected DxD were also shown to mimic heparin or heparan sulfate by their ability to interact with, stabilise and protect the heparin-binding growth factor of the fibroblast growth factor family against trypsin digestion (Tardieu et al., J. Cell. Physiol. 1992; 150: 94). The wound healing action of these DxD was explained by postulating that the endogenously released heparin-binding growth factors could be protected within the wound. To further understand the action of these DxD on tissue repair, we have studied their effect on the human neutrophil elastase (HNE) activity, one of the proteases involved in wound repair. These DxD inhibited HNE in an hyperbolic non-competitive manner. Extent of HNE inhibition by DxD increased with their molecular weight and benzylamide sulfonate substitution levels. One DxD, RGT11, was the best inhibitor (Ki 40 pM) and efficiently inhibited FGF-2 proteolysis by HNE, restoring its growth-promoting activity towards human skin fibroblasts. The data contribute to a better understanding of the wound-healing property and anti-inflammatory activity of these polymers.

Cell Division↗
PubMed1986

Comparative kinetics study of the evolution of freshwater aquatic toxicity and biodegradability of linear and branched alkylbenzene sulfonates.

Evolution of both primary biodegradability and acute toxicity to daphnia and zebra fish of a linear alkylbenzene sodium sulfonate (LAS) and a branched alkylbenzene sodium sulfonate (BAS) have been measured simultaneously. In six of eight experiments, LAS was biodegraded to 90% in 7 days and BAS to 70% in 7 days. In the two other experiments, both LAS and BAS have shown the same biodegradation speed and reached the same biodegradation level in 7 days: 45% in one experiment and 55% in the other. The composition of bacteria population and the level of cellular ATP of the inoculum play a decisive role in the biodegradation. These results confirm that it is essential to know the composition of bacteria population present in the inoculum as well as their biochemical characteristics to accurately interpret results of biodegradation tests. In the case of a rapid primary biodegradation of LAS and BAS, the acute toxicity of LAS remains three times as high as that of BAS for at least 24 hr toward daphnia and 48 hr toward zebra fish. Their acute toxicity to daphnia and zebra fish become equivalent only after 72 hr. When primary biodegradation of both products is slower, the acute toxicity of LAS remains higher than that of BAS for more than 7 days.

Alkanesulfonates↗
PubMed1987

Effect of linear alkyl benzene sulfonate in skin of fish fingerlings (Cirrhina mrigala): observations with scanning electron microscope.

Pathomorphological changes in the skin was noticed under the scanning electron microscope in fish fingerlings (Cirrhina mrigala) exposed to 0.005 ppm (25% of the LC50) concentration to linear alkyl benzene sulfonate. The epithelial cells present in the epidermis of the skin were found to secrete more mucus with linear alkyl benzene sulfonate (LAS) than did controls. The presence or deposition of mucus on the surface of skin indicated likely molecular interaction between constituents of mucus and LAS.

Animals↗
PubMedDate not supplied

Sulfonated dextran inhibits complement activation and complement-dependent cytotoxicity in an in vitro model of hyperacute xenograft rejection.

In the present study, we demonstrate that a substituted soluble dextran derivative bearing 73% carboxylic groups and 15% benzylamide sulfonate groups, termed CMDBS25, inhibits complement activation and complement-mediated damage in an in vitro model of xenogeneic rejection. Incubation of porcine aortic endothelial cells with normal human serum resulted in time-dependent complement consumption as assessed by C3a generation in the fluid phase and deposition of activated complement fragments C3, C5 and of C5b-9 on target cells. The presence of C5b-9 membrane attack complex was associated with 51Cr release from prelabelled endothelial cells. The addition of 5-25 mg of CMDBS25/ml under the experimental conditions used, inhibited complement activation and C3a generation in a dose-dependent fashion. CMDBS25 (25 mg/ml) totally suppressed iC3b, C5 and C5b-9 cytolytic complex deposition on cells and inhibits by 42% lysis of target endothelial cells. Native dextran had no effect. Our observations document the anti-complementary properties of sulfonated dextran derivatives and their potential as therapeutic agents for the prevention of complement-dependent hyperacute xenograft rejection.

Animals↗
PubMed1982

Thermal inhibition of repair of methylmethane sulfonate-damaged DNA in chick embryo fibroblasts.

Chick embryo fibroblasts were treated with the monofunctional alkylating agent methylmethane sulfonate at various concentrations for 1 h at 42 degrees C, rinsed and then incubated post-treatment at various temperatures at which the kinetics of alkali-labile bond disappearance was followed. Growth experiments showed that these cells grew similarly at temperatures of either 37 degrees C or 42 degrees C. Repair as assessed by removal of alkali-labile bond was also similar for postincubation in the temperature range 37-42 degrees C for damage due to methylmethane sulfonate treatment at concentrations less than 1.5 mM. When the postincubation temperature was raised higher than 42.5-43 degrees C, this type of repair was stopped. The normal internal body temperature of adult chickens is about 41.6 degrees C. Hence the present finding indicates that chick cells are much more severely restricted in DNA repair at temperatures above normal than are mammalian cells, which can function in this respect for several deg. C above 37 degrees C.

Animals↗
PubMed1983

Inactivation of Bacillus cereus 569/H beta-lactamase I by 6-beta-(trifluoromethane sulfonyl)amidopenicillanic acid sulfone and its N-methyl derivative.

6-beta-(Trifluoromethane sulfonyl)amidopenicillanic acid sulfone and its N-methyl derivative were found to be potent inhibitors of Bacillus cereus 569/H beta-lactamase I. The rate of the inactivation of the enzyme by both compounds was found to increase with the decreasing pH of the reaction medium. The reaction of the enzyme with 6-beta-(trifluoromethane sulfonyl)amidopenicillanic acid sulfone was found to be irreversible at the pH values investigated. In contrast, the reaction with the N-methyl derivative at neutral pH was consistent with the partitioning of the acyl enzyme intermediate in three pathways which included (a) deacylation to yield active enzyme, (b) conversion to a transiently inhibited species, and (c) conversion to an irreversibly inactive form. The amino acid composition of the chromophoric peptide obtained from the enzyme inactivated by either of the compounds was consistent with the occurrence of an initial acylation of serine-70 of the protein.

Amino Acids↗
PubMed1988

A study of the interaction of avidin with 2-anilinonaphthalene-6-sulfonic acid as a probe of the biotin binding site.

The environment of the biotin binding site on avidin was investigated by determining the fluorescence enhancement of a series of fluorescent probes that are anilinonaphthalene sulfonic acid derivatives. Of the compounds tested, 2-anilinonaphthalene-6-sulfonic acid (2,6-ANS) exhibited the greatest enhancement under the conditions used (which would reflect both molar fluorescence enhancement and binding affinity) and exhibited more than 95% reversal upon addition of biotin. Thus, 2,6-ANS was chosen for more detailed characterization of the interaction with avidin. Only a single class of binding sites for 2,6-ANS was identified; the mean value for the Kd was 203 +/- 16 microM (X +/- 1 S.D.), and the molar ratio of 2,6-ANS binding sites to biotin binding sites was approx. 1. These results provide evidence that the biotin binding site and the 2,6-ANS binding site are at least partially overlapping, but the possibility that the probe binding site is altered by a conformational change induced by biotin binding cannot be excluded. At excitation = 328 nm and emission = 408 nm, the molar fluorescence of the bound probe was 6.8 +/- 1.0 microM-1 and that of the free probe was 0.061 +/- 0.008 microM-1 giving an enhancement ratio (molar fluorescence of bound probe/molar fluorescence of free probe) of 111 +/- 22. Upon binding, the wavelength of maximum fluorescence decreases. These findings also provide evidence that the fluorescence enhancement associated with the interaction of 2,6-ANS and avidin reflects the environment of the biotin binding site. The Kosower's Z factor, an empirical index of apolarity, was 82.1 for the 2,6-ANS binding site on avidin. This value reflects a degree of apolarity that is similar to apolar environments observed for substrate binding sites on several enzymes; although not the dominant factor, this environment may contribute to the strong binding of biotin.

Anilino Naphthalenesulfonates↗