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PubMed1995

Antineoplastic drugs sulindac sulfide and sulfone inhibit cell growth by inducing apoptosis.

The nonsteroidal anti-inflammatory drug sulindac is known to inhibit chemical carcinogenesis in rodent models and cause regression of adenomas in patients with adenomatous polyposis coli. Sulindac is a prodrug that is metabolized to a pharmacologically active sulfide derivative that potently inhibits prostaglandin synthesis. Recent studies, however, have shown that a sulfone derivative of sulindac, which essentially lacks prostaglandin synthesis inhibitory activity, also inhibits chemical carcinogenesis, suggesting that reduction of prostaglandin levels is not necessary for the antineoplastic activity of this class of drugs. Both sulindac sulfide and the sulfone inhibit the growth of cultured tumor cells, although the cellular mechanism(s) responsible for the antineoplastic activity of sulindac derivatives is unknown. In this study, we investigated the effects of sulindac sulfide and sulfone on the proliferation, differentiation, and apoptosis of HT-29 human colon carcinoma cells. Sulindac sulfide and sulfone significantly reduced cell number in both preconfluent and confluent cultures of HT-29 cells with the sulfide showing approximately 4-fold greater potency. In addition to HT-29 cells, both drugs inhibited the growth of a variety of tumor cell lines derived from other tissues, as well as normal epithelial cells and fibroblasts. Neither sulindac sulfide nor sulfone inhibited cell proliferation under conditions where the drugs were growth inhibitory. Only under specific conditions involving mitogenic stimulation did sulindac sulfide and sulfone cause cell cycle arrest. Neither sulindac sulfide nor the sulfone induced differentiation of HT-29 cells, but both drugs strongly induced apoptosis. The apoptotic response to sulindac sulfide and sulfone was both time- and dose-dependent and involved a mechanism independent of their inhibitory effect on cell cycle progression. These data suggest that apoptosis is responsible for the cell growth inhibitory activity of sulindac sulfide and sulfone and represents a potential mechanism for the antineoplastic activity of these drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Physicochemical properties and platelet interactions of segmented polyurethanes containing sulfonate groups in the hard segment.

The adhesion of platelets to a series of segmented polyurethanes having sulfonate groups in the hard segment is reported. The polyurethanes were synthesized using sulfonated chain extenders of different structure. Analogous control materials without sulfonate groups also were studied. Adhesion was measured in vitro using washed human platelets in a carrier fluid consisting of Tyrode's buffer with apyrase, albumin, and red cells at normal concentration. The polymers were characterized by gel permeation chromatography and elemental analysis. Water absorption and thermal transitions also were determined. It was found that the sulfonated materials absorb significant amounts of water while the nonsulfonated analogs do not. The surfaces of polymer films were characterized by water contact angle and XPS. The contact angles of the sulfonated surfaces were relatively low. Platelet adhesion to the sulfonated polymers was found to be very high compared to the nonsulfonate analogs. The local environment of the sulfonate groups (different chain extenders) also appears to have an effect on platelet interactions. Albumin adsorption was high on all the materials and was not correlated with platelet adhesion. It appears from this work that platelets may have a binding site that is specific for sulfonate groups.

Adsorption↗
PubMed1996

Sulfonates: novel electron acceptors in anaerobic respiration.

The enrichment and isolation in pure culture of a bacterium, identified as a strain of Desulfovibrio, able to release and reduce the sulfur of isethionate (2-hydroxyethanesulfonate) and other sulfonates to support anaerobic respiratory growth, is described. The sulfonate moiety was the source of sulfur that served as the terminal electron acceptor, while the carbon skeleton of isethionate functioned as an accessory electron donor for the reduction of sulfite. Cysteate (alanine-3-sulfonate) and sulfoacetaldehyde (acetaldehyde-2-sulfonate) could also be used for anaerobic respiration, but many other sulfonates could not. A survey of known sulfate-reducing bacteria revealed that some, but not all, strains tested could utilize the sulfur of some sulfonates as terminal electron acceptor. Isethionate-grown cells of Desulfovibrio strain IC1 reduced sulfonate-sulfur in preference to that of sulfate; however, sulfate-grown cells reduced sulfate-sulfur in preference to that of sulfonate.

Anaerobiosis↗
PubMed1978

Species variability in plasma S-sulfonate levels during and following sulfite administration.

It has been shown that S-sulfonate compounds (R-S-SO-3) are produced by the action of sulfite on reactive disulfide bonds [4,5]. Plasma S-sulfonate production was determined as a function of sulfite ingestion and intraperitoneal injection in rats, mice and rhesus monkeys. The tendency of these species and of the rabbit [8] to produce S-sulfonates in plasma was related to the availability of sulfite and of reactive disulfide bonds and to the stability of plasma protein S-sulfonates. The rhesus monkey and the rabbit accumulated plasma S-sulfonates much more readily than did the rat, while the mouse produced little, if any, under the same test conditions. Plasma protein S-sulfonate fractions in the rat and rhesus monkey were characterized by half-lives of approximately 4 and 8 days respectively. The sensitivity and precision of the analytical method for plasma protein S-sulfonate were improved by incorporation of 35S into the outer sulfur atom of the S-sulfonate moiety (R-S-35SO-3).

Animals↗
PubMed2006

Lithium carbenoids-ultra-reactive yet selective reagents for methylenation and halomethylenation of sulfones.

The first efficient, one-pot method for methylenation of p-toluyl sulfones (i.e., the transformation of p-MePhSO2CHR2 into R2CCH2) is described. Methods for effecting that transformation involving alkylation of sulfones with reagents of the general formula MCH2X, where M = SiMe3, SnR3, and MgCl (the Julia method) have been previously described. However, the silicon reagent is completely unreactive toward many sulfones, the tin reagent typically affords only moderate yields, and the magnesium reagent typically gives incomplete reaction (9-40% starting material). This article reports that excellent yields are obtained by alkylating the sulfone with the more ionic lithium methylene carbenoids (LiCH2X, where X = Cl, Br, and I). For example, treatment of sulfone 1 with 3 equiv of n-BuLi (THF, -100 degrees C) followed by 2 equiv of CH2Br2 affords olefin 2 in 96% yield. Although the carbenoid is generated in the presence of a 1:2 mixture of alpha-lithio-sulfone and n-BuLi, it reacts selectively with the alpha-lithio-sulfone (Krel = 9.6 +/- 0.8 with LiCH2Br). The chlorocarbenoid LiCH2Cl reacts somewhat less selectively (Krel = 3.5). The alkyl-substituted carbenoid n-BuCHBrLi reacts > or = 40 times more slowly than LiCH2Br, suggesting that olefination occurs by the SN2 mechanism rather than by metal-assisted ionization (MAI), the mechanism by which cyclopropyl and vinylidene carbenoids react with nucleophiles. Finally, sulfones can be transformed into vinyl halides by treatment with 3 equiv of n-BuLi (THF, -78 degrees C), followed by >2 equiv of diisopropylamine, followed by 3 equiv of dihalomethane (CH2X2, where X2 = Cl2, BrCl, Br2, or I2). All products are formed in high yield and purity.

Alkenes↗
PubMed1990

Thiophene-degrading Escherichia coli mutants possess sulfone oxidase activity and show altered resistance to sulfur-containing antibiotics.

We have previously isolated mutants of Escherichia coli which show increased oxidation of heterocyclic furan and thiophene substrates. We have now found that strains carrying the thdA mutation express a novel enzyme activity which oxidizes a variety of substrates containing a sulfone (SO2) moiety. Both heterocyclic sulfones (e.g., tetramethylene sulfone) and simple aliphatic sulfones (e.g., ethyl sulfone) were oxidized. The thdA mutants were more resistant than wild-type strains to aromatic sulfone antibiotics such as dapsone. In contrast they showed increased susceptibility to thiolutin, a cyclic antibiotic containing sulfur at the sulfide level of oxidation. Several new thdA mutant alleles were isolated by selecting for increased oxidation of various aliphatic sulfur compounds. These new thdA mutants showed similar sulfone oxidase activity and the same map location (at 10.7 min) as the original thdA1 mutation. The constitutive fadR mutation was required for the phenotypic expression of thdA-mediated oxidation of sulfur compounds. However, the thdA-directed expression of sulfone oxidase activity was not fadR dependent. The thdC and thdD mutations probably protect against the toxicity of thiophene derivatives rather than conferring improved metabolic capability.

Anti-Bacterial Agents↗
PubMedDate not supplied

Effect of sulfonates on the esterase activity of carboxypeptidase A.

The effects of sulfonates on the carboxypeptidase A catalyzed hydrolysis of the ester substrate benzoylglycyl-L-phenyllactate were determined. The modifiers examined were benzenesulfonate, p-toluenesulfonate, 2-phenylethane-sulfonate, methanesulfonate, ethanesulfonate, propanesulfonate, butanesulfonate, pentanesulfonate, hexanesulfonate, heptanesulfonate, and 2,2-dimethyl-2-silapentane-5-sulfonate. Sulfonate activators of peptide hydrolysis were inhibitors of esterase activity. Of the sulfonates studied, 2,2-dimethyl-2-silapentane-5-sulfonate was the most effective inhibitor. 2-Phenylethanesulfonate, hexanesulfonate, heptanesulfonate, and 2,2-dimethyl-2-silapentane-5-sulfonate exhibited uncompetitive inhibition. The remaining sulfonates either did not inhibit or the inhibition was too weak to properly characterize.

Carboxypeptidases↗
PubMed1997

Sulfone derivatives with anti-HIV activity.

Following the discovery of anti-HIV properties of suramin great efforts were devoted to design novel NNRT agents with the aims to find novel drugs for the clinical therapeutic management of AIDS. Sulfone and sulfonamide derivatives were studied by NCI at Bethesda as potential anti-HIV-1 agents and nitrophenyl phenyl sulfone (NPPS) was selected as lead compound for further investigations. At the same time Merck Laboratories discovered L-737,126, a potent indolyl aryl sulfone with inhibitory activity against reverse transcriptase. These studies stimulated novel search in the sulfone series and both diarylsulfones and cyclic sulfone derivatives were investigated. Our decennial interest in chemotherapeutic agents containing a pyrrole ring pulsed us to synthesize and test as anti-HIV-1 agents a number of pyrryl aryl sulfones (PASs), pyrrolobenzothiadiazepine (PBTDs) and pyrrolobenzothiazepine related sulfones. The new sulfone derivatives inhibit selectively HIV-1 and were inactive against HIV-2. Most of them were as active as, if not more active than, nevirapine.

Anti-HIV Agents↗
PubMed2000

A semi-empirical approach to the modeling of the electrophoretic mobility in free solution: application to polystyrenesulfonates of various sulfonation rates.

This work focuses on the understanding of the electrophoretic behavior of flexible chains of polystyrenesulfonates (PSSs) in free solution. It deals mainly with the variation of the electrophoretic mobility with (i) the polymerization degree (N) of fully sulfonated PSSs and (ii) the sulfonation rate of randomly sulfonated PSSs. In both cases, the electrophoretic mobility was modeled following a semi-empirical approach which involves parameters retaining a physical meaning. Fully sulfonated PSS oligomers, having a length smaller than or similar to the Debye length, exhibit a particular electrophoretic behavior, in-between that observed for multicharged small molecules and that for polyelectrolytes. The electrophoretic mobility of these oligomers increases strongly with N, which is attributed to a hydrodynamic coupling between monomers. Then the mobility is maximum for an N of about 10, for which the PSS oligomers are still in a rod-like conformation. Afterwards, as N increases and the PSSs are larger than the Debye length, the electrophoretic mobility decreases slowly until it reaches a constant value corresponding to the free-draining behavior. Next, the electrophoretic behavior of long PSS (N about 1,200) differing in their sulfonation rates was investigated. The effective charge rates were determined independently by conductimetric measurements and the mobilities were modeled as a function of the sulfonation rate. The PSS behavior observed was compared to the one previously reported for classical polyelectrolytes having hydrophilic backbones, such as copolymers of poly(acryamide-coacrylic acid). A specific behavior has been pointed out for these partially sulfonated PSSs, which is attributed to the hydrophobicity of their backbone. Finally, it is shown that separations of PSSs of different sulfonation rates can be obtained with electrolytes containing an anionic surfactant or methanol.

Electrophoresis↗
PubMed1978

Fluorescence of 1,8-anilinonaphthalene sulfonic acid bound to proteins and to lipids of sarcolemma.

Relative contributions to fluorescnece of 1,8-anilinonaphthalene sulfonic acid-sarcolemma by 1,8-anilinonaphthalene sulfonic acid bound to proteins and to lipid were assessed on the basis of fluorescence lifetime and steady-state emission spectra. The lifetime spectrum of lipid-poor proteins prepared from sarcolemma had a major time constant of 16 ns; that of lipids extracted from sarcolemma had a major time constant of 7 ns and a minor one of 4 ns. In sarcolemma, components having all three time constants were observed with weighting factors 0.33, 0.6 and 0.07, respectively, indicating the fraction of 1,8-anilinonaphthalene sulfonic acid bound to protein and to lipid. Steady-state emission spectra of 1,8-anilinonaphthalene sulfonic acid-sarcolemma were resolved into and resynthesized from contributions by 1,8-anilinonaphthalene sulfonic acid bound to proteins and to lipids. The latter was at least two thirds of total 1,8-anilinonaphthalene sulfonic acid bound. Results of analyses of spectra obtained with various concentrations of sarcolemma and 1,8-anilinonaphthalene sulfonic acid suggest that the proteins have a higher affinity, but only about half the binding capacity for 1,8-anilinonaphthalene sulfonic acid as do lipids.

Anilino Naphthalenesulfonates↗
PubMed2003

Modulation of adhesion, spreading and cytoskeleton organization of 3T3 fibroblasts by sulfonic groups present on polymer surfaces.

The early phase of 3T3 fibroblast interaction with sulfonated styrene copolymer surfaces, of two sulfonic group densities and thus of differing wettability, was studied. The sulfonic groups present on copolymer surfaces affected the behaviour of cells, i.e. they stimulated cell adhesion, activated cell spreading and influenced cytoskeleton reorganization. The relative number of adhering cells correlated, while the number of spreading cells inversely correlated, with the surface density of sulfonic groups. Cell shape and the pattern of distribution of F-actin, alpha-actinin and vinculin in the interacting cells also depend on the surface density of sulfonic groups. On surfaces of high sulfonic group density, highly polarized cells were observed with F-actin bundles. On surfaces of low sulfonic group density, the cells spread with a square-like morphology with F-actin organized in stress fibres. In contrast, the cells spread poorly on nonsulfonated surfaces and cell adhesion was unaffected by surface wettability. The contribution of alpha(5)beta(1), alpha(4), and beta(5)integrins to the cell interaction with fibronectin (FN) and vitronectin (VN) adsorbed from serum-containing medium on polymer surfaces was examined. Our results suggest that surface sulfonic groups influence the conformation of FN and VN adsorbed on polymer surfaces and, in turn, determine the integrins that are involved in cell adhesion.

3T3 Cells↗
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↗
PubMed2001

Reaction of arylsulfonylhydrazones of aldehydes with alpha-magnesio sulfones. A novel olefin synthesis.

Reactions of representative tosylhydrazones of aldehydes and ketones with alpha-metalated sulfones were examined in order to develop a practical olefination method. Treatment of aldehyde tosylhydrazone 2 with an excess of alpha-lithiated methyl phenyl or dimethyl sulfones yielded 3a. The reaction of 2 with sterically unhindered lithiated alkyl sulfones gave mixtures of the respective olefination products 3b-d along with the Shapiro fragmentation product 4. Sterically hindered lithiated sulfones afforded Shapiro products exclusively. In contrast, aldehyde tosylhydrazones 2 or 6 in reactions with a variety of alpha-magnesio primary or secondary alkyl sulfones gave olefination products 3a-j and 7a-c in high yields (Tables 1 and 2). beta-Branched alkyl sulfones afforded predominantly (E)-alkenes, whereas unhindered primary sulfones gave mixtures of (E)- and (Z)-alkenes with low selectivity. Reaction of the 2,4,6-triisopropylbenzenesulfonylhydrazone (trisylhydrazone) of cyclodecanone 11c with alpha-magnesio methyl phenyl sulfone afforded the methylidene derivative 12a contaminated with the Shapiro product 13. Tosylhydrazone 2 resisted reaction with i-PrMgCl and gave only a small amount of the addition product in reaction with Bu(2)Mg. Some mechanistic aspects of the reaction of tosylhydrazones with organomagnesium compounds are discussed.

Journal Article↗
PubMed2005

Solvation behavior of short-chain polystyrene sulfonate in aqueous electrolyte solutions: a molecular dynamics study.

We analyze the solvation behavior of short-chain polystyrene sulfonate (PSS) in aqueous electrolyte solutions by isothermal-isochoric molecular dynamics simulation to determine the solvation effects on the structure and conformation of the polyelectrolyte as a function of the aqueous environment. To that end, we study these aqueous systems including the explicit atomistic description of water, the PSS chain, and their interactions with all species in solution. In addition, we investigate the effect of the degree of sulfonation and its distribution along the PSS chain on the resulting conformation as well as solvation structure. Moreover, we assess the impact of added salts on the net charge of the PSS backbone, placing emphasis on the valence of the counterion and the extent of the ion-pair formation between the sulfonate group and the counterions. Finally, we present evidence for the so-called like-charge attraction between sulfonate groups through the formation of counterion-mediated interchain sulfonate-sulfonate and water-mediated intrachain sulfonate-sulfonate bridges, as well as between unlike counterion-counterion interactions.

Journal Article↗
PubMed2003

Cyclooxygenase-independent induction of apoptosis by sulindac sulfone is mediated by polyamines in colon cancer.

Sulindac, a non-steroidal anti-inflammatory prodrug, is metabolized into pharmacologically active sulfide and sulfone derivatives. Sulindac sulfide, but not sulindac sulfone, inhibits cyclooxygenase (COX) enzyme activities, yet both derivatives have growth inhibitory effects on colon cancer cells. Microarray analysis was used to detect COX-independent effects of sulindac on gene expression in human colorectal cells. Spermidine/sperm-ine N1-acetyltransferase (SSAT) gene, which encodes a polyamine catabolic enzyme, was induced by clinically relevant sulindac sulfone concentrations. Northern blots confirmed increased SSAT RNA levels in these colon cancer cells. Deletion analysis and mutational studies were done to map the sulindac sulfone-dependent response sequences in the SSAT 5'-flanking sequences. This led us to the identification of two peroxisome proliferator-activated receptor (PPAR) response elements (PPREs) in the SSAT gene. PPRE-2, at +48 bases relative to the transcription start site, is required for the induction of SSAT by sulindac sulfone and is specifically bound by PPAR gamma in the Caco-2 cells as shown by transfection and gel shift experiments. PPRE-1, at-323 bases relative to the start site, is not required for the induction of SSAT by sulindac sulfone but can be bound by both PPAR delta and PPAR gamma. Sulindac sulfone reduced cellular polyamine contents in the absence but not in the presence of verapamil, an inhibitor of the export of monoacetyl diamines, inhibited cell proliferation and induced apoptosis. The induced apoptosis could be partially rescued by exogenous putrescine. These data suggest that apoptosis induced by sulindac sulfone is mediated, in part, by the COX-independent, PPAR-dependent transcriptional activation of SSAT, leading to reduced tissue polyamine contents in human colon cancer cells.

Acetyltransferases↗
PubMed1996

S-methyl-N,N-diethylthiocarbamate sulfoxide and S-methyl-N,N-diethylthiocarbamate sulfone, two candidates for the active metabolite of disulfiram.

The mechanism of action of disulfiram involves inhibition of hepatic aldehyde dehydrogenase (ALDH). Although disulfiram inhibits ALDH in vitro, it is believed that the drug is too short-lived in vivo to inhibit the enzyme directly. The ultimate inhibitor is thought to be a metabolite of disulfiram. In this study, we examined the effects of S-methyl-N,N-diethylthiocarbamate (MeDTC) sulfoxide and S-methyl-N,N-diethylthiocarbamate sulfone (confirmed and proposed metabolites of disulfiram, respectively) on rat liver mitochondrial low K(m) ALDH. MeDTC sulfoxide and MeDTC sulfone, in 10-min incubations with detergent-solubilized mitochondria, inhibited ALDH activity with an IC50 (mean +/- SD) of 0.93 +/- 0.04 and 0.53 +/- 0.11 microM, respectively, compared with 7.4 +/- 1.0 microM for the parent drug disulfiram. Inhibition by MeDTC sulfone and MeDTC sulfoxide, both at 0.6 microM, was time-dependent, following apparent pseudo-first-order kinetics with a t1/2 of inactivation of 3.5 and 8.8 min, respectively. Dilution of ALDH inhibited by either sulfoxide or sulfone did not restore activity, an indication of irreversible inhibition. Addition of glutathione (50 to 1000 microM) to ALDH before the inhibitors did not alter the inhibition by MeDTC sulfoxide. In contrast, the inhibition by MeDTC sulfone was decreased > 10-fold (IC50 = 6.3 microM) by 50 microM of glutathione and almost completely abolished by 500 microM of glutathione. The cofactor NAD, in a concentration-dependent manner, protected ALDH from inhibition by MeDTC sulfoxide and MeDTC sulfone. In incubations with intact mitochondria, the potency of the two compounds was reversed (IC50 of 9.2 +/- 3.6 and 0.95 +/- 0.30 microM for the MeDTC sulfone and sulfoxide, respectively). Our results suggest that MeDTC sulfone is highly reactive with normal cellular constituents (e.g., glutathione), which may protect ALDH from inhibition, unless this inhibitor is formed very near the target enzyme. In contrast, MeDTC sulfoxide is a better candidate for the ultimate active metabolite of disulfiram, because it is more likely to be sufficiently stable to diffuse from a distant site of formation, such as the endoplasmic reticulum, penetrate the mitochondria, and react with ALDH located in the mitochondrial matrix.

Alcohol Deterrents↗
PubMed1996

Coal tar, pine tar and sulfonated shale oil preparations: comparative activity, efficacy and safety.

BACKGROUND: Tar and sulfonated shale oil preparations are used in the treatment of a variety of inflammatory skin diseases, including psoriasis vulgaris; due to the high polycyclic aromatic hydrocarbon (PAH) content of tars, a possible relationship with cancer in humans has been postulated. On the other hand, the purity of sulfonated shale oils concerning PAHs guarantees a good tolerability during dermatologic therapy. AIM: In this review, it is attempted to compare activity, efficacy and safety of coal tar, pine tar and sulfonated shale oil preparations which currently play a role in dermatologic treatment. RESULTS AND CONCLUSIONS: Primary sources of PAHs in the normal human environment are forest fires, cigarette smoke and combustion of fossil fuels for heating and energy. Thermal processing of fossil substances is also required for the production of tars and sulfonated shale oils. Due to individual manufacturing techniques, tars and sulfonated shale oils differ completely in their chemical composition. Still, sulfonated shale oils are often falsely grouped as tars because of their related origin and similar dermatologic indications. There is at least limited evidence of the activity and efficacy of various tars as well as sulfonated shale oil preparations in different frequent inflammatory skin diseases. This includes psoriasis vulgaris and atopic eczema of glabrous as well as hairy skin. There is still some concern about the long-term tolerability of tar preparations at least in some contexts. This, however, does not apply to sulfonated shale oil preparations. Consequently, at least their use should still be considered a rational drug treatment in dermatology.

Animals↗
PubMed1993

Bile acid sulfonates alter cholesterol gallstone incidence in hamsters.

The prevention of cholesterol gallstone formation by three bile acid analogs, sodium 3 alpha,7 alpha-dihydroxy-5 beta-cholane-24- sulfonate, sodium 3 alpha,7 beta-dihydroxy-5 beta-cholane-24-sulfonate and sodium 3 alpha,6 alpha-dihydroxy-5 beta-cholane-24-sulfonate, was examined in a hamster model of cholesterol cholelithiasis. Sodium taurochenodeoxycholate, sodium tauroursodeoxycholate and sodium taurohyodeoxycholate were studied simultaneously for comparison. Gallstones and cholesterol crystals were induced in 14 of 15 hamsters fed a bile acid-free, semipurified lithogenic diet containing 0.3% cholesterol and 4% butterfat for 6 wk. The addition of 0.1% sodium taurochenodeoxycholate and sodium tauroursodeoxycholate to the lithogenic diet had little effect on the formation of gallstones or biliary cholesterol crystals. In contrast, sodium 3 alpha,7 alpha-hydroxy-5 beta-cholane-24- sulfonate and sodium 3 alpha,7 beta-dihydroxy-5 beta-cholane-24-sulfonate, when fed at the same dose, prevented cholesterol gallstone formation significantly. Sodium taurohyodeoxycholate and sodium 3 alpha,6 alpha-dihydroxy-5 beta-cholane- 24-sulfonate inhibited cholesterol gallstone formation effectively. The cholesterol saturation index of bile was greater than 1.00 in all groups, with the exception of the group fed sodium 3 alpha,7 alpha-dihydroxy-5 beta-cholane-24-sulfonate. Liver and serum cholesterol levels tended to be lower in most of the groups that were fed bile acids. This effect was most pronounced in the animals receiving sodium taurohyodeoxycholate. At the end of the experiment, the administered sulfonate analogs were detected in gallbladder bile.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗