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PubMed2006

Characterization of four clones derived from human adenocarcinoma cell line, HT29, and analysis of their response to sodium butyrate.

The differentiation of colorectal cancer cells is associated with the arrest of tumor growth and tumor regression. However, the mechanism of such tumor cell differentiation has not yet been elucidated. Several adenocarcinoma cell lines, including HT29 which differentiates only upon stimulation with a differentiation agent, have been used for the study of colorectal cells. Since we had previously obtained variable results during analyses of these cells, we selected several clones of this cell line. In this study, four clones of the parental HT29 cells, H8, G9, G10 and A3, were characterized. All of them differentiated upon treatment with sodium butyrate as the differentiation agent but they appeared different in their response regarding some of the markers of differentiation. As revealed by ultrastructural analysis, H8 and G10 clones formed numerous intercellular cysts with microvilli whereas these structures were found only occasionally in G9 and A3 clones. An elevated level of the indicator of cell differentiation, CEACAM 1, was found in H8 and G10 clones and the activity of alkaline phosphatase, another important marker of colorectal cell differentiation, was up-regulated and highly increased upon butyrate treatment in the H8 clone. Phosphorylation of p38 MAPK was increased in H8 and A3 butyrate-treated clones. According to the levels of cleaved PARP and activated caspase-3, the apoptotic response to butyrate appeared similar in all four clones, while electronoptic analysis revealed that clones G9 and A3 were more perceptive to butyrate-induced apoptosis. In conclusion, our data showed considerable heterogeneity in morphology and some enzymatic activity of the cloned cells. This fact may contribute to the evidence that many HT29 cells possess multipotent information similar to that of stem cells of the normal intestinal crypt.

Adenocarcinoma↗
PubMed1975

[A new butyric acid-producing bacteroides species: B. splanchnicus n. sp. (author's transl)].

Three butyric acid-producing saccharolytic Bacteroides cultures (1651/6, BM 158, and IPP 3751) were described by WERNER and REICHERTZ in 1971 (Zbl.Bakt.Hyg., I. Abt. Orig. A 217,206-216). Since then, 6 strains closely resembling 1651/6 were isolated from stool specimens and surgically removed appendices. In the present communication, strains 1651/6, S2/34, S3/38, S4/28, S6/6, A5/2 are described as members of a new species, Bacteroides splanchnicus n.sp. The strains were morphologically very similar (Gram negative non-sporing non-motile rods, 1-2.5 mu in length and 0.7 mu in width) and fermented glucose, fructose, galactose, mannose, lactose, and arabinose (pH values of 4.6-5.4, moderate gas formation). Negative reactions (pH values of 5.8-7.2) were observed with 20 other carbohydrates. The strains were positive in the glutamic acid decarboxylase test and formed indole and H2S. In peptone-yeast extract broth and peptone-yeast extract-glucose broth acetic, propionic, isobutyric, butyric, and isovaleric acids were produced. Washed cells of strains 1651/6 and S4/28 incubated anaerobically in sterile solutions of single amino acids produced butyrate from lysine only. Abundant butyric acid was also produced from glucose. The in vitro activity of 15 antibiotics on 5 strains was studied by broth dilution tests. Uniformly, the strains showed resistance to aminoglycosides and polymyxins (MIC values, 60-500 mug/ml) and susceptibility to tetracyclines, lincomycin, clindamycin, rifampicin, and erythromycin (MIC values, 0.05-0.5 mug/ml). Chloramphenicol, penicillins, and cephalosporins showed bacteriostatic activity at concentrations of 5-40 mug/ml. The serological behaviour of 5 strains was studied in cross-agglutination and gel-diffusion experiments. Cross-reactivity was pronounced in gel-diffusion tests using rabbit antisera and autoclaved extracts and extracts prepared by repeated deep-freezing and thawing of whole cell suspensions as antigens. However, antisera against the B. splanchnicus strains did not react with antigens of B. fragilis 6869, B. thetaiotaomicron AS 126, B. vulgatus AM 45 a, B. distasonis AII 104 and butyric acid-producing strains BM 158 and IPP 3751 in agglutination and gel-diffusion experiments, and there were no cross-reactions between B. splanchnicus antigens and antisera against B. fragilis 6869 and the other aforementioned strains. The new species has been confirmed by members of the ICSB Taxonomic Subcommittee for Gram negative anaerobic rods. Strains 1651/6 and S4/28 have been deposited in The National Collection of Type Cultures, London (NCTC numbers 10825 and 10826). Strain NCTC 10825 (= 1651/6) is the type of the species, B. splanchnicus.

Acetates↗
PubMed1990

Alteration of differentiation state of human hepatocytes cultured with novobiocin and butyrate.

Chang liver cells cultured in the simultaneous presence of novobiocin and butyrate stopped proliferating and changed into fibroblast-like cells with remarkably elongated cytoplasm. In these fibroblast-like cells, the cellular content of both protein and DNA was increased 2- to 3-fold. In addition, the production of specific proteins such as type III procollagen, actin, and tubulin was increased and the expression of proliferation-associated nuclear antigen which was reactive with Ki-67 monoclonal antibody was reduced remarkably. Therefore, Chang liver cells cultured with novobiocin and butyrate were considered to be arrested at the premitotic G2 phase of the cell cycle and then enter into the noncycling resting state. These actions of novobiocin and butyrate were not mediated by the pathway of epidermal growth factor action or modulated by the diacylglycerol agonist 1-oleoyl-2-acetylglycerol and the C kinase inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine. On the other hand, novobiocin was disclosed to be a stimulator of [3H]acetate uptake and acted synergistically with butyrate in enhancing nuclear protein acetylation. From these results it can be speculated that novobiocin and butyrate chemically modulate nuclear proteins and thereby alter the gene expression and the differentiation state of Chang liver cells.

Acetylation↗
PubMedDate not supplied

Low level toxicity and antitumor activity of butyric mono- and polyester monosaccharide derivates in mice.

This study compares the antitumor activity of five mono- and polyesters of n-butyric acid derived from monosaccharides in the murine model of Crocker 180 TG Sarcoma. Tumor incidence at ten days, mean survival time and final survival rate were significantly affected in all cases. Combined treatment by butyric esters, alpha/beta interferon (IFN) and/or Corynebacterium parvum used as immunestimulator improved the antitumor protection. Studies of acute toxicity in mice, performed by i.p. and oral routes, showed the low toxicity of butyric esters, which were devoid of detectable side effects with no incidence on ponderal growth when administered per os in rats daily for one month. Finally, a comparative study of antitumor activity, toxicity and water-solubility of various butyric esters enabled us to select among these new molecules two isomers (carbon-3 and carbon-6 of the glucose ring substituted with n-butyric acid) derived from monoacetone glucose for further investigations of their biological mechanism in vivo and in vitro.

Animals↗
PubMed1989

[Studies on mechanism of carcinogenesis in cell culture. III. Butyric acid-induced phenotypic reversion of malignant transformed Syrian hamster lung cells (BHLB4)].

The MNNG transformed Syrian hamster lung fibroblast cell line (BHLB4) established in our laboratory was treated with 2.0 mmol/L butyric acid. We obtained a butyric acid-dependent partially reversed cell line (ButB4) similar to normal cells in morphology, membrane properties, proliferation rate, colony-forming ability on solid agar culture, etc. However, when transplanted into nude mice, this cell line's tumorigenicity remained intact. Detection of cAMP levels in the cytoplasm showed much higher levels in ButB4 cells than in transformed cells. Butyric acid activity is evidently associated with changes of cAMP. In addition to phenotypical analysis, the karyotypes of ButB4 and BHLB4 were analyzed in detail. It was found that the disomy rate of C15 was significantly increased in ButB4 cells (73%) as compared with BHLB4 cells (33%). These results show that butyric acid not only induces phenotypic reversion in BHLB4 cells directly, but can also selectively kill C15 monosomy cell clones, allowing rapid growth of C15 disomy cell clones. Butyric acid may also influence maintenance of the reversion phenotype.

Animals↗
PubMed1980

Antagonism between phorbol myristate acetate and butyric acid on isoproterenol elevation of cyclic adenosine 3':5'-monophosphate and their effects on beta-adrenergic receptors in mouse epidermis.

Butyric acid enhanced adenosine 3':5'-monophosphate accumulation in both untreated and isoproterenol-stimulated epidermis. A single treatment with 17 nmol of the potent tumor promoter, phorbol myristate acetate (PMA), inhibited cyclic adenosine 3':5'-monophosphate accumulation in isoproterenol and in butyric acid-stimulated epidermis. beta-Adrenergic receptors in mouse epidermis were measured by the binding of L-[3H]dihydroalprenolol. The apparent dissociation constant was 52 nM, and 33 fmol L-[3H]dihydroalprenolol were bound per microgram DNA. An increase in receptors was induced in vivo with 200 nmol butyric acid. The induction exhibited a 2-fold maximum at 72 hr and a decline to control values at 120 hr. PMA had no effect on the number or availability of the beta-receptors, nor did it affect the butyric acid induction. The biochemical antagonism between PMA and butyric acid on the beta-adrenergic responsiveness of mouse epidermis may be a result of opposing actions on the coupling of beta-receptors to adenyl cyclase. The alteration in the function of membrane receptors involved in cell metabolism may be responsible for some of the biological effects of PMA and other promoters.

Animals↗
PubMed1980

Cell cycle-specific enhancement of type C virus activation by sodium n-butyrate.

The effect of sodium n-butyrate on chemical induction of xenotropic virus from synchronized Kirsten sarcoma virus-transformed BALB mouse cells was examined. When added during the last part of the G1 phase, n-butyrate produced a large increase in cycloheximide induction during S phase. Under similar conditions, activation by 5-iododeoxyuridine was inhibited. When added with cycloheximide during the S phase, n-butyrate inhibited activation of virus. Studies with synchronized cultures showed that n-butyrate delayed the onset of DNA synthesis, characteristic of the S phase, and inhibited histone deacetylation in log-phase cells. The effects produced by n-butyrate could, therefore, be the result of lengthening the G1 phase of the cell cycle or a modification of histones affecting transcription during virus activation.

Animals↗
PubMed1982

Enhancement of 5-lipoxygenase activity in mastocytoma P-815 cells by n-butyrate treatment.

Cloned mastocytoma P-815, 2-E-6 cells were used to investigate regulation of 5-lipoxygenase activity. 2-E-6 cells had high 5-lipoxygenase activity with slight 12-lipoxygenase activity. The 5-lipoxygenase activity was increased over 5-fold by treatment of the cells with 1 mM n-butyrate for 18 h. the most effective dose range being 0.1-5.0 mM. Treatment with n-butyrate for 18 h was more effective than treatment for 40 h. Addition of n-butyrate to an untreated cell homogenate had no stimulatory effect. The enhancement of 5-lipoxygenase activity by n-butyrate was accompanied by new synthesis of protein(s). 12-Lipoxygenase activity was not increased so much as 5-lipoxygenase activity by the treatment. This is the first report of stimulation of 5-lipoxygenase activity in cultured cells. The different responses of the two lipoxygenases to n-butyrate treatment strongly suggest that 5-lipoxygenase is a different enzyme from 12-lipoxygenase.

Animals↗
PubMed1980

Morphologic and morphometric analyses of butyrate-induced alterations of rat glioma cells in vitro.

The effect of butyrate on cellular morphologic features and morphometric parameters was examined in vitro with clonal glioma cells of the inbred CD Fischer rat. Untreated cells were multipolar with a high nuclear:cytoplasmic ratio, contained few attenuated rough endoplasmic reticular (RER) and cytoskeletal components in the cytoplasm, and were devoid of junctional complexes. Following exposure to butyrate, the glioma cells appeared epithelioid, and each was characterized by a polygonal cell body with a substantially reduced nuclear:cytoplasmic ratio. In contrast to the coarsely clumped nuclear chromatin of untreated glioma cells, the nuclei of the butyrate-exposed cells consisted of finely dispersed chromatin. The cytoplasm of treated cells contained numerous distended RER packed with proteinaceous material and had an elaborate cyto-skeletal network. Butyrate also induced the development of junctional devices between apposed surface membranes of adjacent cells. The acquisition of these phenotypic traits more characteristic of normal glial cells makes butyrate a potent, naturally occurring reverse transformation agent.

Animals↗
PubMed1981

Differential expression of the globin genes in human leukemia K562(S) cells induced to differentiate by hemin or butyric acid.

Human leukemia K562(S) cells were induced to differentiate by 50 microM hemin or 1.4 mM butyric acid, and the types of hemoglobins synthesized were compared. In both cases, embryonal hemoglobins [Portland, Gower 1, Hb X, and fetal hemoglobin (Hb-F)] were detected. Butyric acid-treated K562(S) cells contained mostly Hb Gower 1 (zeta 2 epsilon 2) and a hemoglobin with the electrophoretic characteristics of Portland (gamma 2 zeta 2). For hemin-treated K562(S), the most abundant hemoglobin synthesized by Hb X (epsilon 2 gamma 2), and the second most abundant was Bart's (gamma 4). Traces of Gower 1 were observed in nontreated K562(S) cells. The kinetics of hemoglobin induction as a result of the two treatments differed; increased hemoglobin synthesis was detected after only 24 hr of hemin treatment, whereas 4 days were required in butyric acid-treated cells. Both hemin and butyric acid were able to induce their respective patterns of hemoglobin synthesis independent of the presence of serum in the K562(S) growth medium. Analysis of the globin chains in induced K562(S) cells induced to differentiate indicated that, with both inducers, adult alpha- but not beta-globin chains were present. Karyotype analysis of K562(S) cells revealed a nearly triploid chromosome complement with a modal number of 68 chromosomes. Three copies of chromosome 11 and four copies of chromosome 16 (coding for the beta-like and alpha-like globin genes, respectively) were present. A large marked chromosome, involving chromosome 7, and a Philadelphia chromosome were also seen. These data characterize the K562(S) subline and also indicate that hemin and butyric acid differ in their effects on the expression of embryonal globin genes.

Butyrates↗
PubMedDate not supplied

Discordant effects of butyrate analogues on erythroleukemia cell proliferation, differentiation and histone deacetylase.

Actions of butyrate and structural analogues on histone deacetylase activity were compared with effects on proliferation and differentiation of erythroleukemia cells. Proliferation was inhibited by 5 mM tert- butylacetate, phenylacetate, phenylbutyrate, 3-bromopropionate and ethyl butyrate without induction of hemoglobin synthesis. n - Butyramide was a stronger inhibitor of cell proliferation and a more effective inducer of hemoglobin synthesis than isobutyramide. The data from combination studies were compatible with butyramide and isobutyramide being weaker agonists that competed for a common site with butyrate. Butyramide and isobutyramide were weaker inhibitors of histone deacetylase than 4-phenylbutyrate and phenylacetate, which in turn were less effective than 3-bromopropionate and butyrate. Butyrate and analogues had similar inhibitory effects on histone deacetylase activity in nuclei from mouse DS19 cells and human K562 cells. Effects on histone deacetylase did not show a consistent correlation with inhibition of cell proliferation or induction of hemoglobin synthesis.

Amides↗
PubMed1998

Alterations in protein-DNA interactions in the gamma-globin gene promoter in response to butyrate therapy.

The mechanisms by which pharmacologic agents stimulate gamma-globin gene expression in beta-globin disorders has not been fully established at the molecular level. In studies described here, nucleated erythroblasts were isolated from patients with beta-globin disorders before and with butyrate therapy, and globin biosynthesis, mRNA, and protein-DNA interactions were examined. Expression of gamma-globin mRNA increased twofold to sixfold above baseline with butyrate therapy in 7 of 8 patients studied. A 15% to 50% increase in gamma-globin protein synthetic levels above baseline gamma globin ratios and a relative decrease in beta-globin biosynthesis were observed in responsive patients. Extensive new in vivo footprints were detected in erythroblasts of responsive patients in four regions of the gamma-globin gene promoter, designated butyrate-response elements gamma 1-4 (BRE-G1-4). Electrophoretic mobility shift assays using BRE-G1 sequences as a probe demonstrated that new binding of two erythroid-specific proteins and one ubiquitous protein, alphaCP2, occurred with treatment in the responsive patients and did not occur in the nonresponder. The BRE-G1 sequence conferred butyrate inducibility in reporter gene assays. These in vivo protein-DNA interactions in human erythroblasts in which gamma-globin gene expression is being altered strongly suggest that nuclear protein binding, including alphaCP2, to the BRE-G1 region of the gamma-globin gene promoter mediates butyrate activity on gamma-globin gene expression.

Adolescent↗
PubMed1990

Dietary butyrate (tributyrin) does not enhance AOM-induced colon tumorigenesis.

Butyrate has induced differentiation in neoplastic cells grown in vitro, among them being colon cancer cell lines. In vivo, only one major study used sodium butyrate in the drinking water and showed an elevation in 1,2-dimethylhydrazine induced colon cancer in rats. Seeking to show that it was the sodium and not the butyrate which was responsible for the enhancement, we fed tributyrin at a 5% level to mice for 48 weeks. Mice experienced normal growth and development at this dose. Analysis of short chain fatty acids in the feces after 6 months in tributyrin feeding showed a 10-fold increase in butyric acid. However no difference in AOM induced focal areas of dysplasia or colonic tumor incidence was observed between tributyrin fed and control mice. At least two conclusions have been reached by this study, (1) that the dietary use of a sodium salt can contribute to the enhancement of chemically induced colon neoplasia and (2) butyrate may be discounted as providing any major therapeutic benefit against colonic tumorigenesis.

Animals↗
PubMed1993

Induction of germ-cell alkaline phosphatase by butyrate and cyclic AMP in BeWo choriocarcinoma cells.

BeWo choriocarcinoma cells synthesize two alkaline phosphatase isoenzymes: germ-cell alkaline phosphatase and tissue-unspecific alkaline phosphatase. We have made use of the differential heat-stabilities of these two isoenzymes to study the induction of germ-cell alkaline phosphatase by sodium butyrate and cyclic AMP (cAMP). Sodium butyrate causes a large induction of germ-cell alkaline phosphatase activity (approx. 35-fold after 96 h) after an initial lag period of 12-24 h. We showed that butyrate increases germ-cell alkaline phosphatase mRNA. Dibutyryl cAMP also induces germ cell alkaline phosphatase (approx. 2.5-fold after 96 h). When optimal concentrations of butyrate and dibutyryl cAMP were added simultaneously to cells, they caused a synergistic induction of activity. This suggested that these compounds use separate mechanisms to induce germ-cell alkaline phosphatase activity and that it is the cAMP moiety of dibutyryl cAMP that induces enzyme activity. This was confirmed by the use of two additional cAMP analogues, 8-(4-chlorophenylthio) cAMP and 8-bromo cAMP, and of two compounds, 3-methyl-1-isobutylxanthine and cholera toxin, which raise the endogenous concentration of cAMP. All four compounds caused a 2-fold increase in enzyme activity. Treatment of cells with 8-(4-chlorophenylthio) cAMP, 8-bromo cAMP and cholera toxin increased germ-cell alkaline phosphatase mRNA between 2- and 7-fold. These data suggest that this alkaline phosphatase isoenzyme is regulated at the level of its mRNA by cAMP, in a manner distinct from that of butyrate.

1-Methyl-3-isobutylxanthine↗
PubMed2002

Randomized comparison of the type 4 phosphodiesterase inhibitor cipamfylline cream, cream vehicle and hydrocortisone 17-butyrate cream for the treatment of atopic dermatitis.

BACKGROUND: Therapeutic options to treat atopic dermatitis are limited. Leukocytes from atopic patients have an abnormally high activity of cyclic adenosine monophosphate (AMP)-phosphodiesterase (PDE), which can be normalized in vitro by PDE inhibitors. Cipamfylline is a new potent and selective inhibitor of PDE-4. OBJECTIVES: To compare the efficacy and safety of up to 14 days' topical treatment with cipamfylline (0.15%) cream with vehicle and with hydrocortisone 17-butyrate (0.1%) cream. PATIENTS AND METHODS: International, multicentre, prospective, randomized double-blind, left-right studies of cipamfylline vs. vehicle and cipamfylline vs. hydrocortisone 17-butyrate in adult patients with stable symmetrical atopic dermatitis on the arms. RESULTS: Both cipamfylline and hydrocortisone 17-butyrate reduced the Total Severity Score significantly (P < 0.001). The reduction with cipamfylline was significantly greater than that with vehicle (difference vehicle-cipamfylline 1.67 95% confidence interval (CI) 1.06, 2.28; P < 0.001) and was significantly less than with hydrocortisone 17-butyrate (difference hydrocortisone-cipamfylline -2.10 95% CI -2.93, -1.27; P < 0.001). Investigator and patient assessments of the overall treatment response showed a similar picture. CONCLUSIONS: Cipamfylline cream is significantly more effective than vehicle, but significantly less effective than hydrocortisone 17-butyrate cream in the treatment of atopic dermatitis.

Administration, Topical↗
PubMed2003

Eumovate (clobetasone butyrate 0.05%) cream: a review of clinical efficacy and safety.

Topical steroid creams and ointments have been available as over-the-counter (OTC) medications for the self treatment of acute dermatitis and other steroid responsive skin disorders for more than ten years. Despite earlier fears, widespread availability and use of these creams is not associated with clinically significant adverse effects. In dermatological practice, hydrocortisone 1% remains the mainstay of treatment for facial eczema, but it is often not effective in eczema affecting other body areas. Eumovate(TM) (clobetasone butyrate 0.05%) cream has recently been made available as a pharmacy medication for the short-term management of acute eczema and allergic dermatitis by adults and children aged 10 or older, based on evidence derived from clinical trials involving over 3500 patients. This review summarises the key efficacy and safety data derived from 29 clinical trials and the post-licensing pharmacovigilance safety information, which supported the reclassification of this product for OTC use. These data show clobetasone butyrate 0.05% is more effective than 1.0% hydrocortisone in the treatment of eczema and more effective than flurandrenolone 0.0125% (p=0.01%) and a potent topical steroid hydrocortisone butyrate (p<0.05), in the treatment of psoriasis. A review of the effect of topical steroids on skin thickness concluded that, following short term application, there was no clinically significant difference between hydrocortisone 1.0% and clobetasone butyrate 0.05% in terms of potential for skin thinning. Similarly, even under extreme conditions, clobetasone butyrate 0.05% has negligible systemic absorption and has almost no effect on HPA axis function.

Acute Disease↗
PubMed1994

Isobutyramide, an orally bioavailable butyrate analogue, stimulates fetal globin gene expression in vitro and in vivo.

Butyrate and other short-chain fatty acids stimulate fetal globin gene expression and have potential for ameliorating the beta globin disorders. Butyrate, however, is rapidly metabolized in vivo and reaches only micromolar concentrations in plasma. We report here that a branched-chain derivative of butyrate, isobutyramide, increases gamma globin gene expression in cultured human erythroid progenitors in vitro and stimulates activity from a minimal gamma globin gene promoter linked to a reporter gene in stable and transient expression assays, with slightly less activity in these in vitro assays than butyrate. In vivo, administration of isobutyramide to anaemic adult baboons rapidly stimulates fetal globin synthesis and F-reticulocyte production. Plasma concentrations at millimolar levels are achieved after a single intravenous or oral dose (500-600 mg/kg), and these concentrations are maintained for 9.5-10.5 h. These results indicate that although isobutyramide has slightly less activity than butyrate in vitro in enhancing fetal globin expression at the cellular and molecular level, its prolonged in vivo half-life may provide superior activity as a therapeutic agent for reactivating fetal globin gene expression in vivo.

Administration, Oral↗
PubMed1991

Screening for corticosteroid contact sensitivity. Comparison of tixocortol pivalate, hydrocortisone-17-butyrate and hydrocortisone.

3 corticosteroids have so far been tried as markers for corticosteroid contact sensitivity: hydrocortisone, tixocortol pivalate and hydrocortisone-17-butyrate. The present study compared these steroids for screening in addition to a standard patch test series. Of 727 patients, 28 (3.9%) reacted to tixocortol pivalate and 10 (1.4%) to hydrocortisone-17-butyrate; hydrocortisone gave an allergic reaction in 2 of 521 (0.4%) patients. Serial dilutions suggested that tixocortol pivalate, not marketed in Finland, caused allergic reactions which could possibly be cross-reactions to hydrocortisone. In contrast to previously published data, frequent cross-reactions occurred with hydrocortisone-17-butyrate and tixocortol pivalate. All allergic reactions to other corticosteroids found by testing with tixocortol pivalate concurred with reactions to hydrocortisone-17-butyrate. The study suggests that the most effective choice for routine testing for corticosteroid contact sensitivity would be both tixocortol pivalate and hydrocortisone-17-butyrate.

Administration, Topical↗