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PubMed2000

The response of Culex quinquefasciatus (Diptera: culicidae) to traps baited with carbon dioxide, 1-octen-3-ol, acetone, butyric acid and human foot odour in Tanzania.

The responses of Culex quinquefasciatus Say to traps baited with carbon dioxide, 1-octen-3-ol, acetone, butyric acid and human foot odour were studied in the field in Muheza, north-east Tanzania using Counterflow Geometry (CFG) and Centers for Disease Control (CDC) traps. It was found that significantly more C. quinquefasciatus responded to foot odour collected on nylon stockings than to clean nylon stockings (P < 0.05). Significantly more mosquitoes were caught in a CFG trap baited with carbon dioxide than in traps with either human foot odour, acetone or butyric acid. It was also found that in an outdoor situation a carbon dioxide baited CDC unlit trap collected over 12 times more C. quinquefasciatus than an unbaited CDC unlit trap and nine times more mosquitoes than CDC traps baited with 1-octen-3-ol alone (P < 0.05). The number of mosquitoes caught in a CDC trap baited with 1-octen-3-ol did not differ significantly from that of the unbaited CDC trap (P > 0.05). These results indicate that the Afrotropical C. quinquefasciatus respond significantly better to traps baited with carbon dioxide than to either octenol, acetone or butyric acid, and that human foot odour contains stimuli to which C. quinquefasciatus is attracted under field conditions.

Acetone↗
PubMed2005

Inhibition of biohydrogen production by undissociated acetic and butyric acids.

Glucose fermentation to hydrogen results in the production of acetic and butyric acids. The inhibitory effect of these acids on hydrogen yield was examined by either adding these acids into the feed of continuous flow reactors (external acids), or by increasing glucose concentrations to increase the concentrations of acids produced by the bacteria (self-produced). Acids added to the feed at a concentration of 25 mM decreased H2 yields by 13% (acetic) and 22% (butyric), and 60 mM (pH 5.0) of either acid decreased H2 production by >93% (undissociated acid concentrations). H2 yields were constant at 2.0 +/- 0.2 mol H2/mol glucose for an influent glucose concentration of 10-30 g/L. At 40 g glucose/L, H2 yields decreased to 1.6 +/- 0.1 mol H2/mol glucose, and a switch to solventogenesis occurred. A total undissociated acid concentration of 19 mM (self-produced acids) was found to be a threshold concentration for significantly decreasing H2 yields and initiating solventogenesis. Hydrogen yields were inhibited more by self-produced acids (produced at high glucose feed concentrations) than by similar concentrations of externally added acids (lower glucose feed concentrations). These results show the reason hydrogen yields can be maximized by using lower glucose feed concentrations is that the concentrations of self-produced volatile acids (particularly butyric acid) are minimized.

Acetates↗
PubMed1992

Novel anticancer prodrugs of butyric acid. 2.

The antitumor activity of novel prodrugs butyric acid was examined. The in vitro effect of the compounds on induction of cytodifferentiation and on inhibition of proliferation and clonogenicity showed that (pivaloyloxy)methyl butyrate (1a) (labeled AN-9) was the most active agent. SAR's suggested that its activity stemmed from hydrolytically released butyric acid. In vivo, 1a displayed antitumor activity in B16F0 melanoma primary cancer model, manifested by a significant increase in the life span of the treated animals. Murine lung tumor burden, induced by injection of the highly metastatic melanoma cells (B16F10.9), was decreased by 1a. It also displayed a significant therapeutic activity against spontaneous metastases which were induced by 3LL Lewis lung carcinoma cells. Moreover, 1a has the advantage of low toxicity, with an acute LD50 = 1.36 +/- 0.1 g/kg (n = 5). These results suggest that 1a is a potential antineoplastic agent.

Animals↗
PubMed2005

The role of intracellularly released formaldehyde and butyric acid in the anticancer activity of acyloxyalkyl esters.

Previous studies described a family of anticancer histone deacetylase inhibitor prodrugs of formula Me(CH(2))(2)COOCH(R)OR(1), which upon intracellular hydrolysis release acids and aldehydes. This study examines the mechanisms by which the prodrugs affect tumor cells and the contribution of the released aldehyde (formaldehyde or acetaldehyde) and acids to their anticancer activity. Type I prodrugs release 2 equiv of a carboxylic acid and 1 equiv of an aldehyde, and of Type II release 2 equiv of acids and 2 equiv of an aldehyde. SAR studied inhibition of proliferation, induction of differentiation and apoptosis, histone acetylation, and gene expression. Formaldehyde, measured intracellularly, was the dominant factor affecting proliferation and cell death. Among the released acids, butyric acid elicited the greatest antiproliferative activity, but the nature of the acid had minor impact on proliferation. In HL-60 cells, formaldehyde-releasing prodrugs significantly increased apoptosis. The prodrugs affected to a similar extent the wild-type HL-60 and MES-SA cell lines and their multidrug-resistant HL-60/MX2 and MES-Dx5 subclones. In a cell-free histone deacetylase (HDAC) inhibition-assay only butyric acid inhibited HDAC activity. The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism.

Acetaldehyde↗
PubMed2000

Novel mutual prodrug of retinoic and butyric acids with enhanced anticancer activity.

Acyloxylalkyl esters of retinoic acid and small carboxylic acids (C3-5) were evaluated for anticancer activity. The derivative of butyric acid (BA) and all-trans-retinoic acid (ATRA)-retinoyloxymethyl butyrate (RN1)-acting as a mutual prodrug was a more potent inducer of cancer cell differentiation and inhibitor of proliferation than the parent acids. ED50 of RN1 for differentiation induction in HL-60 was over 40-fold lower than that of ATRA. The differentiating activity of ATRA compared to that of the acyloxylalkyl esters derived from butyric (RN1), propionic (RN2), isobutyric (RN3), and pivalic (RN4) acids was found to be: RN1 > RN2 > RN3 > ATRA approximately RN4. This observation implies that the activity of the prodrugs depends on the specific acyl fragment attached to the retinoyl moiety, and the butyroyl fragment conferred the highest potency. The IC50 values for inhibition of Lewis lung (3LLD122) and pancreatic (PaCa2) carcinoma cell line colony formation elicited by RN1 were significantly higher than those of ATRA. In addition to its superiority over ATRA or BA as growth inhibitors of the above cell lines, RN1 was also able to overcome the resistance to ATRA in 3LLD122 cells.

Antineoplastic Agents↗
PubMed2004

Hyaluronic-acid butyric esters as promising antineoplastic agents in human lung carcinoma: a preclinical study.

New promising compounds, derived from the esterification of hyaluronic acid with butyric acid, were investigated in vitro on a non-small cell lung carcinoma cell line (NCI-H460) and an its metastatic subclone (NCI-H460M). All new compounds exerted a dose-dependent inhibitory effect on both cell lines, which expressed CD44, the specific surface receptor for hyaluronic acid, in a very high percentage of cells (90%). HE1, the most effective of these compounds, was 10-fold more effective than sodium butyrate (NaB) in inhibiting cell proliferation. Similarly to NaB, after 24 hours of treatment, HE1 affected the expression of three cell cycle-related proteins (p27(kip1), p53 and p21(waf1)) responsible for growth arrest, indicating that the presence of the hyaluronic acid backbone does not interfere with the biologic activity. Intratumoral treatment with HE1 demonstrated a marked efficacy on primary tumor growth and on lung metastases formation of the murine Lewis Lung Carcinoma model. Altogether, present findings suggest a possible clinical application of these novel butyric pro-drugs in primary and metastatic lung cancer.

Animals↗
PubMed2001

Epstein--Barr virus post-transplant lymphoproliferative disease and virus-specific therapy: pharmacological re-activation of viral target genes with arginine butyrate.

Lymphoproliferative disorders associated with the Epstein-Barr virus (EBV) include non-Hodgkin's lymphoma, Hodgkin's lymphoma, and "post-transplant lymphoproliferative disorders" (PTLD), which occur with immunosuppression after marrow and organ transplantation. PTLD is characterized by actively proliferating, latently infected EBV(+) B-lymphocytes, and often manifests a rapidly progressive fatal clinical course if the immunosuppression cannot be reversed. Lung transplant recipients are a subset of patients at special risk for developing PTLD. The incidence of PTLD development in these patients has been estimated at 5--10%. Whereas immunologic and antiviral therapy have been moderately effective for treating EBV-associated infections in the lytic phase, they have been less useful in the more common latent phase of the disease. One common treatment for herpesvirus infections has targeted the virus-specific enzyme thymidine kinase (TK). The lack of viral TK expression in EBV(+) tumor cells, due to viral latency, makes anti-viral therapy alone ineffective as an anti-neoplastic therapy, however. We have developed a strategy for the treatment of EBV-associated lymphomas/PTLD using pharmacologic induction of the latent viral TK gene and enzyme in the tumor cells, followed by treatment with ganciclovir. Arginine butyrate selectively activates the EBV TK gene in latently EBV-infected human lymphoid cells and tumor cells. A Phase I/II trial has been initiated, employing an intra-patient dose escalation of arginine butyrate combined with ganciclovir. In six patients with EBV-associated lymphomas or PTLD, all of which were resistant to conventional radiation and/or chemotherapy, this combination produced complete clinical responses in four of six patients, with a partial response occurring in a fifth patient. Pathologic examination in two of three patients demonstrated complete necrosis of the EBV lymphoma, with no residual disease, following a single three-week course of the combination therapy. Possible side-effects of the therapy included nausea and reversible lethargy at the highest doses. One patient suffered acute liver failure, thought to be secondary to release of FasL from the necrotic tumor. Analysis of patient-derived tumor cells in culture demonstrated that arginine butyrate produced selective induction of the EBV TK gene, which then conferred sensitivity to ganciclovir, resulting in tumor apoptosis. Additional patient accrual is sought for further evaluation of this therapy.

Antineoplastic Agents↗
PubMed1977

The actions of cyclic AMP, its butyryl derivatives and Na butyrate on the proliferation of malignant trophoblast cells in vitro.

Cyclic AMP, and its derivatives N6-monobutyryl cyclic AMP and dibutyryl cyclic AMP, have been found to inhibit the proliferation of trophoblast cells of the BeWo cell line in vitro. Sodium butyrate (1 mM), a possible degradation product of the butyrate derivatives, also inhibited cell proliferation, giving similar growth rates to equimolar dibutyryl cyclic AMP. The inhibition by butyrate was however, not sufficient to account for the action of 1 mM N6-monobutyryl cycli AMP, which, like cyclic AMP, completely inhibited cell proliferation. The potency, specificity and toxicity of the substances were compared. The results suggest different modes of action for cyclic AMP and dibutyryl cyclic AMP.

Bucladesine↗
PubMed1999

Sodium butyrate enhances STAT 1 expression in PLC/PRF/5 hepatoma cells and augments their responsiveness to interferon-alpha.

Although interferon-alpha (IFN-alpha) has shown great promise in the treatment of chronic viral hepatitis, the anti-tumour effect of this agent in the therapy of liver cancer is unclear. Recent studies have demonstrated that differentiation-inducing agents could modulate the responsiveness of cancer cells to IFN-alpha by regulating the expression of signal transducers and activators of transcription (STAT) proteins, a group of transcription factors which play important roles in the IFN signalling pathway. We have reported that sodium butyrate is a potent differentiation inducer for human hepatoma cells. In this study, we investigated whether this drug could regulate the expression of STAT proteins and enhance the anti-tumour effect of IFN-alpha in hepatoma cells. We found that sodium butyrate specifically activated STAT1 gene expression and enhanced IFN-alpha-induced phosphorylation and activation of STAT1 proteins. Co-treatment with these two drugs led to G1 growth arrest, accompanied by down-regulation of cyclin D1 and up-regulation of p21WAF-1, and accumulation of hypophosphorylated retinoblastoma protein in hepatoma cells. Additionally, internucleosomal DNA fragmentation, a biological hallmark of apoptosis, was detected in hepatoma cells after continuous incubation with a combination of these two drugs for 72 h. Our results show that sodium butyrate potently enhances the anti-tumour effect of IFN-alpha in vitro and suggest that a rational combination of these two drugs may be useful for the treatment of liver cancer.

Antineoplastic Agents↗
PubMed1998

Sodium butyrate induces apoptosis and accumulation of ubiquitinated proteins in human breast carcinoma cells.

To investigate the possible relationship between apoptosis and the ubiquitin pathway we examined the patterns of ubiquitinated proteins in the human breast carcinoma MCF-7 cell line following induction of apoptotic death by sodium butyrate. Apoptosis in these cells was associated with internucleosomal DNA fragmentation and proteolytic cleavage of poly(ADP-ribose) polymerase. By dual in situ antiubiquitin immunofluorescence and chromatin DNA staining, we demonstrated that ubiquitin fluorescence was increased specifically in cells that underwent sodium butyrate-mediated apoptosis. The extent of ubiquitin incorporation into protein conjugates was examined in both adherent (not yet apoptotic) and floating (apoptotic) cell populations. We found that apoptotic cells exhibited enhanced intensity of ubiquitin-immunoreactive conjugates, whereas adherent cells did not. In addition, two-dimensional immunoblot analysis of proteins from apoptotic cells identified a set of isomeric ubiquitinated conjugates located at a pI range of 4. 2 - 4.6 and a Mr approximately of 30 kDa. These data indicate that the ubiquitin pathway may play a role in the sodium butyrate-induced apoptotic program in breast carcinoma cells.

Apoptosis↗
PubMed1967

The gas-liquid chromatography of carboxylic acid esters of the urinary 11-deoxy-17-oxo steroids. Determination as n-butyrates.

1. The gas-liquid-chromatographic separations of the acetate, propionate, n-butyrate, isobutyrate and n-valerate esters of androsterone, aetiocholanolone and dehydroepiandrosterone were studied on a 1% neopentyl glycol sebacate column. The n-butyrate, isobutyrate and n-valerate esters were well resolved. 2. The three steroids derived from hydrolysed urinary 17-oxo steroid conjugate extracts were analysed by gas-liquid chromatography after conversion into their n-butyrate esters. The results were compared with independent determinations involving chromatography on alumina.

17-Ketosteroids↗
PubMed1972

Ketogenesis from butyrate and acetate by the caecum and the colon of rabbits.

1. When studied in vitro, tissue from the caecum and the proximal colon of rabbits converted butyrate into ketone bodies. The conversion was similar to that observed with liver slices. The ketogenic activity was associated with the mucosa rather than the muscle of the gut wall and, in the colon, diminished as the distance from the caecal-colonic junction increased. 2. Tissue from the wall of the ileum, caecum, proximal colon and distal colon was also shown to metabolize [1-(14)C]butyrate to carbon dioxide. 3. Enzyme assays showed that in both liver tissue and caecal mucosa the activity of hydroxymethylglutaryl-CoA synthase was more than ten times that of acetoacetyl-CoA deacylase. Labelling experiments in vitro gave confirmation of the hydroxymethylglutaryl-CoA pathway. 4. The significance of the conversion of butyrate into ketone bodies is discussed.

Acetates↗
PubMedDate not supplied

Protozoa involved in butyric rather than lactic fermentative pattern during latent acidosis in sheep.

We used six ruminally cannulated Texel wethers to study the relative role of protozoa and lactate-metabolizing bacteria in ruminal fermentative patterns during an induced latent acidosis. The sheep were fed an alfalfa hay diet (H) and latent acidosis was induced, following a short transition period of one week, with a grain-rich acidotic diet (W, 60% wheat + 40% alfalfa hay). Ruminal pH, ruminal volatile fatty acids (VFA), lactate and NH3 concentrations, protozoa and lactate-utilizing bacterial counts, the relative proportions of three main bacteria implicated in lactate metabolism (a lactate-producing species, Streptococcus bovis, and two lactate-utilizing species, Selenomonas ruminantium, and Megasphaera elsdenii) using specific 16S-rRNA-targeting oligonucleotide probes, and lactate dehydrogenase (LDH) activity were determined for both diets. The pH parameters (mean, minimum, maximum, time and area under pH 6.0 and 5.5) measured with the W diet were indicative of a latent (i.e., subacute and maintained) acidosis. However, a butyric rather than lactic latent acidosis was observed in this study. Total ruminal lactate concentration remained at low levels with the acidotic diet (< 4 mmol x L(-1)), but changes were observed in VFA composition, which was oriented towards butyrate at the expense of acetate (P < 0.05), while propionate remained constant. In agreement with the low ruminal lactate concentration, no changes in the proportion of S. bovis 16S-rRNA were observed. The lactate-metabolizing bacterial population also remained fairly constant in number, proportion and activity. The increase in butyrate concentration was accompanied by a proliferation of entodiniomorphs (P < 0.01). These results suggest that the protozoa limited lactate accumulation and possibly also the decrease in pH during latent acidosis. Experiments with defaunated and faunated sheep could provide further evidence of the role of protozoa in the development of rumen latent acidosis.

Acidosis↗
PubMed2003

Biochemical effect of intravenous arginine butyrate in X-linked adrenoleukodystrophy.

OBJECTIVES: To determine the biochemical and clinical effects of intravenous arginine butyrate in X-linked Adrenoleukodystrophy (X-ALD). STUDY DESIGN: Arginine butyrate was intravenously infused over a 4-month period in a patient with the rapid cerebral form of X-ALD. Very long chain fatty acids (VLCFA), complete blood counts, and serum chemistries were monitored, and serial MRI of the brain and clinical neurologic examinations were performed. RESULTS: All blood chemical and hematologic values remained within the normal range for age throughout the therapy. After completion of the first day of infusion, the C 26:0 value fell from 1.01 microg/mL to 0.445 microg/mL, which is below the mean value for an X-ALD heterozygote. Throughout the remainder of the trial, all C26:0 levels fell below the mean -1 SD for X-ALD hemizygotes (mean, 1.18 microg/mL, 1 SD = 0.53), ranging from 0.321 to 0.565 microg/mL. Despite reduction of the plasma VLCFA, the patient continued to deteriorate neurologically. CONCLUSIONS: Intravenous arginine butyrate resulted in a rapid decrease in plasma VLCFA but no effect on the neurologic progression of the disease in this patient. Additional studies are needed to determine minimum effective dosage and interval, what proportion of patients respond, and whether the agent can prevent neurologic degeneration.

Adrenoleukodystrophy↗
PubMed1981

Enhanced phosphorylation of high-mobility-group proteins in nuclease-sensitive mononucleosomes from butyrate-treated HeLa cells.

The protein composition of nucleosome fractions differing in their sensitivity to micrococcal nuclease and derived from butyrate-treated or untreated HeLa cells has been compared. Most of the high-mobility-group-14 (HMG-14) and HMG-17 content of HeLa cell chromatin is associated with those nucleosomes that are preferentially sensitive to micrococcal nuclease. Furthermore, electrophoresis of these two HMG proteins from the transcriptionally active chromatin fraction MN1 of butyrate-treated cells resolves them into a series of bands. The multiple band pattern of HMG-14 and -17 from butyrate-treated cells results from hyperphosphorylation rather than hyperacetylation. Phosphorylation of these two small nonhistone proteins may play some role in the modulation of the structure of transcriptionally active chromatin.

Acetylation↗
PubMed2000

B-ind1, a novel mediator of Rac1 signaling cloned from sodium butyrate-treated fibroblasts.

Sodium butyrate is a multifunctional agent known to inhibit cell proliferation and to induce differentiation by modulating transcription. We have performed differential display analysis to identify transcriptional targets of sodium butyrate in Balb/c BP-A31 mouse fibroblasts. A novel butyrate-induced transcript B-ind1 has been cloned by this approach. The human homologue of this transcript contains an open reading frame that codes for a protein of 370 amino acids without known functional motifs. In transfected cells, the B-ind1 protein has been found to potentiate different effects of the small GTPase Rac1, such as c-Jun N-terminal kinase activation and transcriptional activity of nuclear factor kappaB (NF-kappaB). In addition, we have demonstrated that B-ind1 forms complexes with the constitutively activated Rac1 protein. To investigate the role of B-ind1 in Rac1 signaling, we have constructed several deletion mutants of B-ind1 and tested their ability to affect the activation of NF-kappaB by Rac1. Interestingly, the fragment encoding the median region of human B-ind1 acted as a dominant-negative variant to block Rac1-mediated NF-kappaB activity. These data define B-ind1 as a novel component of Rac1-signaling pathways leading to the modulation of gene expression.

Animals↗
PubMed2002

Novel mode of interference with nuclear factor of activated T-cells regulation in T-cells by the bacterial metabolite n-butyrate.

The transcription factor nuclear factor of activated T-cells (NF-AT) plays an essential role in the activation of many early immune response genes. A dynamic equilibrium between calcineurin and cellular kinases controls its phosphorylation and thus regulates its activity by determining its subcellular localization. Here, we demonstrate that T-cell activation in the presence of the bacterial metabolite n-butyrate, which leads to inhibition of interleukin-2 transcription, is characterized by the maintenance of the activity of counter-regulatory kinases glycogen synthase kinase 3 and protein kinase A as well as persistence of intracellular cAMP levels, whereas calcium response and mitogen-activated protein kinase activation were indistinguishable from cells stimulated in the absence of n-butyrate. Nuclear binding of NF-AT was decreased but other transcription factors implicated in interleukin-2 expression such as AP1 and nuclear factor kappaB were unaffected. The effect on NF-AT binding appeared to be the result of increased nuclear export because the export inhibitor leptomycin B completely restored nuclear binding of NF-AT. We, therefore, provide first evidence for interference with NF-AT regulation alternative to the currently understood inhibition of nuclear import. This mechanism might represent a bacterial strategy to subvert host defense, which could be of particular clinical importance in the gastrointestinal tract where high amounts of n-butyrate are physiologically present.

Butyrates↗
PubMed2006

Butyrylated starch is less susceptible to enzymic hydrolysis and increases large-bowel butyrate more than high-amylose maize starch in the rat.

Large-bowel fermentation of resistant starch produces SCFA that are believed to be important in maintaining visceral function. High-amylose maize starch (HAMS) and acylated starches are sources of resistant starch and are an effective means of increasing colonic SCFA. Cooking increases digestibility of starches but its effects on the capacity of these starches to raise large-bowel SCFA are unknown. We have examined the effects of cooking of HAMS and butyrylated HAMS (HAMSB) on amylolysis in vitro and their capacity to raise caeco-colonic SCFA in rats. The starches were boiled in excess water and microwaved, followed by drying at 100 degrees C. Cooking increased in vitro glucose release for both starches but significantly less from HAMSB. Rat growth rates were unaffected when fed cooked resistant starch. Digesta pH was increased in the caecum and proximal colon of rats fed cooked HAMS. Distal colonic pH was highest in rats fed cooked HAMSB. Factorial analyses (2x2) of caecal SCFA pools showed significant differences between HAMS and HAMSB, and that cooking significantly lowered caecal butyrate pools. Portal venous butyrate concentrations were higher in both HAMSB groups than those fed HAMS. The data suggest that HAMSB is less susceptible to in vitro amylolysis than HAMS following cooking and delivers more butyrate to rat caecum than HAMS. This attribute may be useful in food applications for specific delivery of SCFA to the colon. Preparation of carbohydrates to simulate human food in animal experiments may be important to assess nutritional and physiological effects accurately.

Amylose↗