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PubMed1989

Factors responsible for variable reported lineages of HL-60 cells induced to mature with butyric acid.

HL-60 is a multipotential human leukemia cell line widely used as an in vitro model to investigate myeloid differentiation. A variety of compounds can reproducibly induce these cells to differentiate towards specific lineages. However, under what appear to be similar experimental conditions, various laboratories have reported either neutrophilic differentiation or monocytic differentiation after butyric acid induction. We investigated different hypotheses to explain these dissimilar findings. First, the potential role of variable 1,25-dihydroxyvitamin D3 (VD3) concentrations in commercial fetal calf serum was assessed. Second, possible differences between laboratories inherent to the HL-60 cells themselves were explored. Lineage was assessed by morphology, histochemistry (nonspecific esterase), and neutrophil-specific (CD15) and monocyte-specific (MO2) surface antigens. We found that increasing concentrations of VD3 spanning the range reported in commercial fetal calf serum (25 to 155 pg/ml) act in synergy with butyric acid to result in higher monocyte/neutrophil ratios at the higher VD3 concentrations. Different lots of serum led to monocyte/neutrophil ratios in proportion to their VD3 concentrations. Starting with HL-60 cells obtained from different laboratories, several single-cell clones were derived which yielded either high percentages of monocytes, high percentages of neutrophils, or intermediate mixes of both cell types after induction with butyric acid. We conclude that the wide variation of VD3 concentration found in different lots of commercial fetal calf serum and intrinsic differences in HL-60 cells are two identifiable factors that can explain the discrepancies in lineage observed by different investigators after butyric acid induction of HL-60 cells.

Antigens, Differentiation↗
PubMed1985

Effect of n-butyrate on superinfection of Raji lymphoblastoid cell line by Epstein-Barr virus.

The effect of n-butyrate on superinfectability of virus-nonproducer Raji cells by the P3HR-1 strain of Epstein-Barr virus (EBV) was investigated. n-Butyrate is known to be a potent inducer of virus antigen synthesis in virus-producer cell lines and of cell differentiation in virus nonproducers. The drug inhibited the growth of Raji cells but did not interfere markedly with cell viability. It induced a low rate of early antigen (EA) synthesis in about 1-2% of noninfected Raji cells. While the number of superinfectable cells remained relatively constant after treatment with butyrate, an increase in antigen positivity was noted in untreated cells. This relative decrease in sensitivity to superinfection in butyrate-treated Raji cells was more pronounced in cultures that had been treated with the drug for 48 or 72 hr as compared to those treated for 24 hr. A blocking of the treated cells in the certain cell-cycle phase and their drug-induced differentiation towards plasma cells might have been involved in the phenomenon described.

Antigens, Viral↗
PubMed1987

Induction of B-lymphocyte antigens on the chronic myeloid leukemic cell line K562 using sodium butyrate.

Chronic myeloid leukemia (CML) is a disorder arising from a defect in the hemopoietic stem cell. Consequently, the malignant clone can involve all cells within the stem cell's capacity for differentiation, including erythrocytes, granulocytes, monocytes, megakaryocytes, and lymphocytes. Similarly, the K562 cell line, which was derived from a patient with CML, has been shown to be capable of differentiation towards erythrocytes, granulocytes, monocytes, and megakaryocytes, and in this respect may represent a model of the hemopoietic stem cell. However, although K562 shows properties of a myeloid stem cell, no lymphocyte-specific features or differentiation have yet been described. In the present study, K562 cells have been induced to differentiate by culture in the presence of sodium butyrate. The direction and extent of induced differentiation over 12 days were determined with a panel of monoclonal antibodies and with cytochemical stains. This treatment consistently induced expression of pre-B-cell markers, including B-lymphocyte-specific B4 and B1, and of the common acute lymphoblastic leukemia antigen (CALLA), recognized by J5. In addition to the increased expression of B-lymphocyte markers, butyrate induction of K562 resulted in a decrease in granulocyte markers, increases in certain monocyte and platelet markers, and an increase in beta 2 microglobulin expression. Butyrate-induced expression of B-lymphocyte markers was not observed with the myelomonocytic cell line U937. The expression of B-lymphocyte-specific antigens on butyrate-induced K562 may result from the relaxed control of gene expression, but alternatively these observations may indicate the lymphoid-myeloid stem cell nature of K562.

Antibodies, Monoclonal↗
PubMed1988

Evidence for a labile intermediate in the butyrate induced reduction of the level of c-myc RNA in SW837 rectal carcinoma cells.

We have found that the differentiation inducer butyric acid causes the synthesis of a cellular protein(s) that mediates a rapid decline in the level of myc RNA in SW837, a cell line derived from a human adenocarcinoma of the rectum. This effect was dose-dependent and was maximal at 1 mM. Among the short chain fatty acids tested, butyric acid was found to be the most potent. Valeric acid was less effective, and acetic, propionic, isobutyric, and caproic acids did not cause a significant change in myc RNA level. Dimethylsulfoxide, another inducer of differentiation, also caused a marked diminution of myc RNA level, but was only tested at a relatively high dose (282 mM). The reduction in myc RNA level caused by butyrate was blocked by inhibitors of protein synthesis, and was rapidly reversed by removing the inducer. This suggests that butyrate causes the induction of a labile activity that has a negative effect on myc RNA abundance.

Adenocarcinoma↗
PubMed1987

Sodium butyrate stimulates cellular recovery from UV damage in xeroderma pigmentosum cells belonging to complementation group F.

Possible stimulation of the DNA repair capacity by sodium butyrate in normal and xeroderma pigmentosum (XP) cells was investigated. XP cells belonging to the complementation group F showed considerable stimulation of DNA repair by sodium butyrate in terms of both the amount of unscheduled DNA synthesis (UDS) and the colony-forming ability after UV irradiation. UDS in XP cells belonging to the complementation group A was not enhanced, while normal cells showed slight enhancement, but less than that of XP F cells. In XP A, XP C, and normal cells, sodium butyrate treatment enhanced the killing effect of UV irradiation. The residual repair capacity in XP F cells appeared to be stimulated by sodium butyrate.

Butyrates↗
PubMed1988

Molecular analysis of sodium butyrate-induced growth arrest.

Sodium butyrate has been shown to exert dramatic effects on the growth of cells in culture. It inhibits DNA synthesis, arrests actively proliferating cells in G1 and induces differentiation. The mechanism responsible for these various anti-proliferative effects is presently unknown. We wished to study the effects of sodium butyrate on cell growth at the molecular level, by analyzing the pattern of expression exhibited by several growth-associated genes (e.g., c-fos, c-myc, p53 and thymidine kinase) in Swiss 3T3 cells following treatment with sodium butyrate. Our results suggest that sodium butyrate-induced growth arrest of Swiss 3T3 cells (1) can be distinguished at a molecular level from the arrest brought about by other means of growth arrest; (2) does not result from a generalized mechanism which non-specifically shuts down the expression of growth-associated genes but rather occurs via a more specific mechanism which leads to the reduction in the expression of certain genes (e.g., c-myc, p53, thymidine kinase) while inducing the expression of others (e.g., c-fos, aP2); and (3) may involve one or more of the molecular events leading to adipocyte differentiation.

Animals↗
PubMed1988

Transcriptional and posttranscriptional modulation of calcitonin gene expression by sodium n-butyrate in cultured human medullary thyroid carcinoma.

The TT cell line of human medullary thyroid carcinoma produces large quantities of calcitonin (CT) and calcitonin gene-related peptide (CGRP) mRNAs by alternative splicing of a primary CT gene transcript. We have previously shown that the relative levels of these mRNAs depend on the growth stages of the TT cells in culture and that these mRNAs can be increased acutely at the transcriptional level by phorbol esters (12-O-tetradecanoylphorbol-13-acetate) and the cyclic nucleotide, cyclic AMP. We show here that the naturally occurring fatty acid butyrate, unlike 12-O-tetradecanoylphorbol-13-acetate or cyclic AMP, has a delayed stimulatory effect on CT gene transcription, and also can modulate the posttranscriptional processing of RNA from this gene. Treatment of the TT cells with butyrate leads to a 5-fold increase in CT gene transcription after a lag period of 48 h and to a sustained decrease in the calcitonin gene-related peptide to CT mRNA ratio throughout the growth curve of these cells. In addition to its effects on CT gene expression, butyrate also decreases cellular proliferation and c-myc expression in the TT cells. These changes suggest that butyrate induces cultured human medullary thyroid carcinoma cells to acquire in vitro properties more consistent with the differentiated phenotype of the mature thyroid C-cell which is characterized by a low calcitonin gene-related peptide to CT ratio.

Butyrates↗
PubMed1987

The impact of butyric acid on the cardiovascular system.

The influence of sodium salt of butyric acid (C4H7NaO2) on the functional state of the cardiovascular system was studied on 12 guinea-pigs and 15 rabbits by the thermodilution method. The following parameters were determined: cardiac output (CO), arterial blood pressure (AP), total peripheral vascular resistance (TPVR), and in rabbits the heart rate (HR). It was found that butyric acid induces significant changes in TPVR, which correlate with changes in CO and AP. These changes could to a considerable extent be prevented by the administration of indomethacin. Haemodynamic changes induced by butyric acid are primarily connected with changes in vascular tonus, induced by the action of F2 alpha prostaglandins whose synthesis is intensified by the influence of butyric acid.

Animals↗
PubMed1985

Kinetics of Ii synthesis, processing, and turnover in n-butyrate-treated Burkitt's lymphoma cell lines which express or do not express class II antigens and in hairy leukemic cells.

We have sought to understand the role of the electrophoretically invariant chain (Ii) in class II antigen functions, particularly in certain transformed cells in which we have previously demonstrated hyperexpression of Ii. Molecular structures and relative kinetics of Ii synthesis, processing and turnover were compared in paired, Ia+ and Ia- Burkitt's lymphoma (BL) cell lines and in hairy cell leukemia (HCL) cells. Cells were metabolically labeled with [35S] methionine for 15 min (with or without a cold methionine chase to 3 hr) or were continuously labeled for 3 hr. One- and two-dimensional gel electrophoresis resolved immunoprecipitates formed with a) a heteroantiserum to purified class II antigen (demonstrating alpha and beta chains and Ii associated with that complex), b) a heteroantiserum to hairy cell leukemia (HCL) membranes (demonstrating principally the dominant, basic form of Ii molecules, class I antigens, and some additional proteins), and c) a monoclonal antibody to human Ii. Treatment of Ia+ Jijoye and its daughter, Ia- P3HR-1, BL cells with 4 mM butyrate for 48 hr enhanced the synthesis of the dominant, basic form of Ii but did not affect apparent turnover rates of that pool of Ii chains in either cell line. In Ia+ Jijoye cells but not in Ia- P3HR-1 cells Ii was terminally processed to more acidic, sialic acid-derivatized forms. Butyrate treatment did not alter the relative turnover rate of terminally processed Ii in Jijoye cells. The level of the dominant, basic form of Ii in HCL cells equaled that in butyrate-treated Jijoye cells, and relative turnover rates of this terminally unprocessed Ii pool were similar in HCL and Jijoye cells. However, HCL Ia-associated Ii was not terminally processed, as was Ia-associated Ii in Jijoye cells. The expression of Ia auxiliary proteins, p41 and p25, was also enhanced in Jijoye cells by butyrate treatment and was prominent in HCL cells. From these experiments, we may hypothesize the following. In lymphoblastoid cells, two pathways for Ii turnover could exist. One is through association with Ia complexes and progressive terminal processing of carbohydrate side chains and a second is not associated with Ia or, apparently, with such processing. Because Ii is not found to be terminally processed in the absence of class II antigen, Ia might be considered to direct the processing of a subset of Ii towards some function (rather than vice versa).(ABSTRACT TRUNCATED AT 400 WORDS)

Antigens, Differentiation, B-Lymphocyte↗
PubMed1985

13C NMR studies of butyric fermentation in Clostridium kluyveri.

The fermentation of 13C-labeled ethanol and acetate into butyrate and caproate by Clostridium kluyveri has been studied by using 13C NMR. The pathway involves the conversion of both ethanol and acetate into acetyl coenzymes A, two of which condense to form CoA-linked precursors of butyrate. If butyryl-CoA is involved in the condensation, caproate is the ultimate product. ATP is produced from acetyl-CoA via the reactions catalyzed by phosphotransacetylase and acetate kinase with acetate, a required carbon source, as a co-product. In spectra of whole cells incubated with the labeled carbon sources, label from ethanol appears rapidly in acetate, which then reaches a lower, steady-state concentration due to its re-entry into the pathway. The rapid initial production of acetate indicates equally rapid production of ATP. Label from acetate appears in ethanol only if ethanol is already present, indicating that this process is one of isotopic equilibration rather than net synthesis of ethanol from acetate. The ratio of butyrate to caproate produced depends strongly on the initial ratio of ethanol to acetate in the medium. The relative rates of utilization of ethanol and acetate vary as the fermentation proceeds. 13C-13C coupling in the butyrate and caproate produced from [1-13C]ethanol and [2-13C]acetate can be used to determine if the acetyl-CoA molecules arising from ethanol and acetate enter the same pool or if they remain separated. The data are consistent with random mixing of the acetyl-CoA produced from the two carbon sources.

Acetates↗
PubMed1984

[Modulation of alkaline phosphatase by butyrate and prednisolone in uterine cervical cancer cell line (SKG-III)].

The production of late placental alkaline phosphatase (ALP) isoenzyme and the co-presence of a small amount of tissue-unspecific ALP isoenzyme was confirmed in the newly established uterine cervical epidermoid cancer cell line SKG-III. Sodium butyrate (3mM), which has been shown to modulate oncodevelopmental gene expression, was examined after introduction of the agents into confluent cultures. 72 hours after the first sodium butyrate treatment, the amount (per mg cell protein) of total ALP activity increased to 5 times that of control cells and tissue-unspecific insoenzyme occupied about two thirds of the concentration of the modulated ALP. Treatment of SKG-III cells with prednisolone (5 micrograms/ml) for 48 hours caused a 3.5 times increase in total ALP activity, and most of the modulated ALP was occupied by late placental isoenzyme. From these data, it was concluded that sodium butyrate mainly induced tissue-unspecific isoenzyme, while prednisolone induced late placental isoenzyme. The results suggested that SKG-III cells had at least two ALP isoenzyme genes and chemical agents such as sodium butyrate or prednisolone could modulate the ALP isoenzyme profile of these cultured cells in vitro.

Alkaline Phosphatase↗
PubMed1983

Excess rumen product anions in cattle. II. Toxic and lethal effects with butyrate.

Toxicity to butyrate was observed in 100-250 kg male Holstein calves following intravenous injection of 0.7-3.6 mmole/kg body weight, intravenous infusion with 0.12-0.53 mmole/min/kg body weight and intraruminal dosage with 19.4 mmole/kg body weight butyrate. Lower doses produced ataxia and serous nasal discharge. Higher doses produced sudden flaccid paralysis and death from asphyxia. No postmortem lesions, gross or histological, were observed. Plasma K+ was reduced to 2.2-2.5 mEq/L. When infusions were stopped, rapid recovery preceded clearance of butyrate and low K+ remained. Nerve depolarization in the central nervous system may be the cause of the toxic effects. Butyrate acidosis is suggested as a factor in unexplained sudden deaths in ruminants.

Acidosis↗
PubMed1995

Sodium butyrate stimulation of HIV-1 gene expression: a novel mechanism of induction independent of NF-kappa B.

Nuclear factor-kappa B (NF-kappa B) has been shown to play a central role in stimulating human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR)-directed viral gene expression. We have previously described a cell line (TE671/RD) that fails to respond to phorbol myristate acetate (PMA) or tumor necrosis factor-alpha (TNF-alpha) in terms of amplifying HIV-1 LTR-driven gene expression unless it is concurrently treated with sodium butyrate. It was not determined whether this lack of response stemmed from an inability of these cells to produce free NF-kappa B or from ineffectual interaction of this sequence-specific transcriptional factor with its target. We now show that these cells are in fact capable of inducing a free nuclear NF-kappa B-binding activity when stimulated with PMA but not when treated with sodium butyrate alone. Furthermore, we show that sodium butyrate alone is equally potent in stimulating HIV-1 LTR-directed gene expression in latently infected U1 and ACH-2 cells in the absence of induction of nuclear NF-kappa B, as compared with PMA, which induces NF-kappa B activation in these cells. We also show that stimulation of HIV-1 expression in U1 cells with sodium butyrate is not blocked by N-acetylcysteine, whereas that of PMA stimulation is blocked. These observations are discussed in the context of a model where chromatin structure participates in the maintenance of restricted HIV-1 viral gene expression in these cells.

Acetylcysteine↗
PubMed1994

Antagonistic effects of deoxycholic acid and butyrate on epithelial cell proliferation in the proximal and distal human colon.

Colon cancer is a major malignant disease in Western countries where--for unknown reasons--it occurs predominantly in the distal colon. Fecal secondary bile acids are an important risk factor whereas butyrate may be a protective agent. In this in-vitro study biopsies from the normal ascending and sigmoid colon of 24 subjects were incubated with 5 microM DCA (proximal vs. sigmoid colon) or DCA and DCA plus 10 mM butyrate (DCA vs. DCA/BUT, only sigmoid colon) and cell proliferation measured by bromodeoxyuridine immunohistochemistry. Whole crypt labeling index (LI) after DCA-incubation was similar in the ascending (15.4%) and sigmoid colon (15.4%) indicating an equal mucosal response of the two colonic subsites to DCA. Compared to DCA/BUT, incubation with DCA alone resulted in a significantly higher LI for the whole crypt (16.8 vs. 11.4%, p < 0.01) and for the upper 40% of the crypt (4.5 vs. 0.8%, p < 0.01). This may indicate a butyrate-related decrease in the susceptibility for colon cancer. Since luminal concentrations of DCA and butyrate are influenced by dietary interventions the findings of this study may be of particular interest with regard to colon cancer development and prevention.

Butyrates↗
PubMed1993

Differential elimination of synthetic butyric triglycerides in vivo: a pharmacokinetic study.

New butyrate derivatives were synthesized to investigate the residence time of potent butyric acid in vivo. These derivatives were triglycerides in which one, two, or three butyric acid molecules were bound to glycerol or to mono- and dipalmitic esters of glycerol. Pharmacokinetic studies showed that a constant plasma level of each compound was maintained for a long time; all molecules had identical volumes of distribution, but differed about their mean residence time. Triesters in which palmitic acid was present displayed no toxicity and seemed to be even more stable in the organism; this may be due to their adsorption on the tissue. Other triglycerides constituted by butyric acid and various long fatty acids may be synthesized and useful in long-term clinical treatment.

Animals↗
PubMed1994

Treatment of refractory ulcerative proctosigmoiditis with butyrate enemas.

BACKGROUND: It is well established that the colonic mucosa is highly dependent upon the luminal presentation of nutrients. This dependence is most marked in the distal colon. The major luminal nutrients are short chain fatty acids (SCFA) that are produced as a by-product of colonic fermentation of carbohydrates. Butyrate appears to be the SCFA that is most avidly metabolized by the colonic mucosa. It has been suggested that ulcerative colitis (UC) is, at least in part, related to an energy deficiency state of the colonic mucosa which may be secondary to impaired SCFA production, uptake, or utilization. OBJECTIVE: To determine if butyrate enemas are safe and effective in refractory distal UC. METHODS: Ten patients with distal UC, refractory to all other available forms of rectal therapy and to oral sulfasalazine or mesalamine (5-ASA), were treated with nightly butyrate enemas in an open-label study. Enemas consisted of 60 ml of 80 mM sodium butyrate titrated to a pH of 7.0. Patients were assessed clinically and endoscopically at baseline and at 3- to 6-wk intervals, and a disease activity score from 0 to 12 was determined. Response to therapy was determined by changes in the activity score. RESULTS: Six of 10 patients responded to therapy. Four of these six had complete responses. The mean disease activity score of all 10 patients fell from 8.0 +/- 2.4 (mean +/- SD) to 4.3 +/- 4.1 at the end of follow-up. Response to therapy could not be predicted based on any of the baseline characteristics analyzed. CONCLUSIONS: In this open-label study, patients with distal UC who were refractory to all previous therapy had a 40% complete response rate and an overall 60% response rate. Controlled studies of this promising therapy are indicated.

Adult↗
PubMed1993

Sodium butyrate causes an increase in the block to transcriptional elongation in the c-myc gene in SW837 rectal carcinoma cells.

Elevated expression of the c-myc oncogene is a frequent finding in tumors and cell lines derived from carcinomas of the colon and rectum. In a previous study we demonstrated that the differentiation agent sodium butyrate causes a rapid reduction in the expression of c-myc RNA in the rectal carcinoma cell line SW837. This effect was blocked by inhibitors of protein synthesis, suggesting that butyrate causes the induction of an activity that has a negative effect on c-myc expression. In the present work we demonstrate that the rapid decrease in the level of c-myc RNA, upon treatment of SW837 cells with 2 mM butyrate, is followed by a slower decrease in the level of p53 RNA and an increase in the RNA levels for fibronectin and a placental type alkaline phosphatase. Using in vitro elongation of nascent transcripts to measure transcription and actinomycin D chase experiments to measure RNA stability, we show that the reduction in expression of c-myc RNA is due to an increase in the block to transcriptional elongation, rather than a decrease in transcriptional initiation or an increase in degradation of the RNA. We conclude that sodium butyrate induces an activity that increases the transcriptional block in SW837 cells, and that regulation of transcriptional elongation is an important mechanism for regulating c-myc expression in this cell type. A shift in relative usage of the two major promoters in the c-myc gene accompanies the reduction in expression. The potential significance of this finding with respect to transcriptional elongation is discussed. Mutations in the exon 1/intron 1 boundary region of the c-myc gene cause an increase in transcriptional elongation in Burkitt lymphoma. We sequenced this region in a series of cell lines derived from colorectal carcinomas, all of which had an elevated level of c-myc expression, to determine if a similar mutational mechanism is at work in this disease. All of the lines examined had a normal c-myc DNA sequence, suggesting that the deregulation of c-myc expression in colon cancer is not due to a cis mutation in this region.

Antisense Elements (Genetics)↗
PubMed1995

[Isolation and reassociation of acetogen and methanogen in a syntrophobic coculture degrading butyrate anaerobically].

Anaerobic coculture BF2 which degraded butyrate into acetate and produced methane was isolated from granular methanogenic sludge. The coculture is associated syntrophically the Syntrophomonas subsp. saponavida strain CF2 with Methanobacterium formicicum strain MF2 and appeared to degraded C4 approximately C18 fatty acids including isobutyrate. The optimal temperature and pH for growth was 37 degrees C and 7.7 respectively. The strain CF2 was obtained in pure culture with crotonate as substrate and produces acetate and butyrate. The doubling time of strain CF2 in crotonate media was about 20 hours. Strain CF2 is Gram negative, slightly curved 0.2 approximately 0.3 x 2.0 approximately 3.0 micron with round ends, motile by lateral flagellation at the concave side, non sporeforming. With a hydrogen scavenging organism, such as Methanospillum hungatei JF1, Methanobacterium formicicum 1535, Methanobrevibacterium bryantii 1125 and Desulfovibrio sp. B11, the strain CF2 paired up and the defined coculture degraded butyrate to acetate. When the strain CF2 associated with the original accompanist, Methanobacterium formicius strain MF2, the reassociated couculture degraded butyrate to acetate and produced methane again.

Butyrates↗