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At least 1,225 records · Page 68Linked to original sources
PubMed1996

Antibodies to butyrate-inducible antigens of Kaposi's sarcoma-associated herpesvirus in patients with HIV-1 infection.

BACKGROUND: The recent identification in patients with Kaposi's sarcoma of DNA sequences with homology to gammaherpesviruses has led to the hypothesis that a newly identified virus, Kaposi's sarcoma-associated herpeslike virus (KSHV), has a role in the pathogenesis of Kaposi's sarcoma. We developed serologic markers for KSHV infection. METHODS: KSHV antigens were prepared from a cell line (BC-1) that contains the genomes of both KSHV and the Epstein-Barr virus (EBV). We used immunoblot and immunofluorescence assays to examine serum samples from 102 patients with human immunodeficiency virus type 1 (HIV-1) infection for antibodies to KSHV-associated proteins and to distinguish these antibodies from antibodies to EBV antigens. A positive serologic response was defined by the recognition of an antigenic polypeptide, p40, in n-butyrate-treated BC-1 cells and by the absence of p40 recognition in untreated BC-1 cells or EBV-infected, KSHV-negative cells. The detection by the immunofluorescence assay of 10 to 20 times more antigen-positive cells in n-butyrate-treated BC-1 cells than in untreated cells was considered a positive response. RESULTS: Antibodies to the p40 antigen expressed by chemically treated BC-1 cells were identified in 32 of 48 HIV-1-infected patients with Kaposi's sarcoma (67 percent), as compared with only 7 of 54 HIV-1-infected patients without Kaposi's sarcoma (13 percent). These results were confirmed by an immunofluorescence assay. The positive predictive value of the serologic tests for Kaposi's sarcoma was 82 percent, and the negative predictive value 75 percent. CONCLUSIONS: The presence of antibodies to a KSHV antigenic peptide correlates with the presence of Kaposi's sarcoma in a high-risk population and provides further evidence of an etiologic role for KSHV.

Antibodies, Viral↗
PubMed1988

Butyrate infusions in the ovine fetus delay the biologic clock for globin gene switching.

The switch from fetal to adult hemoglobin expression is regulated in many mammalian species by a developmental clock-like mechanism and determined by the gestational age of the fetus. Prolonging fetal globin gene expression is of considerable interest for therapeutic potential in diseases caused by abnormal beta-globin genes. Butyric acid, which is found in increased plasma concentrations in infants of diabetic mothers who have delayed globin gene switching, was infused into catheterized fetal lambs in utero during the time of the normal globin gene switch period. The globin gene switch was significantly delayed in three of four butyrate-treated fetuses compared with controls and was entirely prevented in one fetus in whom the infusion was begun before the globin switch was under way. These data provide a model for investigating and arresting the biologic clock of hemoglobin switching.

Animals↗
PubMed1995

Sodium butyrate inhibits c-myc splicing and interferes with signal transduction in ovarian carcinoma cells.

Sodium butyrate (NaB), a physiologically produced short chain fatty acid, dramatically changes the growth rate and also the morphology of a fast growing subclone (N.1) derived from the heterogenous human ovarian carcinoma HOC-7. The mRNA of the growth related proto-oncogene c-myc, constitutively expressed in N.1 cells decreased significantly within 24 h of NaB treatment and remained suppressed until the NaB block was released. Down-regulation was accomplished partially by accelerating degradation of c-myc mRNA and by inhibiting splicing of c-myc transcripts. We demonstrated that NaB blocked general mechanisms in signal transduction, such as the release of Ca2+ from intracellular stores, and modulated the activity of serine/threonine kinases. The multiple effects of sodium butyrate on HOC-7 derivatives, as well as on a variety of other cell types investigated by others, may be due to interference with general mechanisms of signal transduction.

Adenocarcinoma↗
PubMed1983

Expression of recombinant plasmids in mammalian cells is enhanced by sodium butyrate.

We have studied the effects of sodium butyrate on DNA-mediated gene transfer in an effort to investigate interrelationships between chromatin structure and expression of recombinant plasmids. Our results demonstrate that butyrate affects the early stages of gene activity following DNA uptake at least two levels. First, the number of cells able to express foreign DNA increases from 10% to up to 40%. Second, there is an increase in enhancer-dependent transcription, approximately 30 fold in HeLa cells, involving the SV40 early promoter. Stable transformation efficiencies increase to 4% and 10% in HeLa S3 and monkey kidney CV-1 cells, respectively. Finally, expression of integrated recombinant plasmid genes is reinducible by a second treatment five weeks after initial exposure to this agent.

Butyrates↗
PubMed1981

The extent of histone acetylation induced by butyrate and the turnover of acetyl groups depend on the nature of the cell line.

Cells possessing widely different physiological and morphological features have been treated with substances known to stimulate the differentiation of erythroleukemia cells. Only short fatty acids are capable of causing a hyperacetylation of the core histones and of enhancing the level of an H1-like protein in Chinese hamster ovary cells. While the time courses of a butyrate-mediated acetylation are similar for all cells, the maximum histone acetyl contents are much higher for the transformed cell of a given type. A withdrawal of butyrate rapidly (within 45 min) gives rise to a 'hypoacetylated state' for fibroblasts and transformed fibroblast (epithelial) cells from which there is a slow recovery. Lymphoid cells, on the other hand, display a marked persistance of the highly acetylated forms of histone H4.

Acetylation↗
PubMed1998

Diagnosis of diabetes mellitus in a bull by means of butyrate infusion.

A 9-month-old bull was presented with a history of runting and glucosuria. The bull showed major signs of diabetes mellitus, such as polyuria, polydipsia, polyphagia, emaciation, glucosuria, and ketonuria, but persistent hyperglycemia was missing. Because in an intravenous glucose tolerance test glucose disappearance was only insignificantly more rapid in a non-diabetic age-matched control than in the diabetic bull a butyrate-stimulated insulin response test was performed. Insulin response to butyrate infusion was markedly impaired in the diabetic bull compared with the non-diabetic bull. At necropsy hepatic cirrhosis was noticed and suggestive signs for diabetes mellitus were seen in liver and kidneys.

Animals↗
PubMed1983

Inhibitory effect of cerulenin and sodium butyrate on germination of Candida albicans.

Candida albicans germination in liquid medium was inhibition by the antilipogenic agent cerulenin and the fatty acid sodium butyrate. Although these inhibitors prevented germ tube emergence at concentrations of 1 microgram/ml and 20 mM, respectively, neither significantly affected cell viability as judged by trypan blue staining or the rate of protein biosynthesis throughout the time course of the experiments. Cerulenin treatment resulted in inhibition of lipid biosynthesis, but lipid biosynthetic capabilities remained unaltered in sodium butyrate-supplemented cultures. Because each inhibitor blocks germination by different mechanisms, their utility in distinguishing events directly correlated to germination was examined. In this context, chitin synthase activity was inhibited by both compounds, confirming the importance of chitin biosynthesis in C. albicans germination.

Antifungal Agents↗
PubMed1990

Transcriptional activation of the adenine phosphoribosyltransferase promoter by an upstream butyrate-induced Moloney murine sarcoma virus enhancer-promoter element.

It has been documented that the activity of a specific promoter can be occluded by the presence of another promoter element upstream. We present evidence for a phenomenon contradictory to that predicted by the promoter occlusion theory. Transcription from the hamster aprt (adenine phosphoribosyltransferase) promoter was augmented instead of repressed in transfected mouse L cells when an upstream Moloney murine sarcoma virus enhancer-promoter element was induced with butyrate. Without an adjacent Moloney murine sarcoma virus element, butyrate could not activate the aprt promoter.

Adenine Phosphoribosyltransferase↗
PubMed1996

n-Butyrate, a cell cycle blocker, inhibits early amplification of duck hepatitis B virus covalently closed circular DNA after in vitro infection of duck hepatocytes.

During chronic hepadnavirus infection, virus persistence depends on the regulation of the pool of covalently closed circular DNA (cccDNA), which is the template for transcription of viral RNA species. The development of in vitro infection of duck hepatocyte primary cultures by duck hepatitis B virus (DHBV) provides a unique opportunity to study the regulation of cccDNA synthesis. After DHBV in vitro infection, cccDNA is detected 1 day later and is amplified to a high copy number after 1 week in culture. We studied whether this amplification occurs during cell cycle progression of duckling hepatocytes. By using [3H]thymidine incorporation, we found that hepatocytes obtained from 3-week-old ducklings spontaneously entered the S phase of the cell cycle when cultured in serum-free medium without added growth factors. Bromodeoxyuridine labeling confirmed that cellular DNA synthesis took place in more than 50% of parenchymal cells. Cytofluorometry analysis revealed the presence of asynchronous populations and polyploidization processes. The addition of a cell cycle blocker, n-butyrate, completely inhibited [3H]thymidine incorporation and blocked duckling hepatocytes in the G1 phase of the cell cycle. Simultaneously, butyrate inhibited cccDNA amplification and allowed the establishment of DHBV infection, as demonstrated by the detection of a basal level of cccDNA in treated hepatocytes. Both effects were reversible since active cell DNA synthesis was restored and cccDNA accumulated after drug withdrawal.

Animals↗
PubMed1984

Induction of EBV DNA demethylation and of EBV-specific transcription in Daudi cells treated with TPA and n-butyrate.

The Epstein-Barr virus (EBV) abortive producer cell line Daudi may be induced to an incomplete cycle of viral production by chemicals such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and n-butyrate. These chemicals greatly increase expression of the early antigen but not that of viral capsid antigen. DNA from these cells was cleaved with various restriction enzymes specific for the mCG sites. Viral sequences (mostly in an episomal form) were tested for their methylation patterns and compared to the methylation pattern of the producer cell line B95-8. The BamHI C, V, and H EBV DNA fragments appeared to be nonmethylated in B95-8 whether or not induced by TPA. The same fragments were partially methylated in noninduced Daudi cells. Treatment of the latter with TPA and n-butyrate increased the amount of viral DNA per cell, and hypomethylation of some EBV DNA sites occurred in parallel. Transcription changes were noted only at the level of the BamHI H fragment; cytoplasmic RNA molecules specific for this region were detected only after induction.

Burkitt Lymphoma↗
PubMed1993

Acetate, butyrate and proline uptake in the caecum and colon of prairie voles (Microtus ochrogaster).

We have measured unidirectional uptake (not transmural flux) of acetate, butyrate and proline by everted sleeves of intact tissue from the jejunum, caecum, proximal colon and distal colon of prairie voles (Microtus ochrogaster). There was active (i.e. Na(+)-dependent) transport of L-proline in the jejunum, but we found no evidence for it in any region of the hindgut (i.e. the caecum, proximal colon and distal colon). Uptake of acetate was carrier-mediated in all three regions of the hindgut, but the Jmax and apparent Km (< or = 1.5 mmol l-1) were low, and uptake was primarily passive over the concentration range 10-50 mmol l-1, which spanned measured acetate levels in the caecum and proximal colon. At 100 mmol l-1, acetate uptake (nmol min-1 cm-2) was higher (P < 0.001) in distal colon (359 +/- 33) than in the proximal colon (225 +/- 17) and caecum (150 +/- 5) (mean +/- S.E., N = 8). Uptakes summed over the length of each region were also higher (P < 0.001) in the distal colon at 100 mmol l-1, but not at low concentrations (0.1 mmol l-1). Uptakes normalized to diffusion coefficients were higher for butyrate than acetate and were lowest for L-glucose (which is absorbed passively via an aqueous pathway) in all regions, indicating that uptake of the short-chain fatty acids involves solubilization in the lipid bilayer of the apical membrane. The short-chain fatty acids absorbed from the hindgut of the vole were equivalent to 22% of standard metabolic rate or 15% of resting (but fed) metabolic rate.

Acetates↗
PubMed1992

Etiology of acetonemia in Norwegian cattle. 2. Effect of butyric acid, valeric acid, and putrescine.

A feeding experiment was performed on 16 cows in order to test the effect of naturally occurring substances in silage on forage intake, ketonemia, and milk yield. The cows were divided into a control group and three experimental groups. The cows in the three experimental groups were fed 100 g/d of putrescine, 200 g/d of valeric acid, or 200 g/d of butyric acid through a ruminal tube for 3 d. Butyric acid increased plasma acetoacetate; the effect was largest in high yielding cows. Putrescine influenced both milk yield and forage intake and may possibly be a contributory factor, alone or combined with other amines, for the development of ketonemia. Valeric acid did not influence feed intake or plasma acetoacetate concentration. A rapid method for acetoacetate analysis also is described.

Acetoacetates↗
PubMed1992

Inhibition of butyric acid-induced colitis in mice by 16,16-dimethyl prostaglandin E2.

A standard colitic lesion was induced in male BKA mice by intrarectal administration of butyric acid (7.5%, 0.1 ml, 10 sec contact). Animals were killed after 5 h and the 'colitic score', increase in colonic tissue water ('oedema') and colonic tissue content of myeloperoxidase (MPO, a marker for neutrophils) were determined. Drug was administered intrarectally in 0.2 ml saline 20 min before colitis induction. In colitic animals given vehicle alone, all these parameters increased (P less than 0.05) compared to the non-colitic controls. In colitic animals given 16,16-dimethyl PGE2 (0.2-20000 micrograms/kg), colitic score was reduced (P less than 0.05) at all dose levels when compared with vehicle-treated colitic animals. The oedema and MPO showed a dose-related reduction (r = -0.895 and -0.904 respectively). In mouse colon 16,16-dimethyl PGE2 showed a protective action against butyric acid-induced colitic damage.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Modulation of the cluster 1 and mucin antigens in human small cell lung cancer and other epithelial tumour cell lines after treatment with the differentiation inducing agent, sodium butyrate.

The expression of the human small cell lung cancer (SCLC) cluster 1 antigen and the human milk fat globule membrane (HMFG) antigen were studied in three SCLC, three lung adenocarcinoma, six ovarian adenocarcinoma and three colorectal adenocarcinoma cell lines before and after culture in the presence of the differentiation inducing agent, sodium butyrate. Before treatment, only SCLC and well differentiated ovarian cell lines expressed the cluster 1 antigen. After 4 days culture with sodium butyrate, expression of cluster 1 antigen was induced in poorly differentiated ovarian, colorectal and lung adenocarcinoma cell lines whereas existing antigen expression was enhanced in SCLC and well differentiated ovarian cell lines. The expression of the HMFG antigen was also modified. Induction of cluster 1 antigen correlated with increased levels of alkaline phosphatase in the treated cell lines, this enzyme being associated with a more differentiated state in colon and ovarian carcinoma cell lines. The pattern of induction of cluster 1 antigen expression suggests that several different epitopes of this antigen are recognised by the ten SCLC cluster 1 antibodies studied.

Adenocarcinoma↗
PubMed1990

[Subacute butyric acid exposure in cattle. 5. Effect on the acid-base equilibrium and protein metabolism in cows].

Acid-base balanced in cows were but slightly affected by butyric acid exposure experiment over three weeks. Applications of sodium butyrate over the same period of time, on the other hand, was associated with buildup of alkalosis in the second half of the experimental period, with alternation of loading, compensation, and reloading being recordable. Nitrogen metabolism in cows was but slightly affected under the given experimental conditions. However, clearly noticeable impairment of nitrogen metabolism was exhibited by one cow that had fallen ill, in the course of experimentation.

Acid-Base Equilibrium↗
PubMed1990

3'-Azido-3'-deoxythymidine inhibits globin gene transcription in butyric acid-induced K-562 human leukemia cells.

We previously demonstrated that 3'-azido-3'-deoxythymidine (AZT) inhibits proliferation of human bone marrow progenitor cells in vitro and that incorporation of AZT into nuclear DNA may be one mechanism responsible for AZT-induced bone marrow toxicity [Antimicrob. Agents Chemother. 31:452-454 (1987); Mol. Pharmacol. 36:9-14 (1989)]. The present study explores possible genetic mechanisms involved in AZT-induced anemia by evaluating the effects of AZT on globin gene expression at both the transcriptional and the translational levels in butyric acid-induced K-562 human erythroleukemia cells. AZT, at concentrations ranging from 10 to 250 microM, was added to cells 25 hr after initiation of induction of hemoglobin (Hb) synthesis with 1.4 mM butyric acid. Hb synthesis, as measured by benzidine staining, was inhibited by AZT in a dose- and time-dependent manner in these cells. AZT inhibition of cell growth was not the major contributing factor in the net inhibition of Hb synthesis in K-562 cells. As assessed by Northern blot analysis, AZT inhibition of Hb synthesis was associated with a decrease in globin mRNA steady state levels without inhibition of total RNA synthesis or actin mRNA steady state levels. In particular, a decrease of globin mRNA levels of 23% by 25 microM AZT was observed, reaching a maximum inhibition of 59% in the presence of 250 microM AZT. In vitro translation experiments demonstrated that essentially all nonglobin translatable mRNAs were not inhibited by AZT concentrations as high as 250 microM, whereas globin mRNAs coding for epsilon, zeta, A gamma, G gamma, and alpha chains were substantially inhibited to similar levels by AZT, in a dose-dependent manner. Transcriptional run-on studies with isolated nuclei from AZT-treated K-562 cells demonstrated a 20 and 50% inhibition of in vitro synthesized globin transcripts from cells exposed to 25 and 100 microM AZT, respectively. 2',3'-Dideoxycytidine also inhibited K-562 cell growth in the same concentration range as AZT but, of importance, had no effects on Hb production. These data suggest that inhibition of globin gene expression may play a role in the cytotoxicity of AZT to the erythroid cell.

Anemia↗
PubMed1989

Increased synthesis of secreted proteins induces expression of glucose-regulated proteins in butyrate-treated Chinese hamster ovary cells.

The effects of increased synthesis of secreted proteins expressed from stably integrated heterologous genes in Chinese hamster ovary (CHO) cells following treatment with sodium butyrate was studied. Butyrate treatment increased expression of mRNA transcribed from the adenovirus major late promoter in combination with the SV40 enhancer for Factor VIII, von Willebrand factor, and erythropoietin. Increased levels of mRNA were compared to increases in intracellular primary translation product and secreted protein. While von Willebrand factor and erythropoietin were efficiently secreted, Factor VIII was not. Increased expression of all these proteins induced expression of the glucose-regulated proteins, GRP78 and GRP94. However, increased Factor VIII synthesis was correlated with an 80-fold increase in GRP78 mRNA and a 10-fold increase in GRP94 mRNA. These data suggest that elevated levels of newly synthesized secretion-competent protein as well as misfolded protein induce the glucose-regulated proteins.

Animals↗
PubMed1987

Differential effects of sodium butyrate and dimethylsulfoxide on gamma-glutamyl transpeptidase and alkaline phosphatase activities in MCF-7 breast cancer cells.

Sodium butyrate and dimethylsulfoxide (DMSO), two known chemical inducers of cell differentiation, were examined on MCF-7 breast cancer cells. Both agents reduce the proliferative capacity of MCF-7 cells, as reflected by inhibition of colony formation in semisolid agar. Sodium butyrate is shown to enhance markedly the activity of two plasma membrane-bound enzymes, alkaline phosphatase and gamma-glutamyl transpeptidase. DMSO does not enhance the activity of these enzymes, but rather induces a small decrease in gamma-glutamyl transpeptidase activity. The present results show that although both agents inhibit cell proliferation, they have a distinct effect on phenotypic expression.

Alkaline Phosphatase↗