Disease relevance of butanoic acid

• The potential to inhibit muscle differentiation reversibly is not specific to DMSO, but is shared by a number of compounds, including dimethylformamide, hexamethylbisacetamide and butyric acid, all potent inducers of gene expression in Friend erythroleukemia cells [1].
• Sodium butyrate treatment of cultures of ChaGo (human lung cancer) cells resulted in increased production of human chorionic gonadotropin (hCG) and its alpha subunit (hCG-alpha) and induced a variety of morphologic changes [2].
• Butyric acid induces apoptosis by up-regulating Bax expression via stimulation of the c-Jun N-terminal kinase/activation protein-1 pathway in human colon cancer cells [3].
• Because butyric acid (BA) is the major short-chain fatty acid produced by fermentation of dietary fiber in the large bowel, it may be an important regulator of apoptosis in colorectal cancer [3].
• BACKGROUND & AIMS: Butyrate is effective in experimental colitis by increasing transglutaminase activity [4].

Psychiatry related information on butanoic acid

• RESULTS: Butyrate enemas (40 mM twice daily for 14 days) decreased colonic pain thresholds in control rats; they did not reduce the TNBS-induced hypersensitivity, but on the contrary increased its duration (without modifying the inflammation score) [5].
• Clusters of NPY-producing neurons in the ARC that coexpress gamma- amino butyric acid and agouti-related peptide, and those in the brain stem (BS) that coexpress catecholamines and galanin, participate in disparate manners to regulate appetitive behavior [6].
• In addition, the involvement of the stress hormone corticotropin-releasing hormone, the peptide cholecystokinin and the amino acid transmitter gamma-amino butyric acid in anxiety disorders is reviewed [7].

High impact information on butanoic acid

• Sodium butyrate in millimolar concentrations causes an accumulation of acetylated histone species in a variety of vertebrate cell lines [8].
• I have grown HeLa cells in 5 mM sodium n-butyrate leading to extensive in vivo histone acetylation, and have characterized the structure of chromatin containing the modified histones [9].
• Sodium butyrate inhibits histone deacetylation in cultured cells [8].
• Butyric acid, a potent inducer of erythroid differentiation in cultured erythroleukemic cells [10].
• Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope [11].

Chemical compound and disease context of butanoic acid

• Friend erythroleukemia cells of line Fw are noninducible for hemoglobin synthesis by dimethyl sulfoxide, butyric acid, and other agents [12].
• In a strain of murine erythroleukemia cells resistant to dimethyl sulfoxide (DR-10), the preferential stimulation of betamaj synthesis by hexamethylene bisacetamide of the betamin synthesis by butyric acid is more pronounced than with the dimethyl sulfoxide-sensitive cells (DS-19) [13].
• All-trans-retinoic acid (RA), sodium n-butyrate (NaB), hexamethylene bisacetamide (HMBA), and dimethyl sulfoxide (DMSO) induce differentiation of the human acute myeloid leukemia cell line HL60 [14].
• The effect of oxamflatin on the transcriptional activity of the cytomegalovirus (CMV) promoter was examined and compared with known HDAC inhibitors, TSA, sodium n-butyrate, and FR901228 [15].
• Effect of sodium n-butyrate on induction of prostaglandin synthase activity in cloned mastocytoma P-815 2-E-6 cells [16].

Biological context of butanoic acid

• Furthermore, experiments with the deacetylase inhibitor sodium-n-butyrate do not support the proposed connection between diacetylated H4 (H4Ac2) and DNA replication [17].
• Erythroid differentiation can be readily induced by butyric acid in cultured erythroleukemic cells in the presence of inhibitors of DNA synthesis and in the absence of cell division [18].
• Sodium butyrate, which initiates differentiation to mature eosinophils, also induces the appearance of high affinity (Kd 1-5 X 10(-11) M) IL-5 binding sites on these cells [19].
• These results suggest that the increase in TGase activity in DMSO- or butyric acid-treated FL cells may be related to cell differentiation [20].
• BACKGROUND & AIMS: Butyrate serves as the major source of energy for colonic epithelial cells, and has profound effects on their proliferation, differentiation, and apoptosis [21].

Anatomical context of butanoic acid

• Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol [11].
• To test for the possibility that an allele of the beta 3Gal-T gene might be repressed instead of mutated, we have investigated whether 5-azacytidine or sodium n-butyrate, both inducers of gene expression, would reactivate expression of beta 3Gal-T in cloned enzyme-deficient T cells derived from a patient affected by the Tn syndrome [22].
• Sodium butyrate downregulated CXCR4 expression and induced differentiation of HT-29 cells, suggesting a role for CXCR4 in maintenance and renewal of the colonic epithelium [23].
• To this end, we exposed isolated chicken osteoclasts to a metabolic (butyric) acid and observed a fall in both intracellular pH and cytosolic calcium [( Ca2+]i) [24].
• RESULTS: Butyrate induces a time- and concentration-dependent increase in hsp25, but not hsp72 or hsc73, protein expression in rat IEC-18 cells but not 3T3 fibroblasts [25].

Associations of butanoic acid with other chemical compounds

• Although both DMSO and n-butyric acid induced rapid erythroid cell differentiation of the GM 979 cells, and both resulted in increased hemoglobin synthesis, only DMSO treatment enhanced the susceptibility of the cells to natural cytotoxicity by normal splenocytes [26].
• In contrast, no changes were seen in the incidence of small bowel tumors, luminal butyric acid concentrations, mucosal morphology, or brush-border enzyme activities (i.e., sucrase, alkaline phosphatase) [27].
• Expression in a yeast mutant demonstrated that LeProT1 transports proline and gamma-amino butyric acid with low affinity and glycine betaine with high affinity [28].
• This restricted binding of propidium iodide to chromatin is observed in MELC cultured with other inducing agents, such as butyric acid and dimethyl-acetamide, but is not detected with an Me2SO-resistant cell line cultured with Me2SO [29].
• The profile of butyric-acid-induced changes on globin gene expression is also quite distinct from changes produced by trichostatin A, a known histone deacetylase inhibitor [30].

Gene context of butanoic acid

• Quantitation of transcripts of CD86 accompanied with RNA synthesis inhibition assay and nuclear run-on assay revealed that SB up-regulates the CD86 expression transcriptionally [31].
• Treatment of HL-60 eosinophilic sublines with either interleukin-5 or butyric acid increased the expression of GATA-1 mRNA concomitant with the expression of eosinophil-specific genes, whereas levels of GATA-2 mRNA remained relatively constant [32].
• Butyric acid promoted the synthesis of hemoglobin in UT-7/Epo, but not UT-7 [33].
• The expression of CD80, CD86, human leukocyte antigen (HLA)-DR, HLA-ABC, and intracellular adhesion molecule-1 (ICAM-1) was tested in human AML cell lines after the addition of HDACI, sodium butyrate (SB) [31].
• Pretreatment of cells with the JNK inhibitor SP600125 attenuated the effect of butyric acid on apoptosis, whereas no effect was seen with the p38 inhibitor SB202190 or the ERK inhibitor PD98059 [34].

Analytical, diagnostic and therapeutic context of butanoic acid

• METHODS: Butyrate oxidation was measured by means of a 14CO2-breath test after rectal instillation of 14C-butyrate [35].
• The glycolipid-binding cytotoxin produced by Shigella dysenteriae 1, Shiga toxin, binds to MDCK cells (strain 1) only after treatment with short-chain fatty acids like butyric acid or with the tumor promoter 12-O-tetradecanoylphorbol 13-acetate [36].
• Intracellular acidification was forced by introducing butyric acid into the recording medium, and subsequent changes in pHi and membrane potential were determined with intracellular microelectrodes [37].
• Finally, the allogeneic mixed leukocyte reaction (allo-MLR) against HL60 cells pretreated with SB was enhanced 4-fold compared with allo-MLR obtained with non-treated HL60 cells [31].
• Activation with IFN-gamma and LPS of these cocultures brought about a sharp decrease in uptake of gamma-amino butyric acid and a marked reduction in neuronal cell survival [38].

References