Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BUTYRATES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,333 records · Page 74Linked to original sources
PubMed2001

Effects of sodium butyrate on expression of members of the IGF-binding protein superfamily in human mammary epithelial cells.

Dietary factors play an important role in both the development and prevention of human cancers, including breast carcinoma. One dietary micronutrient, sodium butyrate (NaB), is a major end product of dietary starch and fiber, produced naturally during digestion by anaerobic bacteria in the cecum and colon. NaB is a potent growth inhibitor and initiates cell differentiation for many cell types in vitro. In this study, we investigated the effects of NaB on three human mammary epithelial cells and regulation of the IGF axis, specifically, IGF-binding protein-3 (IGFBP-3), a known growth regulator in human mammary cells, and IGFBP-related protein 2 (IGFBP-rP2)/connective tissue growth factor. NaB inhibited DNA synthesis, as measured by [3H]thymidine incorporation, in estrogen-responsive (MCF-7) and estrogen-non-responsive (Hs578T) breast cancer cells, and normal human mammary epithelial cells (HMEC) to a similar degree (up to 90% inhibition at 1-10 mM concentrations). Treatment of cells with NaB induced histone hyperacetylation, suggesting that NaB exerts its biological effects, at least in part, as a histone deacetylase inhibitor in mammary epithelial cells. Treatment of Hs578T cells with NaB caused an induction of apoptotic cell death. NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type. In the same context, among the IGFBP superfamily members tested, NaB specifically upregulated the expression of IGFBP-3 and IGFBP-rP2. These two proteins are known to be involved in inhibition of mammary epithelial cell replication. Northern blot analysis showed that NaB treatment at 1-10 mM concentrations caused a dose-dependent stimulation of IGFBP-3 mRNA expression in cancerous cells and IGFBP-rP2 mRNA expression in both cancerous and non-cancerous cells. Protein data from Western ligand blot and immunoblot analyses demonstrated parallel results. In summary, we have demonstrated that NaB (i) uniformly suppresses DNA synthesis in both cancerous and non-cancerous mammary cells, and (ii) upregulates IGFBP-3 and IGFBP-rP2 mRNA and protein levels in cancerous and non-cancerous mammary cells. These results provide the first demonstration that butyrate regulates the IGFBP system in the human mammary system.

Acetylation↗
PubMed2003

Effects of hydrochloric, acetic, butyric, and propionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses.

OBJECTIVE: To identify the pathogenesis of gastric ulcers by comparing injury to the nonglandular gastric mucosa of horses caused by hydrochloric acid (HCl) or volatile fatty acids (VFAs). SAMPLE POPULATION: Gastric tissues from 30 horses. PROCEDURE: Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance calculated for tissues after addition of HCl and VFAs to normal Ringer's solution (NRS). Tissues were examined histologically. RESULTS: Mucosa exposed to HCl in NRS (pH, 1.5) had a significant decrease in Isc, compared with Isc for mucosa exposed to NRS at pH 4.0 or 7.0. Also, exposure to 60mM acetic, propionic, and butyric acids (pH, 4.0 or 1.5) caused an immediate significant decrease in Isc. Recovery of sodium transport was detected only in samples exposed to acetic acid at pH 4.0. Recovery of sodium transport was not seen in other mucosal samples exposed to VFAs at pH < or = 4.0. CONCLUSIONS AND CLINICAL RELEVANCE: Acetic, butyric, and propionic acids and, to a lesser extent, HCl caused decreases in mucosal barrier function of the nonglandular portion of the equine stomach. Because of their lipid solubility at pH < or = 4.0, undissociated VFAs penetrate cells in the nonglandular gastric mucosa, which causes acidification of cellular contents, inhibition of sodium transport, and cellular swelling. Results indicate that HCl alone or in combination with VFAs at gastric pH < or = 4.0 may be important in the pathogenesis of gastric ulcers in the nonglandular portion of the stomach of horses.

Acetic Acid↗
PubMed2006

Effects of butyrate, avilamycin, and a plant extract combination on the intestinal equilibrium of early-weaned pigs.

We evaluated the effects of 3 additives, sodium butyrate (AC), avilamycin (AB), and a combination of plant extracts (XT), on the productive performance and the intestinal environment of the early-weaned pig. The XT was a standardized mixture with 5% (wt/wt) carvacrol (from Origanum spp.), 3% cinnamaldehyde (from Cinnamonum spp.), and 2% capsicum oleoresin (from Capsicum annum). Pigs (n = 32) weaned at 18 to 22 d of age with an initial BW of 6.0 +/- 0.10 kg were allocated to 8 pens that, in turn, were allocated to 4 treatments. The treatments included a basal diet (CT) or the basal diet supplemented with 0.3% of AC, 0.04% of AB, or 0.03% of XT. Productive performance was determined during the initial 14 d postweaning. On d 19 and 21 of the experiment, the pigs were killed to allow collection of digesta and intestinal tissue to evaluate variables indicative of aspects of the gastrointestinal environment. Treatments AB and AC improved G:F (P = 0.012 and 0.003, respectively) compared with the CT. Butyrate included in the diet was only detected in the stomach but not in cranial jejunum. When compared with CT, AC produced a lower ileal starch digestibility (P = 0.002) and a lower whole-tract OM and starch digestibility (P = 0.001 and 0.003, respectively), related to a lower VFA concentration in the cranial colon (P = 0.082) and a numerically reduced branched VFA percentage in the rectum. The AB treatment diminished propionate production in caudal colon (P = 0.002) and rectum (P = 0.012) compared with CT. The AC group exhibited deeper crypt depth in the jejunum without variations in villus height compared with CT (P = 0.042). The AC and AB groups also increased goblet cell presence in the colon (P = 0.001 and 0.032, respectively). On the other hand, AB and XT diminished intraepithelial lymphocytes in the jejunum (P = 0.003 and 0.034, respectively). The XT increased lymphocyte presence in the colon (P = 0.003). These results show the important influence of AB and AC on productive performance and on pig gut dynamics. The intestinal modifications observed for AB and AC compared with CT suggest distinct modes of action for each additive.

Animal Feed↗
PubMed2000

Cultures of human colonic epithelial cells isolated from endoscopical biopsies from patients with inflammatory bowel disease. Effect of IFNgamma, TNFalpha and IL-1beta on viability, butyrate oxidation and IL-8 secretion.

Cytokine-mediated impairment of viability and metabolic function of epithelial cells has been suggested as a possible early pathogenic event in the development of inflammatory bowel disease (IBD). It is currently unknown whether pro-inflammatory cytokines have a direct effect on human nontransformed colonic epithelial cells. We investigated the effects of TNFalpha, IFNgamma and IL-1beta on viability, short chain fatty acid (butyrate) oxidation and IL-8 secretion in human colonic epithelial cell cultures in vitro obtained from macroscopically normal mucosa from IBD patients and controls. Colonic crypts were isolated from endoscopical biopsies by ultra-short (10 min) EDTA/EGTA treatment, and exposed to TNFalpha, IFNgamma and IL-1beta for 24 hours. The combination of TNFalpha+IFNgamma induced a significant decrease in cell viability as judged by methyltetrazoleum (MTT) metabolism which decreased to median 68% of unexposed cultures (P < 0.01). This effect was more pronounced than that observed after addition of TNFalpha (median 88%) (P < 0.05), but not IFNgamma alone (median 78%), whereas IL-1beta had no significant effect. Cells from IBD patients were significantly less sensitive to TNFalpha + IFNgamma exposure (median 74%) compared to cells from controls (median 58 %) (P < 0.05). Butyrate oxidation, as measured by entrapment of 14CO2, was not inhibited in cells exposed to TNFalpha + IFNgamma, neither from controls (median 112%) nor from IBD patients (median 108%), suggesting a relative increase of this specific metabolic function in living cells in response to immunoinflammatory stress. IL-8 levels in cell supernatants were increased by TNFalpha + IFNgamma, supporting the role of the epithelium in signalling between luminal factors and mucosal immune cells. In conclusion, we report that TNFalpha and IFNgamma damage and influence human colonic epithelial cell function in vitro and that such mechanisms, if operative in vivo, also may be involved in the pathogenesis of IBD.

Adult↗
PubMed1998

Germinated barley foodstuff increases fecal volume and butyrate production in humans.

Germinated barley foodstuff (GBF), derived from the aleurone layer, scutellum and germ of germinated barley, contains a large quantity of fermentable dietary fibers, especially hemicellulose. Ten grams of GBF were given to 10 healthy volunteers 3 times a day (30 g/day/person) for 28 consecutive days. Fecal weight, water contents and short chain fatty acid content were measured before GBF administration and from days 25 to 28 after initiation of GBF administration. GBF intake significantly increased fecal butyrate content as well as fecal weight and water content. No significant change in body weight resulted from consumption of GBF for 28 days. No major laboratory abnormalities were found in hematologic and urinary analysis. These findings indicate that GBF promotes defecation, produces bacterial short chain fatty acids, especially butyrate, without adverse effects, and is a safe foodstuff for humans.

Adult↗
PubMed2001

Effect of platelet activating factor and butyrate on the expression of interleukin-2 receptor alpha in nasopharyngeal carcinoma cells.

Serum level of soluble interleukin-2 receptor alpha (sIL-2Ralpha) has been shown to correlate with disease progression and prognosis of cancer patients. However, the available information about the source and the pathophysiological regulation of IL-2Ralpha in cancer cells is limited. This study addressed the questions of prognostic value and the source of sIL-2Ralpha in patients with nasopharyngeal carcinoma (NPC). Biological regulation of IL-2Ralpha was characterized in NPC cell lines. Serum sIL-2Ralpha levels of 113 NPC patients were measured by enzyme-linked immunosorbent assay (ELISA). Levels of sIL-2Ralpha in NPC patients were significantly higher than that in the healthy controls, and sIL-2Ralpha levels were correlated with disease progression and patient survival. IL-2Ralpha was identified in cancer cells by immunocytochemistry. In vitro, IL-2Ralpha expression was markedly increased following treatment with platelet activating factor and/or n-sodium butyrate. Increased secretion of IL-2Ralpha was also detected in the culture media. The secreted IL-2Ralpha could functionally bind IL-2. These results indicate that elevated sIL-2Ralpha was often detected in patients with advanced NPC. The elevated sIL-2Ralpha could be shed from NPC cells by a yet to be determined mechanism and IL-2Ralpha expression in NPC cells could be upregulated by platelet activating factor and butyrate.

Adult↗
PubMed2005

Histone deacetylase inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9-dependent apoptosis in human malignant glioma cells.

Histone deacetylase (HDAC) inhibitors have both apoptotic and differentiating effects on various tumor cells. However, the mechanisms underlying the effect of HDAC inhibitors remain unclear. In this study, we investigated the function of anti-proliferative effects of HDAC inhibitors, N-butyric acid and trichostatin A, on human malignant glioma cell lines, U251-MG and D54. MTT assay showed a dose-dependent inhibition of cellular proliferation in both cell lines. Cell cycle analysis revealed increased sub-G1 population in both lines, and G1 arrest only in U251-MG cells. Induction of apoptosis was also supported by the occurrence of DNA fragmentation in tumor cells treated with HDAC inhibitors. Furthermore, caspase inhibition assay indicated that HDAC inhibitor-induced apoptosis was caspase-dependent. Neither mitochondrial membrane potential nor the expression of caspase-9 was changed by treatment with HDAC inhibitors, suggesting the possibility that HDAC inhibitor-induced apoptosis was not mediated by the mitochondrial cell death pathway. On the other hand, immunoblot assay confirmed increased expression of caspase-8 in both lines, and elevation of p21 but not p27 protein in U251-MG cells following HDAC inhibitor treatment. Taken together, the HDAC inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9-dependent apoptosis with or without p21-mediated G1 arrest in human malignant glioma cells.

Apoptosis↗
PubMed2001

The influence of acetoacetate and butyrate on calcium influx and ATP concentrations in HT-29 cells.

The effects of acetoacetate and butyrate on Ca(2+)-influx in HT-29 cells were unknown. Extracellular signals can be transferred to the intracellular environment of the cell via changes in the Ca(2+)-concentration. Extracellular Ca2+ may enter the cell via Ca(2+)-channels in the plasma membrane. Physiological processes occurring within the cell are dependent on Ca(2+)-concentration, including enzyme activity. Intracellular Ca(2+)-concentrations were measured using Fura-2/AM, a fluorescent intracellular Ca(2+)-probe. Ca(2+)-concentrations were measured immediately on application of the inducers to the cells, as well as after a 9 day incubation period. The effect of these inducers on the L-type voltage-operated Ca(2+)-channels were determined using the whole-cell patch-clamp technique. To validate these results for the intestinal epithelial model, membrane current studies were performed on HT-29 cells grown on a polycarbonate membrane. ATP concentrations were measured, and the theoretical effect of the inducers on PDE 4 activity was determined. It was found that both acetoacetate and butyrate blocked Ca(2+)-influx through the L-type voltage-operated Ca(2+)-channels, resulting in the initial low Ca(2+)-concentration (p < 0.05). The blockage effect is short-lived as after a 9 day incubation period in the presence of the inducers, Ca(2+)-concentrations were higher than that of the HT-29 control sample (p < 0.05). ATP concentrations of the cells were decreased in the presence of the inducers (p < 0.05), whilst it was suggested that no interaction between the catalytic site of PDE 4 and the inducers existed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2001

Molecular basis for the synergistic interaction of adriamycin with the formaldehyde-releasing prodrug pivaloyloxymethyl butyrate (AN-9).

The interaction of Adriamycin and pivaloyloxymethyl butyrate (AN-9) was investigated in IMR-32 neuroblastoma and MCF-7 breast adenocarcinoma cells. Adriamycin is a widely used anticancer drug, whereas AN-9 is an anticancer agent presently undergoing Phase II clinical trials. The anticancer activity of AN-9 has been attributed to its ability to act as a butyric acid prodrug, although it also releases formaldehyde and pivalic acid. Adriamycin and AN-9 in combination display synergy when exposed simultaneously to cells or when AN-9 treatment is up to 18 h after Adriamycin administration. However, the reverse order of addition results in antagonism. These interactions have been established using cell viability assays and classical isobologram analysis. To understand the molecular basis of this synergy, the relative levels of Adriamycin-DNA adducts were determined using various treatment combinations. Levels of Adriamycin-DNA adducts were enhanced when treatment combinations known to be synergistic were used and were diminished using those treatments known to be antagonistic. The relative timing of the addition of Adriamycin and AN-9 was critical, with a 20-fold enhancement of Adriamycin-DNA adducts occurring when AN-9 was administered 2 h after the exposure of cells to Adriamycin. The enhanced levels of these adducts and the accompanying decreased cell viability were directly related to the esterase-dependent release of formaldehyde from AN-9, providing evidence for the formaldehyde-mediated activation of Adriamycin.

Adenocarcinoma↗
PubMed2001

IgE production is involved in butyrate-enhanced NK cell activity in vivo.

It has been demonstrated that patients with asthma have a large number of NK cells and show a stronger NK activity. These results indicate that NK cell activity may be related to total IgE level in serum in healthy subjects. Previously, we have found that sodium butyrate (NaBu) markedly enhanced the IL-4-induced IgE production in the LPS-stimulated murine splenocytes in vitro, and inductive rat IgE production in vivo, and enhanced the NK cell activity ex vivo. We hypothesized that the IgE production might be involved in butyrate-enhanced NK cell activity in vivo. Mice were intraperitoneally treated/immunized with NaBu or/and Ascaris suum extract (ASC), and the spleen NK cell activity was evaluated. Furthermore, the effect of serum (NAS) on IL-2- or IFN-gamma-induced spleen NK cell activity was determined. The spleen NK cell activity and IL-2- or IFN-gamma-induced spleen NK cell activity of mice treated/immunized with NaBu or/and ASC were stronger than those of untreated/unimmunized mice. Although IL-4 blocked IL-2 (100 U/ml)- or IFN-gamma (100 U/ml)-induced increase in NK cell activity, these NK cell activities in mice treated/immunized with NaBu/ASC were not inhibited. IgE production showed a tendency to rise in NaBu-treated mice serum, and a synergistic effect was observed with treatment of NaBu and ASC. Moreover, the NAS significantly increased IL-2(25 U/ml)-or IFN-gamma(25 U/ml)-induced NK cell activity, and its effect was inhibited by anti-mouse IgE mAb. These data show that IgE plays an important role in NAS-enhanced IL-2/IFN-gamma-induced NK cell activity, and IL-4 does not inhibit IgE and IL-2/IFN-gamma-induced NK cell activity in mice.

Animals↗
PubMed2004

[The effect of Redix Scutellariae on butyrate of Porphyromonas endodontalis in vitro].

OBJECTIVE: To study the effect of Radix Scutellariae on the growth, metabolism of Porphyromonas endodontalis (P.e), as a preparation for studying the mechanism of Radix Scutellariae in treating pulp and periapical diseases. METHODS: P.e was chosen as the experimental bacteria. Radix Scutellariae was extracted by means of reflux with 80% ethanol. The value of MIC of Radix Scutellariae was measured by minute amount serial dilusion test, and the production of butyrate was measured by high liquid chromatograph(HPLC). RESULTS: Radix Scutellariae could inhibit the growth of P.e, of which the MIC was 100 mg/L. Following the increase in concentration of Radix Scutellariae, the amount of butyrate decreased to (3.527 +/- 0.009) mg/L, (3.048 +/- 0.005) mg/L, (2.490 +/- 0.011) mg/L, (2.209 +/- 0.016) mg/L, respectively (P < 0.05). CONCLUSION: Radix Scutellariae could inhibit the growth and metabolism of P.e and might be an effective agent in treating pulp and periapical diseases.

Bacteroidaceae Infections↗
PubMed2004

Modulation of the HSV-TK/ganciclovir bystander effect by n-butyrate in glioblastoma: correlation with gap-junction intercellular communication.

The efficacy of HSV-TK/ganciclovir gene therapy largely relies on the bystander effect, i.e. the ability of transfected cells to kill the adjacent, untrasfected cells. This mechanism itself depends chiefly on the transfer via gap junctions of phosphorylated ganciclovir between cells, and is often deficient in glioblastomas. In this report, we demonstrate that n-butyrate markedly enhances the gap junction intercellular communication of GJIC-deficient glioma cells, and significantly increases the bystander effect in such cells. This effect of n-butyrate appears to be independent from its HDAC inhibitory effect, since trichostatin A does not reproduce it.

Butyrates↗
PubMed2005

[Changes in telomerase activity decreases in MCF-7 cells during apoptosis induced by sodium butyrate].

OBJECTIVE: To investigate telomerase activity of MCF-7 mammary cancer cells during apoptosis induced by sodium butyrate (SB) in vitro and its mechanism. METHODS: The proliferative activity of MCF-7 cells was assessed by morphology and MTT assay. Cell apoptosis was confirmed by DNA fragmentation and phosphatidylserine (PS) externalization. Telomerase activity was examined by TRAP-ELISA. The expression status of telomerase subunits was analyzed by RT-PCR. RESULTS: A time- and dose-dependent inhibition was detected in MCF-7 cells treated with SB. At 72 hr after SB (2.5 mmol/L) treatment, MCF-7 cells were apoptotic with a rate of 84.3% by flow cytometric assay (AnnexinV/PI double staining). Apoptosis was also confirmed by DNA fragmentation. Telomerase activity and expression level of hTERT, the key subunit of telomerase, decreased at 24-hour time point after SB treatment. No significant changes were observed in the expression of hTR and hTP, the other two subunits of telomerase. CONCLUSION: Telomerase activity decreases in MCF-7 cells during apoptosis induced by sodium butyrate. The underlying mechanism might be related to the down regulation of hTERT transcription.

Apoptosis↗
PubMed2006

[ERK pathway change in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate].

The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB. The expression levels of total ERK and phosphorylated-ERK were determined by Western blot. The effect of NaB in combination with the ERK inhibitor PD98059 on the proliferation/differentiation of SKM-1 cells was studied, and then the expression levels of the P21 and HDAC protein were detected by Western blot. The results showed that the expression level of phosphorylated ERK was down-regulated by the 1 mmol/L NaB, and the level of total ERK had not changed. NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone. It is concluded that the inhibition of ERK may be involved in sodium butyrate inducing differentiation in SKM-1 cells.

Butyrates↗
PubMed1988

Butyrate induces selective transcriptional activation of a hypomethylated embryonic globin gene in adult erythroid cells.

An animal model of hemoglobin switching has been developed in which anemic adult chickens are treated with 5-azacytidine and sodium butyrate or alpha-aminobutyric acid, thereby resulting in activation of the embryonic rho-globin gene in adult erythroid cells. In vitro nuclear runoff transcription assays using erythroid nuclei from treated birds show that the mechanism of activation of the rho-globin gene is transcriptional whereas no transcriptional activation of the embryonic epsilon-globin gene occurs. The action of 5-azacytidine appears to be as an inhibitor of DNA methylation because other S-phase active cytotoxic drugs, when substituted for 5-azacytidine, do not cause demethylation of the embryonic globin genes, nor do they allow transcriptional activation to occur. Embryonic rho-globin gene activation in this model is not due to selection of primitive erythroid cells since a subpopulation of primitive erythroid cells is not evident either morphologically or when cells are probed for embryonic and adult globin RNA by in situ hybridization. These studies show that demethylation by 5-azacytidine is a prerequisite but not sufficient cis-regulatory event for a high level of transcriptional activation of the embryonic rho-globin gene in adult erythroid cells in vivo. The possible basis for the selective transcriptional activation by sodium butyrate in this system is discussed.

Acetylation↗
PubMed1989

The effects of retinoic acid and butyric acid on in vitro migration by murine B16a cells: a quantitative scanning electron microscopic study.

Retinoic acid (RA) and butyric acid (BA) were investigated for their effect on in vitro migration of highly metastatic murine B16a melanoma cells. These potential antitumor agents are known to alter the cytoskeleton. Our initial studies determined the 72 h cytostatic/cytotoxic concentrations of RA (1 X 10(-6) M 1 greater than 1 X 10(-5) M) and BA (1.5 mM)/ greater than 2.0 mM). Cytostasis by RA and BA was confirmed by autoradiography and radioisotope incorporation. For migration assays, cells were plated on 3 and 5 microns diameter pore polycarbonate membranes. Complete media was added containing RA or BA at time of plating. For BA pretreatment studies, BA was added to cells for 72 h prior to plating cells in fresh BA on the membranes. Top and bottom surface of the membranes were examined after 72 h of incubation by scanning electron microscopy. Although RA and BA induced cells on top of the membrane to change morphology as shown by phase, transmission and scanning electron microscopy, only BA enhanced the deformability of cells to allow for passage through the 3 micron diameter pores. Butyric acid enhanced migration through 3 micron diameter pore membrane by 511%. For 5 micron diameter pore membranes, 55.2% of the plated number of untreated early passage cells migrated to the bottom surface as compared to 57.3% for BA-treated cells and 14.9% for RA-treated cells. However, if cellular proliferation over the 72 h period was factored in, BA increased migration by 456% over the controls and pretreatment of cells with BA for 72 h prior to plating increased migration by 893%. Without considering proliferation, RA inhibited migration by 75% over controls. The decrease in migration observed in RA-treated cells was due to an inhibitory effect on cellular migration and a decrease in proliferation.

Animals↗
PubMed1979

Ultrastructural concomitants of sodium butyrate-enhanced ectopic production of chorionic gonadotropin and its alpha subunit human bronchogenic carcinoma (ChaGo) cells.

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. Elongation and flattening of cells were seen by light microscopy. Immunocytochemistry with antisera against hCG and against hCG-alpha showed an increase in cells containing stainable hCG-alpha. Scanning electron microscopy demonstrated enhanced adhesion of cells to glass cover slips, with elongation, flattening, and decreased cytoplasmic blebs. Ultrastructural changes were examined by transmission electron microscopy and evaluated quantitatively by an unbiased observer. Significant findings included increases in perinuclear tonofilaments, smooth endoplasmic reticulum vesicles, dense mitochondrial inclusions, and lipid granules, as well as decreases in intercellular desmosomes, free polyribosomes, mitochondrial dense granules, and Golgi complexes. The most notable change, a marked decrease in condensed chromatin clumps, may have reflected a butyrate-induced biochemical modification of chromatin leading to enhanced accessibility of certain genes for transcription.

Butyrates↗