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At least 793 records · Page 44Linked to original sources
PubMed1993

p145 expression during the cell cycle in HL-60 cell line and normal human lymphocytes: effects of camptothecin, vinblastine, cycloheximide, actinomycin D, retinoic acid and DMSO.

Bivariate flow cytometric analysis of nucleolar antigen p145 was performed on quiescent and phytohemagglutinin-stimulated human lymphocytes and on a promyelocytic cell line (HL-60). Data were acquired on a FACScan flow cytometer and analyzed using LYSYS II. Quiescent lymphocytes did not express p145. PHA-stimulated proliferating lymphocytes expressed p145 maximally after 48 h, similarly to HL-60 cells in exponential growth. Antigen expression in G1 was notably heterogeneous in both cell types. The ratio of p145/DNA was highest in early S and decreased during mid and late S and remained low in G2M. p145 expression was lowest in M-phase cells treated for 6 h with vinblastine. Cycloheximide and actinomycin D had similar effects on p145 in HL-60 cells: expression of p145 gradually decreased from 1 to 6 h incubation in all phases of the cell cycle. Camptothecin did not decrease p145 expression and apoptotic cells from CAM-treated cultures still expressed p145. Retinoic acid and DMSO induced differentiation in HL-60 cells, and as this process progressed, p145 levels gradually fell until they approached isotype antibody control levels at 9 and 6 days, respectively. However, after 5 days treatment with 2 nM retinoic acid apoptotic cells appeared which still expressed p145. The data on drug treatment suggest that p145 exists in undifferentiated and proliferating cells and may not be a specific marker for malignancy, but may prove useful as a monitor of chemotherapeutic effects in cancer treatment.

Antigens, Nuclear↗
PubMed1995

Spontaneous and cycloheximide-induced interleukin-10 mRNA expression in human mononuclear cells.

Interleukin-10 (IL-10) is known to be spontaneously produced by human peripheral blood mononuclear cells. In order to define the cell type in which IL-10 gene is spontaneously expressed we used the reverse polymerase chain reaction for IL-10 mRNA expression, which was also used to study the effects of cycloheximide (CHX). First, we found that IL-10 mRNA is spontaneously expressed in monocytes and B cells but not T cells from healthy donors, and second, we demonstrated that CHX superinduces IL-10 mRNA in monocytes and B cells. Experiments including nuclear run-on analyses established that the effects of CHX on IL-10 gene expression involve both gene transcription and mRNA stabilization.

B-Lymphocytes↗
PubMed1990

Cycloheximide blocks the retention of maternal experience in postpartum rats.

Two studies were done to determine the effects of cycloheximide (CYX), a protein synthesis inhibitor, on maternal experience effects in rats. In the first study eight groups received a 2-h maternal experience 36 h after cesarean (c)-section and two groups received no post c-section experience. Among the experienced groups, two received icv injections of CYX or saline (SAL) 30 min before the maternal experience, two received CYX or SAL 10 min after the experience, and two received the injections 24 h after the experience. One inexperienced group received CYX and the other received SAL 36 h after c-section. Tests for maternal behavior occurred 10 days after c-section. CYX was not able to block or disrupt the "acquisition" or expression of ongoing maternal behavior during the 2-h experience phase. However, CYX was able to block the long-term "retention" of a 2-h maternal experience if the drug was present during or immediately after the experience, prior to "consolidation." The second study investigated the effects of CYX administered immediately after the maternal experience on the expression and retention of maternal behavior 4 and 6 days after c-section, to determine whether the hormonally mediated short-onset latencies of the 4-day group would be blocked by CYX. Eight groups of animals were tested for maternal behavior. Four were tested 4 days after c-section and four were tested 6 days after c-section. Within each of these groups two were experienced and two inexperienced; within each experience condition one group received CYX and one received SAL. Day 4 groups exhibited shorter onset latencies than Day 6 groups. There was also a CYX-SAL difference in maternal onset latencies among experienced Day 6 groups but not among Day 4 groups. These data indicate that the blocking effects of CYX can be seen only when hormonal priming of maternal behavior is no longer in evidence.

Animals↗
PubMed1991

Sexual experience effects are blocked both by the protein-synthesis inhibitor, cycloheximide, and by the noncompetitive NMDA antagonist, MK-801.

Three studies were done to determine the effects of a brief 2-h sexual experience on the maintenance of sexual behavior in male rats; the effects on the experience-based maintenance of sexual behavior of gonadal hormones (study 1), a protein-synthesis inhibitor (study 2), and an N-methyl-D-aspartate receptor blocker (study 3) were determined. Naive male rats were provided with a 2-h sexual experience with sexually receptive hormonally "primed" females or they received no experience. In the first study animals under each of these conditions then underwent castration or sham surgery. In the second study animals under each of the experience conditions received either cycloheximide (CYX) or saline (SAL; 1.5 or 3.0 mg/kg CYX or SAL sc, 10 min after the experience). In study 3 experienced and inexperienced animals received either 0.07 or 0.10 mg/kg MK-801 ip (15 min before the experience). In all studies animals were tested for sexual behavior 3, 6, and 9 days after surgery or injection. These studies showed that the most consistent effect of a 2-h sexual experience was to facilitate the initiation of mounting, especially on the first test; they show, further, that most experience effects were reduced or eliminated if animals were castrated between experience and test, if they received a drug (CYX) at the time of the experience that blocks the synthesis of proteins, or if they received an NMDA receptor antagonist prior to the experience.

Animals↗
PubMed1985

Inhibition of bromodeoxyuridine-associated sister chromatid exchanges in Bloom's syndrome cells with cycloheximide.

Effects of cycloheximide (CH) and deoxycytidine (dC) on the frequency of sister chromatid exchanges (SCEs) in normal and Bloom's syndrome (BS) cells labeled with bromodeoxyuridine (BrdU) during first, second, and third cell cycles were evaluated using endomitotic and three-way differentiation analyses. When CH at 0.2 and 2.0 ng/ml was added to normal and BS cultures of BrdU-labeled endomitoses, the rate of single SCEs was significantly decreased in BS cells, though the rate of reduction in single SCEs was slight in normal cells. No significant change was detected in the twin SCE rate. In BS cells, treatment with CH at 0.2 and 2.0 ng/ml produced significant reductions in SCEs in both the second (SCE2) and third (SCE3) cell cycles, sometimes reaching the normal level. Treatment with dC at 13 and 26 micrograms/ml resulted in almost no significant changes in rates of SCE during first, second, and third cell cycles. When CH was added to BrdU-labeled normal and BS cell cultures, the cell growth rates improved from 35% to 70% over the control level in the BS cells, though in normal cells, the addition of CH resulted in a close-dependent lower cell growth rate. Deoxycytidine did not noticeably affect the cell growth rates in BrdU-labeled normal and BS cultures. The finding that the reduction of BrdU-induced SCEs in BS is paralleled by cell growth improvement is of special interest.

Bloom Syndrome↗
PubMed1989

Inhibition of the adaptive response of human lymphocytes to very low doses of ionizing radiation by the protein synthesis inhibitor cycloheximide.

When human lymphocytes are preirradiated with 1 cGy of X-rays, the cells become less sensitive to subsequent exposures to high doses of about 150 cGy in that approximately one-half as many chromatid aberrations are induced as expected. This adaptation has been attributed to the induction of repair enzymes (proteins) some 4-6 h after the initial low-dose exposure. Experiments have now been carried out showing that application of the protein synthesis inhibitor cycloheximide at this time, but not earlier, prevents the adaptive response.

Adaptation, Physiological↗
PubMed1995

Cycloheximide and buthionine sulfoximine prevent induction of genotoxic adaptation by cadmium salt against methyl mercuric chloride in embryonic shoot cells of Hordum vulgare L.

Presoaked seeds of barley Hordeum vulgare L. pretreated with cycloheximide (CH), 10(-6) M or bythionine sulfoximine (BSO), 10(-4) M, were exposed to methyl mercuric chloride (MMCl), 10(-4) M, with or without prior conditioning with cadmium sulfate (CdSO4), 10(-4) M. Subsequently as the seeds germinated the endpoints measured were mitotic index, cells with mitotic aberrations and micronuclei (MNC) in embryonic shoot cells fixed at 40, 44, 48 and 52 h of recovery. Indicated by the significant reduction (p < or = 0.05) of the yield of cells with aberrations or MNC, the results confirmed that CdSO4-conditioning triggered an adaptive response to MMCl-challenge. Pretreatments of CH and BSO, whereas they potentiated the genotoxicity of MMCl, significantly prevented (p < or = 0.05) the Cd-induced genotoxic adaptation. That underscores a possible involvement of proteins in addition to phytochelatins in the underlaying mechanisms.

Adaptation, Physiological↗
PubMed1986

Regulation of alkaline phosphatase activity in rat hepatoma cells. Effects of serum proteins, cycloheximide, actinomycin D, chloroquine, dinitrophenol and potassium cyanide.

Alkaline phosphatase activity in rat hepatoma cells (R-Y121B) cultured in a monolayer at 0.5% serum was enhanced by serum, bovine serum albumin, casein and gamma-globulin, but ovalbumin, polyvinylpyrrolidone, dexamethasone, insulin and dibutyrylcyclic AMP showed little effect on alkaline phosphatase activity. In addition, cycloheximide, actinomycin D, chloroquine, dinitrophenol and potassium cyanide also increased the enzyme activity, although the incorporation of [14C]leucine into cellular proteins was almost completely inhibited in the presence of these cytotoxic substances. When R-Y121B cell homogenates were incubated at 37 degrees C, alkaline phosphatase activity increased in a pH-dependent manner: the maximal increase was observed at pH 7.1. The magnitudes of the increase differed among cell homogenates and a 4- to 10-fold increase was observed. Alkaline phosphatase in R-Y121B cells was apparently heat-stable, but that in the cells obtained from various treatments was heat labile and the latter activity decreased to less than 50% of the initial activity after 15 min of incubation at 56 degrees C. Alkaline phosphatase in the control and also in the treated cells was more sensitive to L-homoarginine than L-phenylalanine. The Lineweaver-Burk plot showed that the increases in the enzyme activity were accompanied by changes not only in V but also in Km for alkaline phosphatase reaction. Finally, it has been suggested that the increases in alkaline phosphatase activity under various conditions are due to the conversion of the molecule with a low enzyme activity to the molecule with a high enzyme activity in R-Y121B cells.

Alkaline Phosphatase↗
PubMed1991

Glucocorticoids inhibit fructose 2,6-bisphosphate synthesis in rat thymocytes. Opposite effect of cycloheximide.

The content of fructose 2,6-bisphosphate (Fru(2,6)P2) and lactate production in triamcinolone acetonide-treated rats thymocytes was studied. The effect in vitro of corticosterone and dexamethasone on normal thymocytes was also examined. Glucocorticoids produced a marked decrease in Fru(2,5)P2 content and lactate production. The largest effect was observed with triamcinolone acetonide (7.5 mg per kg body weight), which after 20 h of treatment produced over 90% of inhibition. This change was accompanied by the decrease of both phosphofructokinase-1 and -2 activities and ATP levels, without modifications of hexoses phosphate content. The inhibitory actions of glucocorticoids were abolished by cycloheximide, an inhibitor of protein synthesis. Furthermore this drug, by itself, increased Fru(2,6)P2 content by more than 50% compared with the controls.

Animals↗
PubMed1995

The influence of antioxidants and cycloheximide on the level of nitric oxide in the livers of mice in vivo.

When injected into mice prior to the NO generation increase induced with lipopolysaccharide (LPS) from Escherichia coli, exogenous antioxidants diethyldithiocarbamate (DETC) or phenazan (sodium 3.5-di-tert-butyl-4-oxiphenylpropionate) as well as the inhibitor of protein biosynthesis, cycloheximide (CHI) attenuated the NO production in mouse liver in vivo. These data demonstrated the key role of free radicals, which were likely, active oxygen species, in the synthesis of inducible NO-synthase (iNOS) responsible for the NO production in this organ. Similar effects of phenazan and CHI were observed in livers of mice treated with gamma-irradiation or LPS + Fe(2+)-citrate, which suggested that these treatments also induced 1NOS synthesis through initiating the action of active oxygen species. The rate of NO synthesis was estimated by accumulation of paramagnetic mononitrosyl iron complexes with DETC (MNIC-DETC) detected using the EPR method. The formation of MNIC-DETC complexes was found in the brain of mice pre-treated with LPS + Fe(2+)-citrate which seemed to be due to iNOS synthesis stimulated by this treatment.

Animals↗
PubMed1995

Effects of vomitoxin (deoxynivalenol) and cycloheximide on IL-2, 4, 5 and 6 secretion and mRNA levels in murine CD4+ cells.

The effects of continuous in vitro exposure to the trichothecene, vomitoxin (VT) or another protein synthesis inhibitor, cycloheximide (CHX), on interleukin (IL) secretion and mRNA levels were evaluated in murine splenic CD4+ cells. Significant increases were seen in supernatant IL-2, IL-4 and IL-5 obtained from 7 day Concanavalin A (Con A)-stimulated CD4+ cultures containing VT concentrations of 250, 100 and 100 ng/ml, respectively, compared with controls run in the absence of VT. The effect of VT on CD4+ cell proliferation was also assessed after culturing for 3, 5 and 7 days with Con A. Although total cell numbers were not affected at day 3, cultures at day 5 with 50 or more ng VT/ml and at day 7 with 100 or more ng VT/ml had significantly lower cell numbers than controls. In addition, viable cell number was unaffected at day 3, but was significantly decreased at day 5 by VT concentrations of 12.5 ng or more ml and at day 7 by 100 or more ng VT/ml. Elevations in IL-2, IL-4 and IL-5 were also observed in 7-day Con A-stimulated CD4+ cell cultures containing CHX at 50-100, 50 and 10 ng/ml, respectively. When CD4+ cells were stimulated with Con A in the absence of inhibitors and then subjected to reverse transcriptase-polymerase chain reaction coupled with Southern analysis, maximal IL-2, IL-4 and IL-6 mRNA levels were induced at 48 hr whereas peak IL-5 mRNA was observed at 72 hr. Superinduction of IL-2 mRNAs was observed in the presence of VT at 50-100 ng/ml and CHX at 50-250 ng/ml. IL-4 and IL-5 mRNAs were superinduced by VT at 100 ng/ml and CHX at 50 ng/ml. The results suggest that VT and CHX could superinduce both interleukin secretion and mRNA transcript levels in CD4+ cell cultures and that, for VT, these effects occurred concurrently with inhibition of cell proliferation.

Analysis of Variance↗
PubMed1986

Effects of cycloheximide on in vitro testosterone secretion from RANA catesbeiana ovaries.

A 1 hr exposure to 20 micrograms/ml of the protein synthesis inhibitor, cycloheximide (CHX), essentially abolished secretion of testosterone (T) by bullfrog ovarian fragments during simultaneous administration of homologous pituitary extract and CHX. Removal of CHX from the medium after 4 hr of treatment reversed the inhibition of T secretion, allowing it to attain control levels. Pre-exposure of ovarian fragments to CHX was not required to obtain an inhibition of T secretion. These data supported the hypothesis that protein synthesis is required for acute and chronic gonadotropic stimulation of steroidogenesis by the bullfrog ovary.

Animals↗
PubMed1984

Effect of propranolol and cycloheximide on the ethanol-induced increase in liver tryptophan oxygenase activity in starved rats.

Increased supply of tryptophan to the liver, resulting from the lipolytic action of ethanol, is suggested to be responsible for the increased activity of liver tryptophan oxygenase after ingestion of a single large dose of ethanol. This hypothesis was tested using an antilipolytic drug, propranolol, prior to ethanol treatment. It was found that, while propranolol did inhibit the ethanol-induced increase in blood unesterified fatty acids and free tryptophan concentrations, it did not prevent the activation of tryptophan oxygenase by ethanol. In another experiment, where cycloheximide was used to block protein synthesis, it was found that increased protein synthesis rather than decreased protein degradation is probably responsible for the accumulation of liver tryptophan oxygenase after ethanol ingestion.

Animals↗
PubMed1986

Cycloheximide or puromycin can substitute for PDGF in inducing cellular DNA synthesis in quiescent 3T3 cells.

A brief exposure of quiescent (Go) Swiss 3T3 mouse fibroblasts to inhibitors of protein synthesis can replace platelet-derived growth factor in the stimulation of cellular DNA synthesis. When 3T3 cells, after a 6 hr exposure to either cycloheximide or puromycin, are incubated with platelet-poor plasma, a significant percentage of cells enters DNA synthesis. Either inhibition of protein synthesis, or platelet poor plasma by themselves are totally ineffective. A possible mechanism by which inhibitors of protein synthesis may initiate cell cycle progression is through the activation of the c-myc gene.

Animals↗
PubMed1986

Anisomycin and cycloheximide, like growth factors, stimulate rapidly ATP turnover in 3T3 cells.

Addition of EGF and insulin to quiescent cultures of 3T3 cells induce a rapid stimulation of ATP turnover. We show that, like growth factors, anisomycin and cycloheximide, two inhibitors of protein synthesis, induce in 3T3 cells, a rapid increase in ATP turnover. However, this effect was not the result of the inhibition of protein synthesis since puromycin, in the same experimental conditions, did not stimulate ATP turnover.

Adenosine Triphosphate↗
PubMed1987

Effects of glucocorticoids and cycloheximide upon transcription of ribosomal RNA gene in rat liver: application of quantitative S1 nuclease mapping analysis.

The change in the amount of pre-rRNA synthesized in rat liver was examined by S1 nuclease mapping analysis using the probe containing the 5' end of the rat 45S rRNA gene. It was found that the amount of pre-rRNA of adrenalectomized rats, which was about half of the normal level, was increased after administration of dexamethasone attaining to the normal level at 12 h, and that the hormone-induced pre-rRNA synthesis was completely abolished within 1 h after injection of cycloheximide. These results indicate that the glucocorticoids-stimulated initiation of rRNA transcription is mediated by the hormone-dependent short-lived protein(s).

Animals↗
PubMed1987

Studies on ornithine decarboxylase from liver, kidney and tumoral tissues during activity decay following cycloheximide administration.

We have studied the activity, thiol-dependency and Km of ornithine decarboxylase (ODC) from the following sources: liver of rats subjected to partial hepatectomy or administered thioacetamide, the rat 3924A Morris hepatoma, the rat AH130 Yoshida ascites hepatoma, a mouse transplantable mammary carcinoma and kidney of rats administered testosterone propionate. In order to detect possible changes occurring during in vivo ageing of this enzyme we inhibited protein synthesis with cycloheximide. A gradual decrease of Km during ageing was observed in ODC from liver.

Animals↗
PubMed1989

Regression of autophagic vacuoles in mouse pancreatic cells: a morphometric study of the effect of methylamine and chloroquine followed by cycloheximide treatment.

Treatment of mice with methylamine and chloroquine for two hours markedly increased the volume fraction of autophagic vacuoles in the pancreatic acinar cells of the mouse. The autophagic vacuoles disappeared from the cells within 20 min after the administration of a suppressor of autophagic sequestration cycloheximide to animals pretreated with 0.25 mg b.w. dose of methylamine. In contrast, no regression or very slow decay was seen in cells of mice pretreated with higher doses of methylamine (0.50-0.70 mg/g b.w.) and chloroquine (0.08 mg/g b.w.). Our data show that the two drugs retard the disintegration of autophagic vacuole content. It is concluded, that accumulation of autophagic vacuoles due to their slow turnover is an important mechanism of the expansion of autophagic vacuole compartment under the effect of methylamine and chloroquine.

Animals↗