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PubMed1983

Analysis of mutagenic DNA repair in a thermoconditional repair mutant of Saccharomyces cerevisiae. II. Influence of cycloheximide on UV-irradiated exponentially growing rev2ts cells.

The time course of REV2 dependent recovery from prelethal UV damage and UV-induced locus-specific reversion of the his5-2 allele was determined in temperature-shift experiments by use of a thermoconditional allele of the rev2 gene (rad5-8, rev2ts). In UV-irradiated, exponentially growing rev2ts cells the REV2 dependent repair activity persists for up to 8 h at permissive temperature (23 degrees C), while the REV2 dependent mutagenic process is mostly completed within 2 h. The REV2 dependent process in exponentially growing cells is highly impaired by inhibition of protein synthesis. However, a REV2 dependent repair activity independent of de novo synthesis is detectable, even in the presence of up to 200 micrograms/ml cycloheximide, a response not found in stationary phase cells. Thus, the REV2 dependent process seems to be partially constitutive in exponentially growing cells. Additionally, exponentially growing rev2ts cells were considerably more UV-sensitive at restrictive temperature (36 degrees C) than were stationary phase cells.

Cell Cycle↗
PubMed1988

Cycloheximide, an inhibitor of protein synthesis, prevents gamma-interferon-induced expression of class II mRNA in a macrophage cell line.

To characterize the mechanisms by which interferon gamma (IFN-gamma) upregulates major histocompatibility complex class II mRNA levels in mouse macrophages, we studied the effect of IFN-gamma on the transcription rate of class II genes and investigated the requirement for ongoing protein synthesis for the induction of class II mRNA expression. Nuclear run-off assays demonstrate that IFN-gamma induces class II mRNA at the transcriptional level. Treatment with cycloheximide, an inhibitor of protein synthesis, prevented the IFN-gamma-mediated accumulation of E alpha mRNA in the mouse macrophage cell line P388 D.1, indicating that induction of E alpha mRNA in P388 D.1 cells requires de novo synthesis of a protein intermediate. Our studies suggest that this putative protein factor is labile and required throughout the induction period.

Animals↗
PubMedDate not supplied

Effects of serum, cycloheximide and actinomycin D on protein secretion by quiescent mouse embryo fibroblasts.

Quiescent secondary cultures of Swiss mouse embryo fibroblasts secrete several proteins in response to the addition of 20% fetal calf serum (FCS). Of these proteins, a polypeptide of molecular weight (Mr) 48,000 (48 K) was identified in the medium within an hour of mitogenic stimuli. In the next hour an additional protein of Mr26,000 (26 K) appeared in the medium. These two proteins were absent in the conditioned medium of quiescent cells. A third protein of molecular weight 45,000 (45 K) was found in small quantities in the conditioned medium of quiescent cells but a 2-3 fold increase in the level of this protein was observed in the medium of stimulated cells. The level of the serum-induced 45 K protein was much higher in the medium of cells that were treated with cycloheximide (CH) and FCS than that found in the medium of cells treated with FCS alone. A 40,000 dalton protein was found to be a quiescence specific protein which was observed in large amounts in the medium of quiescent cells; the level of this protein gradually declined in the conditioned medium as the cells entered into the proliferative phase. Actinomycin D specifically inhibited the level of the 45 K secreted protein and a 29 K intracellular protein when added along with CH. In contrast to the inhibition of the synthesis of mitogen induced proteins, actinomycin D super-induced the intracellular and extracellular levels of the matrix proteins fibronectin and procollagens.

Animals↗
PubMed1980

Cytochemistry of the microtrabecular network in compact nucleoli of hepatocytes treated with cycloheximide.

Compact nucleoli without the segregation of nucleolar components were produced in hepatocytes by the treatment of experimental rats with cycloheximide to facilitate a cytochemical study on the organization of nucleolar components in such nucleoli. The extraction of pepsin pretreated specimens with nucleases (deoxyribonuclease and ribonuclease) demonstrated that compact nucleoli are characterized by a relatively uniform distribution of RNP components which mask a microtrabecular intranucleolar network. This network apparently consists of proteins and contains fine DNA filaments.

Animals↗
PubMed1975

Chloramphenicol/thiamphenicol and cycloheximide as tools for the measurement of mitochondrial protein synthesis in vitro during organogenesis of rat embryos.

1. A test system was developed to allow the measurement of protein synthesis in vitro in mitochondria from tissues which were accessible only in small quantities. The subcellular fractions which could be isolated are not purely mitochondrial but contain other particles as well, mainly microsomal, which are also active in protein synthesis. The following differences between mitochondrial and microsomal protein synthesis in vitro were used to measure selectively the mitochondrial portion in cell fractions sedimenting between 600 and 10000 X g: selective inhibition of mitochondrial protein synthesis by chloramphenicol/thiamphenicol selective inhibition of microsomal protein synthesis by cycloheximide kinetics of amino acid incorporation a medium favoring mitochondrial protein synthesis Activity of mitochondrial protein synthesis was based on measurements of cytochrome oxidase, a mitochondrial marker enzyme. 2. The technique developed was used for the evaluation of mitochondrial protein synthesis in mammalian embryonic tissues. It may equally well be applied to other tissues available in small amounts and in cases where the isolation of highly purified mitochondrial fractions is met with difficulty. 3. Comparing the rate of 14C-phenylalanine incorporation into mitochondrial protein from rat embryos at different stages of gestation, it was found that mitochondria from 11=day-old rat embryos exhibit an approximately 30-fold higher capacity for protein synthesis than those of day 13-16. On day 12 the capacity is 6 times higher than on the following days.

Animals↗
PubMed1983

Blockade of the renal tubular effects of vitamin D by cycloheximide in the rat.

To further characterize the mechanisms by which 25(OH) vitamin D3 (25(OH)D3) and 1.25(OH)2 vitamin D3 (1,25(OH)2D3) suppress the phosphaturic action of parathyroid hormone (PTH) we have studied the effects of cycloheximide (cyclohex), a protein synthesis inhibitor, on the interaction between PTH and vitamin D metabolites in parathyroidectomized (PTX) rats, both in vivo and in vitro experiments. In clearance studies PTX PTH-infused rats were pretreated with cyclohex 2 h before the administration of vitamin D. In control, PTX PTH-infused rats not pretreated with cyclohex, the administration of 25(OH)D3 and 1,25(OH)2D3 was associated with a fall in fractional excretion of phosphate (CP/CIN) from 0.30 +/- 0.05 to 0.16 +/- 0.02 and from 0.31 +/- 0.05 to 0.13 +/- 0.01 (P less than 0.005) respectively. Cyclohex-pretreated PTX PTH-infused rats failed to respond to both 25(OH)D3 and 1,25(OH)2D3, and CP/CIN, which rose after PTH, remained 0.32 +/- 0.05 and 0.29 +/- 0.03 respectively. In vitro, both 25(OH)D3 and 1,25(OH)2D3 inhibited the PTH-induced activation of adenylate cyclase in the renal isolated membrane fractions. Pretreatment with cyclohex abolished this effect of vitamin D metabolites. These results show that cyclohex blocks the antiphosphaturic effects of both 25(OH)D3 and 1,25(OH)2D3 but does not alter the response to PTH. These findings are consistent with the possibility that the acute renal action of vitamin D depends on de novo synthesis of protein.

Adenylyl Cyclases↗
PubMed1994

Long lasting anti-adrenergic effect of 7-oxo-prostacyclin in the heart: a cycloheximide sensitive increase of phosphodiesterase isoform I and IV activities.

Evidence is accumulating that 7-oxo-prostacyclin (7-oxo-PGI2) induces a delayed indirect anti-adrenergic and cytoprotective effect on the myocardium, the mechanism of which is still unclear. To demonstrate that a single application of 7-oxo-PGI2 (50 micrograms/kg i.m.) 48 h prior to starting experiments attenuates the isoprenaline inducible inotropic response and accumulation of cAMP, isolated hearts of pretreated animals were perfused in the Langendorff mode with and without isoprenaline (1 to 100 nM). The late anti-adrenergic effect of the drug was manifested by a significant attenuation in the elevation of cAMP levels as well as in contractile force development. This effect was not due to changes in cAMP generation as there were identical beta 1-adrenoceptor densities and affinities (as calculated from [3H]-CGP binding studies), Gi and G alpha s protein patterns (as taken from Western blots) as well as adenylyl cyclase activity measurements in the hearts studied. The anti-adrenergic potency of 7-oxo-PGI2, however, was found to be related to a significant rise in cyclic nucleotide hydrolysis by phosphodiesterase (PDE). Using the fast-performance liquid chromatographic separation for PDE isoforms, a significant increase in the activity of PDE isoforms I and IV (260 +/- 28 vs 110 +/- 12 pmol cGMP/min x enzyme fraction and 77 +/- 11 vs 34 +/- 3 pmol cAMP/min x enzyme fraction, respectively) was found in the solubilized fraction of cardiac membranes in comparison to untreated controls; PDE IV activity was also increased in the cytosolic fraction (106 +/- 14 vs 65 +/- 6 pmol cAMP/min x enzyme fraction). The hypothesis that the delayed anti-adrenergic effect of 7-oxo-PGI2 is initiated by an induction and accelerated synthesis of PDE I and IV in the heart is underlined by the fact that cycloheximide suppresses completely both the rise in PDE activities and the anti-adrenergic effects studied. It is suggested that an inducible predominance of cAMP degradation over its generation may be of relevance in processes related to heart protection.

Adenylyl Cyclases↗
PubMed1984

The inhibitory effect of actinomycin D and cycloheximide on the increase in activity of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase in experimentally induced diseased skeletal muscles.

The myotoxic effect of the subcutaneous administration of N,N1-dimethyl-p-phenylenediamine (DPPD) in rats was enhanced by the simultaneous administration of hyaluronidase. The resulting myopathy was associated with an early and dramatic increase in activity of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Administration of actinomycin D or cycloheximide prior to the combined DPPD and hyaluronidase treatment prevented the increase in activity of both pentose phosphate pathway enzymes, indicating that the increase in activity requires RNA synthesis and protein synthesis. The possibility that the increase in activity of both NADPH-regenerating enzymes results from the modification by effectors of existing less active forms of these enzymes leading to more highly active forms was refuted.

Animals↗
PubMed1993

(14C-methyl)-L-methionine uptake in rat brain tumors before and after treatment with the protein synthesis inhibitor cycloheximide.

Autoradiographic study of (14C-methyl)-L-methionine with brain tumor bearing rats aimed at an elucidation of the mechanism of tracer accumulation in the protein synthesis of tumor. Twice as much tracer accumulated in the tumors compared as in the contralateral gray matter (nontumor region) at 90 min post intravenous injection. The protein-bound fraction of the tumors, expressed as acid-insoluble fraction (AIF), was 1.7 +/- 0.6 (mean +/- standard deviation, n = 6), significantly higher than that (0.8 +/- 0.2) of the nontumor region (p < 0.05 by the Mann-Whitney test). The tumor AIF comprised 82.3 +/- 9.2% of the total amount of the tracers accumulated in the tumors. The protein synthesis inhibitor cycloheximide reduced the tracer uptake and the AIF of the tumors to an almost same level as the nontumor region. These findings indicate that metabolic acceleration of protein synthesis may be a main reason for the high accumulation of (14C-methyl)-L-methionine in tumor.

Animals↗
PubMed1993

A preliminary survey of cycloheximide-resistant airborne fungi in Turin, Italy.

Numbers and type of the cycloheximide-resistant part of the aerially transmitted mycoflora of Turin were studied. Samples from three areas characterized by differing human usage were taken in the first week of March. During each sampling, 12 m3 of air were aspirated, using an one-stage volumetric sieve sampler. Fifty-two mesophilic species and eight thermotolerant were isolated. Propagule load varied from 2.92 to 120.31 cfu m-3. The following species appear not to have been reported previously from air samples: Ascotricha bosei, Blastobotrys navarrensis, Cryptendoxyla hypophloia, Chrysosporium an. gymnoascus demonbreunii, Ophiostoma piceae, Penicillium vulpinum, Phialophora mustea, Rhinocladiella pedrosoi, Scopulariopsis croci, S. komngii and Sesquiallium candelabrum. A significant number of potential opportunistic pathogens was isolated.

Air Microbiology↗
PubMed1992

Effects of nefiracetam, DM-9384 on amnesia and decrease in choline acetyltransferase activity induced by cycloheximide.

The effects of nefiracetam, [N-(2,6-dimethyl-phenyl)-2-(2-oxo-pyrrolidinyl)acetamide, DM-9384], a cyclic derivative of GABA, were investigated in the cycloheximide (CXM)-induced amnesia animal model using the passive avoidance task. Pre-training administration of DM-9384 attenuated the CXM-induced amnesia as indicated by prolongation of step-down latency. It protected against CXM-induced inhibition of choline acetyltransferase activity in the cerebral cortex. These results suggest that DM-9384 attenuates CXM-induced amnesia by interacting with AChergic neuronal system and enhancing protein synthesis in the brain.

Amnesia↗
PubMed1992

Morphogenesis of African swine fever virus in monkey kidney cells after reversible inhibition of replication by cycloheximide.

The late cytoplasmic phases of African swine fever virus (ASFV) morphogenesis in monkey kidney cells have been studied by transmission electron microscopy, focusing attention on the synthesis of viral envelopes. Morphogenesis was studied after reversible cycloheximide blockage of monkey kidney cells infected with ASFV. ASFV appears to synthesize its external and internal envelopes within the cellular cytoplasm, at the same time as the capsid is formed, with intracellular and extracellular virions showing similar structure and polypeptide composition.

African Swine Fever Virus↗
PubMed1980

5'-Nucleotidase activity in liver homogenates of rats treated with CCl4, colchicine, cycloheximide, emetine, ethanol, ethionine and 5-fluorotryptophan.

5'-Nucleotidase activity an enzyme marker of the plasma membranes, increases in female rat liver homogenates following ethionine administration, while homogenates from males show no changes. Treatment with CCl4, colchicine, cycloheximide, emetine, ethanol and 5-fluorotryptophan does not significantly modify the 5'-nucleotidase activity of liver homogenates of either female or male rats.

Animals↗
PubMed1989

Cycloheximide inhibits the induction of collagenase mRNA in chondrocytes exposed to synovial factors or recombinant interleukin-1.

Synoviocytes secrete "chondrocyte activating factors" (CAF) which, like recombinant interleukin-1 (IL-1), induce the synthesis of collagenase by cultures of articular chondrocytes. Enzyme synthesis is preceded by the appearance of collagenase mRNA some 3-5 hours after exposure of the chondrocytes to CAF or IL-1. Cycloheximide (CX) inhibits the appearance of this message in a dose-dependent manner. At a concentration of 5 micrograms/ml inhibition by CX is completely reversible, with superinduction being observed in certain experiments. Identification of the newly synthesised proteins which are required for collagenase mRNA induction would greatly advance our understanding of collagenase gene expression.

Animals↗
PubMed1991

Suppression of sodium arsenite-potentiated cytotoxicity of ultraviolet light by cycloheximide in Chinese hamster ovary cells.

Post-treatment with sodium arsenite synergistically increased the cytotoxicity of ultraviolet (UV) light. The potentiation of UV cytotoxicity by sodium arsenite was apparently suppressed by cycloheximide (CHM), a protein synthesis inhibitor. The protective effect of CHM against sodium arsenite-potentiated UV cytotoxicity was well correlated to its activity in inhibiting the synthesis of stress proteins, particularly a small polypeptide with a molecular weight of 8500 dalton. This small stress protein was demonstrated as ubiquitin by immunoprecipitation. Our results also showed that neither ubiquitin induction nor potentiation of UV cytotoxicity by post-treatment with sodium arsenite was observed in the stationary cells. Thus, we suggested that ubiquitin is possibly involved in the action of arsenite in potentiating UV-induced cell killing.

Animals↗
PubMed1992

Serum and insulin inhibit cell death induced by cycloheximide in the human breast cancer cell line MCF-7.

Continuous exposure of cells to cycloheximide (CHM) terminates in cell death. This may result from CHM's inhibition of protein synthesis. In the present study we investigated the effect of serum and insulin on cell death induced by CHM in the human breast cancer cell line MCF-7, and correlated this effect to the inhibition of protein synthesis. Cell death was evaluated by measuring either dead cells by the trypan blue dye exclusion test or by the release of lactic dehydrogenase into the culture medium. CHM (0.1 to 50 micrograms/ml) was shown to induce cell death in a time- and concentration-dependent manner. Including either fetal bovine serum or insulin in the culture medium inhibited this cell death in a concentration-dependent manner. Protein synthesis as measured by [3H]leucine incorporation was inhibited by the increasing concentration of CHM. However, fetal bovine serum and insulin did not alter the protein synthesis inhibition rate induced by CHM. These results indicate that inhibition of protein synthesis is not enough for cell death to proceed. Insulin or factors present in serum may stabilize some crucial cell proteins (key enzymes, cytoskeletal or membrane components) which are vital for cell life.

Blood Proteins↗
PubMed1975

Cycloheximide-induced ultrastructural changes in hepatocyte nuclei in partially hepatectomized rats.

Nearly all the chromatin in regenerating rat hepatocytes appears to decondensed form 24 h after partial hepatectomy. When cycloheximide (CXM) is administered to partially hepatectomized rats, a marked condensation of chromatin occurs; 4 h after administration the quantity of condensed chromatin present is much higher than that found in the hepatocytes of sham-operated, untreated rats. No segregation or fragmentation of the nucleolus were, however, observed; this shows that the condensation of chromatin is not by itself sufficient to induce the segregation and fragmentation of the nucleolus. The mechanism governing CMX-induced chromatin condensation in regenerating hepatocytes is discussed.

Animals↗