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PubMed1989

Cycloheximide-sensitive [35S]methionine labeling of proteins in goldfish retinal ganglion cell axons in vitro.

Polypeptides of retinal ganglion cell axons of the goldfish, regenerating in culture, were labeled by [35S]methionine after decentralization from the explant. Microscopic samples, composed of isolated axonal fields, were analyzed by SDS ultramicroelectrophoresis and autoradiography. Of the several proteins exhibiting cycloheximide-sensitive labeling, beta-tubulin and actin were consistently and prominently labeled, although the possibility of a labeled alpha-isoform with a lower mol. wt. could not be ruled out.

Actins↗
PubMed1991

Estimation of the chloramphenicol and cycloheximide inhibition of protein synthesis in brain cholinergic synaptosomes.

Cholinergic synaptosomes have been prepared from sheep brain cortex by means of an immunoaffinity method using a specific anti-(Chol I) antiserum. The [14C]leucine incorporation into proteins of this preparation shows a low cycloheximide and a high chloramphenicol sensitivity. This fact suggests that the mitochondrial protein synthesis system is the only one present in this fraction.

Animals↗
PubMed1992

Anisomycin and cycloheximide protect cerebellar neurons in culture from anoxia.

Protein synthesis inhibitors have recently been shown to protect from ischemia-induced neuronal death in the rat hippocampus in vivo. In an attempt to further investigate the mechanism of neuronal death resulting from anoxia, cerebellar neurons grown in culture were exposed to an anoxic atmosphere in the presence of protein synthesis inhibitors. Anisomycin and cycloheximide (100 micrograms/ml) offered, respectively, a 97 +/- 4% and 26 +/- 13% protection against anoxia-induced neuronal death.

Animals↗
PubMed1991

The defective in vitro expression of interferon-gamma messenger RNA in rheumatoid arthritis is recovered by cycloheximide.

Circulating T lymphocytes from patients with rheumatoid arthritis (RA) were found to produce low concentrations of interferon-gamma (IFN-gamma) and express low amounts of this messenger RNA (mRNA) in response to stimulation with phytohemagglutinin (PHA). In this study, we have examined the superinduction effect of cycloheximide (CHX) on the IFN-gamma mRNA expression in PHA-stimulated T lymphocytes from nine patients with active RA compared to three healthy individuals. When CHX was added 6 hr postactivation, the expression of IFN-gamma mRNA in RA patients increased significantly at 24 and 48 hr (P less than 0.01) and reached levels similar to those observed in controls. We suggest that posttranscriptional events could play a role in the defective production of IFN-gamma observed in RA.

Arthritis, Rheumatoid↗
PubMed1990

Ovulation blockade through synergism of cycloheximide with assorted anesthetics.

This report addresses the following question: Can ovulation be blocked through a combined action of two drugs, which individually have no effect on ovulation. Ovulation blockade in hamsters was achieved through synergism of two drugs that individually had no effect on ovulation. Treatments were given at 18:00 h on pro-estrus. The keystone finding was that cycloheximide (CX), in a dose too small to affect ovulation, can be made to block ovulation by pretreating hamsters 15 min earlier with pentobarbital. Ovulation blockade was also achieved with phenobarbital + CX, ketamine + CX, and ether + CX. When given alone, none of the four anesthetics interfered with ovulation. The mechanism by which the anesthetic/CX synergism works is not known. The pituitary can be excluded as a target, because it is not necessary for ovulation after 15:30 on pro-estrus. It is speculated that CX reduces the synthesis of ovarian proteins needed for follicle rupture, and the anesthetics augment this process through action on either the ovary, the brain, the liver, or a combination thereof.

Anesthetics↗
PubMed1982

Effect of actinomycin D and cycloheximide on experimental myocardial infarction in rats.

Actinomycin D, an inhibitor of DNA-directed RNA synthesis, or cycloheximide, a protein synthesis inhibitor, administered 24 h and 1 or 4 h respectively, before inducing coronary occlusion in conscious rats, offered marked protection against postinfarction ventricular fibrillation and sudden death. When actinomycin D was given 4 h prior to coronary ligation, the outcome of myocardial infarction was not influenced, the well-established cardioprotective effect of dexamethasone was however completely abolished. These results suggest that protein factors may be involved in the early events of myocardial infarction.

Animals↗
PubMed1982

Cycloheximide prevents apomorphine-induced yawning, penile erection and genital grooming in rats.

Apomorphine (50 micrograms/kg) induced repeated episodes of yawning, penile erection and genital grooming in rats. A dose of cycloheximide, which inhibited brain protein synthesis by 50% totally prevented apomorphine-induced yawning and reduced by approximately 50% the occurrence of episodes of penile erection and genital grooming. However, this treatment failed to modify the stereotyped behaviour induced by 200 micrograms/kg of apomorphine. These results suggest that protein synthesis is required for the behavioural effects of small doses of apomorphine.

Animals↗
PubMed1992

Dynamics of vinblastine-induced autophagocytosis in murine pancreatic acinar cells: influence of cycloheximide post-treatments.

Accumulation of autophagic vacuoles (AVs) was monitored by electron microscopic morphometry in murine pancreatic acinar cells during the 5-hr period after a single injection of vinblastine (VBL). The expansion of the autophagic compartment (AC) occurred in two waves. AVs accumulated in the first 90 min and regressed in the next hour, but thereafter AC expanded again, and 5 hr following the VBL injection, as much as 5.3% of the cytoplasmic volume was found sequestered into the AC. The high rates of accumulation of AVs indicated that VBL stimulated AV formation (segregation) during both expansion phases. To have a deeper insight into the dynamics of the process segregational inhibitor cycloheximide (CHI) was given 1 and 3 hr after VBL and the subsequent regression of the AC and its subcompartments (i.e., early, advanced, and late AVs) were measured during the next 90 min. We found that regression of AVs was fast in the first expansion and slowed down in the second expansion phase during which only early AVs regressed. CHI proved to be a fast and effective inhibitor of autophagic segregation, whether it was given before, simultaneously, or after the VBL injection. The aforementioned results argue for a dual mode of action of VBL (i.e., a prompt stimulation of segregation and a delayed retardation of AV maturation). The two effects of the alkaloid prevail differently along the time course. A further analysis of the behavior of the AC subcompartments showed that CHI perhaps inhibits segregational step(s) occurring prior to the actual formation of the autolysosomes.

Animals↗
PubMed1983

Inhibition of second meiotic division and a switching over to flagellar formation in secondary spermatocytes of newt by cycloheximide.

10.0 micro M cycloheximide (CH) was found to completely inhibit the second meiotic division of newt spermatocytes. Under continuous incubation with CH from the beginning of interphase II, secondary spermatocytes fail to initiate chromosomal condensation and thus remain in interphase II. After 12-15 h of incubation, a single motile flagellum, about 5 micrometers in length, was observed on each of the secondary spermatocytes. These flagella grew to a length of 60-80 micrometers, but thereafter ceased to grow, whereas ordinarily spermatids grew flagella up to 500 micrometers in length in the absence of CH [1]. When CH was applied within 2 h following telophase I, the percentage of meiosis II inhibition was almost 100% and when applied even later, it became less, which showed that the early half period during interphase II was sensitive to CH. Regardless of the length of incubation time with CH, flagella were found to grow within a period of 12-15 h following telophase I. Upon removal of CH, even after 60 h of incubation, the flagella of the secondary spermatocytes shortened and disappeared completely. These spermatocytes underwent the second meiotic divisions. Also, flagella grew on the resulting spermatids. The possibility that a particular centriole which participated in the first meiotic division changes into a basal body for flagellar formation under the influence of CH and vice versa upon removal of it, is discussed in the following.

Animals↗
PubMed1983

Regression of autophagic vacuoles in seminal vesicle cells following cycloheximide treatment.

A 0.25% fraction of cytoplasm was present in the autophagic vacuole compartment of the seminal vesicle cells of fasted and estrogen-treated mice. Autophagic vacuoles regressed rapidly after administration of 0.2 mg/g body weight cycloheximide to the animals and the decay appeared to follow first-order kinetics (average half-life 5.8 min, rate constant of regression 0.120 min-1). Our observations suggest that the drug suppressed the formation of autophagosomes. The fraction of cytoplasm removed by autophagy from the cells was estimated to be about 1.8% h under steady-state conditions.

Animals↗
PubMed1985

Effect of amino acids and cycloheximide on changes caused by vinblastine, leupeptin and methylamine in the autophagic/lysosomal system of mouse hepatocytes in vivo.

The number of autophagic vacuoles in hepatocytes of 24 h fasted mice in vivo increased manyfold following the administration of vinblastine, leupeptin and methylamine. The effect of each chemical is characterized by the predominance of a certain kind of vacuole. Vinblastine treatment is accompanied by a large proportion of vacuoles containing morphologically unaltered organelles, leupeptin causes preferential accumulation of dense and complex vacuoles, methylamine administration produces mostly large, electron-lucent, swollen vacuoles. The amounts of segregated and accumulated cytoplasmic material, expressed as percentage cytoplasm per hour, were 0.84%, 2.08% and 0.74% following vinblastine, leupeptin and methylamine treatment respectively. The actual rate of segregation was probably higher than this. Inhibition of degradation of the sequestered cytoplasmic material is proposed to be a main factor in the increase in the size of the autophagic/lysosomal compartment. Treatment with cycloheximide or exogenously added mixture of amino acids cut down the size of the autophagic/lysosomal system in control cells and strongly inhibited the accumulation caused by vinblastine, leupeptin and methylamine.

Amino Acids↗
PubMed1988

Involvement of serum factor(s) adsorbed to the dish in the response of cycloheximide-pretreated BP-A31 cells to serum pulses.

The mitogenic effect of serum pulses, observed previously in quiescent BP-A31 cells, is an artifact due to adsorption of (unknown) serum mitogens to the culture dish; the continuous presence of growth factors is necessary for these cells to traverse the G1 phase. When pretreated with cycloheximide (CH) during the last 8-24 h of quiescence, the BP-A31 cells are particularly sensitive to the adsorbed serum mitogens, as well as to low concentrations of fetal calf serum (less than 0.25%) and to basic fibroblast growth factor. In contrast, the mitogenic activity of insulin was not influenced by CH pretreatment. The expression of the "competence genes" c-myc and JE was only transiently elevated in quiescent BP-A31 cells during CH exposure and did not correlate with the enhancement of the cells' sensitivity to mitogens.

Adsorption↗
PubMed1990

Death of serum-free mouse embryo cells caused by epidermal growth factor deprivation is prevented by cycloheximide, 12-O-tetradecanoylphorbol-13-acetate, or vanadate.

Serum-free mouse embryo cells cultured in medium supplemented with insulin, transferrin, high-density lipoprotein, and fibronectin are dependent on epidermal growth factor for survival. Cycloheximide or actinomycin D prevented cell death caused by growth factor deprivation, suggesting that cell death required the synthesis of RNA and protein, a phenomenon similar to that reported for neuronal cell death in the absence of nerve growth factor. Orthovanadate, an inhibitor of phosphotyrosine phosphatases, and 12-O-tetradecanoylphorbol-13-acetate, an activator of protein kinase C, also prevented serum-free mouse embryo cell death in the absence of epidermal growth factor.

Adenylyl Cyclases↗
PubMed1992

Cycloheximide can rescue heat-shocked L cells from death by blocking stress-induced apoptosis.

Cultured mouse L cells undergo apoptosis upon 1 h heat shock at 43 and 45 degrees C. Morphologically characteristic apoptotic cells begin to appear soon after the shock. Immunohistochemistry with anti-transglutaminase antibody shows that in most treated cells the enzyme is induced. Its activation results in the formation of highly cross-linked detergent-resistant apoptotic bodies during recovery. Cycloheximide added during hyperthermic stress inhibits the appearance of apoptotic bodies, showing that heat-shock-induced apoptosis is dependent on protein neosynthesis. The analysis of colony-forming ability of heat-shocked L cells shows a survival of 5% at 43 degrees C and less than 0.02% at 45 degrees C. When protein synthesis is inhibited during heat shock the fraction of surviving cells increases to 23% at 43 degrees C and 0.9% at 45 degrees C. This suggest that part of the cells that die upon heat shock are not heavily damaged and would have survived in the presence of a block in protein synthesis.

Animals↗
PubMed1986

A novel mechanism of resistance to alpha-difluoromethylornithine induced by cycloheximide. Growth with abnormally low levels of putrescine and spermidine.

Treatment of the chemically transformed fibroblasts BP-A31 and other cell lines with low concentrations of cycloheximide (CHM) for 72 h followed by the removal of the protein synthesis inhibitor leads to the proliferation of alpha-difluoromethylornithine (DFMO)-resistant phenotypes. These drug-resistant cells contain almost no ornithine decarboxylase (ODC) activity and concomitantly very low levels of putrescine and spermidine. Southern blot analysis and measurements of ODC activity and intracellular polyamine levels showed that the described mechanism of inducing resistance to DFMO triggered by CHM does not involve ODC gene amplification, altered transport of the drug or reduced affinity of the enzyme for DFMO.

Animals↗
PubMed1990

Interleukin 1- and tumor necrosis factor-stimulation of prostaglandin E2 synthesis in MDCK cells, and potentiation of this effect by cycloheximide.

The effects of interleukin (IL)-1 alpha, IL-1 beta and TNF alpha on prostaglandin-E2 synthesis in Madin-Darby canine kidney (MDCK) cells were investigated. IL-1 beta time- and dose-dependently stimulated prostaglandin-E2 synthesis. While TNF alpha produced a comparatively small but significant stimulation of PGE2 release, coincubation of IL-1 beta with TNF alpha produced a marked synergistic stimulation of PGE2 release. The effect of IL-1 beta and of IL-1 beta and TNF alpha was apparent as early as after 2 h of incubation. The enhanced PGE2 synthesis was inhibited by indomethacin as well as actinomycin D, while cycloheximide surprisingly potentiated PGE2 synthesis in response to both IL-1 beta and TNF alpha. IL-1 alpha alone was ineffective in stimulating a significant release of PGE2 at concentrations as high as 10 nM. However, it also showed a marked synergistic interaction with TNF alpha in stimulating PGE2 release.

Animals↗
PubMed1990

Heat shock induces enzymes of trehalose metabolism, trehalose accumulation, and thermotolerance in Schizosaccharomyces pombe, even in the presence of cycloheximide.

Exponentially growing cells of the fission yeast, Schizosaccharomyces pombe, contained virtually no trehalose at 27 degrees C but rapidly accumulated large quantities during heat shock at 40 degrees C. Activities of trehalose-6-phosphate synthase and trehalase also increased upon heat shock. Thermotolerance of the cells, measured as survival at 52 degrees C, increased in parallel to trehalose accumulation and decreased in parallel to the trehalose levels when cells were shifted back to 27 degrees C. Trehalose levels, activities of enzymes of trehalose metabolism and thermotolerance strongly increased upon heat shock even in the presence of cycloheximide, indicating that none of these effects requires protein synthesis. The data support the hypothesis that trehalose acts as a thermoprotectant in Schizosaccharomyces pombe.

Cycloheximide↗
PubMed1990

Effects of cycloheximide and tunicamycin on cell surface expression of pancreatic muscarinic acetylcholine receptors.

The importance of glycosylation in cell surface expression of muscarinic receptors in cultured guinea pig pancreatic acini was investigated. Recovery of the muscarinic receptor population after carbachol-induced down regulation was blocked by cycloheximide but not by tunicamycin, although tunicamycin reduced [3H]mannose incorporation into acinar macromolecules by up to 90%. Tunicamycin treatment also failed to alter carbachol stimulation of amylase secretion from cultured acini. These results indicate that glycosylation of the glandular subtype of muscarinic receptor in the pancreatic acinar cell is not necessary for its insertion in the plasma membrane or for its functional activity.

Animals↗