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PubMed1973

Changes in cellulase and pectinase activities in fruit tissues and separation zones of citrus treated with cycloheximide.

Cellulase activity increased in separation-zone tissues 1 day after "Valencia" orange (Citrus sinensis [L.] Osbeck) was treated with 20 micrograms per milliliter cycloheximide. Exocellulase was detected only in the separation zones of treated fruit, whereas endocellulase was present in zones from both treated and control fruit. Endocellulase activity in separation-zone tissue of treated fruit was nearly three times as great as that in control tissues. Cellulase activity was restricted to separation-zone tissue. Pectinase and an albedo-macerating factor activity were very low and were not influenced by the treatment. The cycloheximide effect in these experiments was apparently caused by ethylene produced by wound tissue.

Journal Article↗
PubMed1973

Effects of Cycloheximide on Indoleacetic Acid-induced Ethylene Production in Pea Root Tips.

Cycloheximide inhibited ethylene production in excised pea root tips treated with high levels of indoleacetic acid (100 mum and 10 mum). In contrast, cycloheximide did not inhibit ethylene production induced by a lower concentration (1 mum) of indoleacetic acid unless it was added 2 hours before the indoleacetic acid treatment. These observations suggest that indoleacetic acid has two effects on the enzyme system involved in ethylene synthesis. At low concentrations (1 mum) indoleacetic acid increases ethylene production without protein synthesis, whereas at the higher concentrations, the synthesis of new protein is associated with increased ethylene production.

Journal Article↗
PubMed1979

Inhibition of Polar Indole-3-acetic Acid Transport by Cycloheximide.

Cycloheximide inhibits polar indoleacetic acid transport in midrib tissues of leaves of citrus (Citrus sinensis [L.] Osbeck) and poplar (Populus deltoides Bartr.) as measured by the donor-receiver agar cylinder technique. It appears that the mechanism of auxin transport inhibition by cycloheximide consists in arresting protein synthesis and not in the disruption of energy flow. The interpretation of the data takes into account the involvement of either a carrier protein or auxin-induced proton excretion in auxin transport.

Journal Article↗
PubMed1981

Cycloheximide stimulation of cyanide-resistant respiration in suspension cultures of senescent pear fruit cells.

Pear fruit cells undergoing a period of senescence in auxin-deprived media develop a substantial cyanide resistant respiration in response to the addition of 0.7 to 3.5 micromolar cycloheximide. The inhibitor does not affect overall cellular repiratory activity and titrations with salicylhydroxamic acid reveal that only a minor portion, about 10%, of the alternate pathway is utilized by the cycloheximide-treated senescent cells. The alternate respiratory pathway appears to be of mitochondrial origin but is not induced by chloramphenicol.

Journal Article↗
PubMed2001

Chemotaxis of the nematode Caenorhabditis elegans toward cycloheximide and quinine hydrochloride.

We investigated the chemotaxis of the nematode Caenorhabditis elegans toward cycloheximide, denatonium benzoate, 6-n-propyl-2-thiouracil, and quinine hydrochloride. Interestingly, C. elegans was strongly attracted to cycloheximide, while avoiding quinine hydrochloride. This is the first report thus far to describe the chemotactic responses of C. elegans toward bitter tastants for humans.

Journal Article↗
PubMed1999

Effects of Fructus schizandrae on cycloheximide-induced amnesia in rats.

The effects of Fructus Schisandrae (Schizandra Chinensis, (FS) on cycloheximide (CXM)-induced amnesia by using a passive avoidance task were studied in rats. FS at 0.25 and 0.75 g/kg administered for 1 week significantly prolonged the CXM-shortened step-through latency (STL). Of the fractions (n-hexane, chloroform and water), only the water fraction at 25 mg/kg administered for 1 week prolonged the CXM-shortened STL. These results suggest that the water fraction is the main active fraction of FS.

Amnesia↗
PubMed1978

Adaptation to cycloheximide of macromolecular synthesis in Tetrahymena.

Cycloheximide (CHI) at 10 ng/ml partially inhibited protein synthesis in exponential cultures of Tetrahymena Sp. At 20 ng/ml or greater, inhibition was complete. When protein synthesis was inhibited to any extent, cell division ceased immediately. In all instances where measured, synthesis of RNA and DNA also ceased. After a period of delay, cellular functions reinitiated in the order: (i) protein synthesis, (ii) DNA synthesis and, (iii) RNA synthesis and cell division. The delay in cell division was divided into three phases of: I, zero; II, low; and, III; fully recovered rates of exponential protein synthesis. The length of the three phases increased with increasing concentration of CHI. Prior growth of cells for one generation in the presence of 7.5 ng/ml CHI (facilitation) eliminated phase I and slightly decreased phases II and III following subsequent challenge with an inhibitory concentration of CHI. Facilitation for six generations further decreased phases II and III. Protein synthesis and cell division were not inhibited during facilitation. In the culture, succinate dehydrogenase activity did not increase during the delay but increased normally at the onset of division. In contrast, NADPH-cytochrome c reductase activity continued to increase for an hour after inhibition of protein synthesis, was constant for a period and did not increase again until an hour after reinitiation of cell division and RNA synthesis. Inhibition of division of all cells was immediate and reinitiation of synthesis and cell division was non-synchronous.

Adaptation, Physiological↗
PubMed1979

Effects of hydrostatic pressure in the range 100-300 atmospheres on cell division and protein synthesis in synchronized Tetrahymena pyriformis: a comparison with cycloheximide and emetine.

Heat-synchronized Tetrahymena pyriformis have been subjected to 5-, 15- and 30-minute pulses of hydrostatic pressure in the range 100-300 atm, without being simultaneously subjected to significant heats of compression. The pressure-induced division delays depend on (1) the level of pressure used, (2) the length of pressure pulse and (3) the time after the synchronizing treatment at which the pressure is applied. A pressure-dependent inhibition of 3H-leucine incorporation into protein was also measured. Comparison of the effects of pressure with those of pulse treatments of cycloheximide and emetine on cell division and protein synthesis revealed that the physical agent produced characteristically different responses from those of the chemical agents. Of particular interest was the fact that the division delays induced by pressures of 200 atm and above were greater than those observed after treatments with cyclohexmide and emetine which produced comparable levels of protein synthesis inhibition. Pressure also delayed cells if it was applied at a time when addition of chemical inhibitors had little effect on the first synchronous division. The results show that inhibition of protein synthesis by pressure cannot entirely account for pressure-induced effects on cell division. The possibility that pressure may also directly affect other processes, such as the assembly of proteins into structure required for division, is discussed.

Amino Acids↗
PubMed1985

Induction and/or selective retention of proteins in mammalian cells exposed to cycloheximide.

Exposure of a number of murine and human cell lines to low graded doses of cycloheximide (CXM) results in a pattern of protein synthesis consisting of enhanced and induced species. These can be divided into two main classes according to molecular weight (20-40 and 70-120 Kd), similar to what has been described for other agents that modify the physiological conditions of growth. In addition, the pronounced synthesis of a hitherto unreported 50-Kd protein species has been consistently observed in all lines tested. Simultaneous exposure of cells to CXM and actinomycin D results in suppressing synthesis of some but not all protein species observed, indicating that control mechanisms at both transcriptional and posttranscriptional levels may be operative in this system.

Animals↗
PubMed1986

Effect of cycloheximide and growth factors on gene expression in quiescent mouse embryo fibroblasts.

Gene expression in quiescent mouse embryo fibroblasts was studied by labelling the cells with [14C] amino acids and analysing the proteins by electrophoresis in polyacrylamide gradient gels containing sodium dodecyl sulfate. Cycloheximide (CH) pretreatment of the cells was found to induce the synthesis of four proteins of molecular weights 72,000, 68,000, 42,000, and 29,000. These proteins were induced by CH both in serum-arrested and serum-stimulated cells. Addition of platelet-derived growth factor to serum-arrested quiescent cells also induced the synthesis of these proteins. Addition of CH and fetal calf serum (20%) to quiescent cells resulted in a dramatic increase in the synthesis of actin and another protein of molecular weight 29,000. The 29,000-dalton protein was present in higher quantities in the nuclei of induced cells. This protein appeared to be an early protein whose synthesis was transiently induced in quiescent cells within 3 hours of addition of 20% fetal calf serum (FCS). The synthesis of this protein was virtually turned off at 5-6 hours after the addition of serum. However, if CH or a combination of CH and FCS was present, a continuous synthesis of the 29 K protein was observed.

Animals↗
PubMed1987

Effect of cycloheximide or puromycin on induction of thermotolerance by sodium arsenite in Chinese hamster ovary cells: involvement of heat shock proteins.

After sodium arsenite (100 microM) treatment, the synthesis of three major heat shock protein families (HSPs; Mr = 110,000, 87,000, and 70,000), as studied with one-dimensional gels, was enhanced twofold relative to that of unheated cells. The increase of unique HSPs, if studied with two-dimensional gels, would probably be much greater. In parallel, thermotolerance was observed as a 100,000-fold increase in survival from 10(-6) to 10(-1) after 4 hr at 43 degrees C, and as a thermotolerance ratio (TTR) of 2-3 at 10(-3) isosurvival for heating at 45.5 degrees C. Cycloheximide (CHM: 10 micrograms/ml) or puromycin (PUR: 100 micrograms/ml), which inhibited total protein synthesis and HSP synthesis by 95%, completely suppressed the development of thermotolerance when either drug was added after sodium arsenite treatment and removed prior to the subsequent heat treatment. Therefore, thermotolerance induced by arsenite treatment correlated with an increase in newly synthesized HSPs. However, with or without arsenite treatment, CHM or PUR added 2-6 hr before heating and left on during heating caused a 10,000-100,000-fold enhancement of survival when cells were heated at 43 degrees C for 4 hr, even though very little synthesis of heat shock proteins occurred. Moreover, these cells manifesting resistance to heating at 43 degrees C after CHM treatment were much different than those manifesting resistance to 43 degrees C after arsenite treatment. Arsenite-treated cells showed a great deal of thermotolerance (TTR of about 10) when they were heated at 45 degrees C after 5 hr of heating at 43 degrees C, compared with less thermotolerance (TTR of about 2) for the CHM-treated cells heated at 45 degrees C after 5 hr of heating at 43 degrees C. Therefore, there are two different phenomena. The first is thermotolerance after arsenite treatment (observed at 43 degrees C or 45.5 degrees C) that apparently requires synthesis of HSPs. The second is resistance to heat after CHM or PUR treatment before and during heating (observed at 43 degrees C with little resistance at 45.5 degrees C) that apparently does not require synthesis of HSPs. This phenomenon not requiring the synthesis of HSPs also was observed by the large increase in thermotolerance to 45 degrees C caused by heating at 43 degrees C, with or without CHM, after cells were incubated for 6 hr following arsenite pretreatment. For both phenomena, a model based on synthesis and redistribution of HSPs is presented.

Animals↗
PubMed1999

LPS-induced signals in activation of caspase-3-like protease, a key enzyme regulating apoptotic cell damage into a macrophage-like cell line, J774.1, in the presence of cycloheximide.

The earliest observed apoptotic change in a macrophage-like cell line, J774.1, treated with lipopolysaccharide (LPS) in the presence of cycloheximide (CHX) was a selective increase in caspase-3-like activity. The addition of polymyxin B, TPCK, herbimycin A, or genistein, all of which inhibited LPS-induced tumor necrosis factor alpha (TNF-alpha) production by macrophages, suppressed the activation of the caspase-3-like protease in these macrophages treated simultaneously with CHX. However, SB202190 and SB203580, inhibitors of MAP kinase, and PD98059, an inhibitor of MAP-kinase kinase (MEK), showed no effect on the activation of the caspase-3-like protease or on the cell damage of the macrophages treated with LPS and CHX, whereas they inhibited LPS-induced TNF-alpha production. These results suggest that some of the early signals in LPS-treated macrophages are common to the subsequent pathways for TNF-alpha production and caspase-3-like protease activation, but the later signals, like MAP-kinase kinase or MAP-kinase, are not involved in the pathways for caspase-3-like protease activation.

Animals↗
PubMed2003

Cycloheximide and actinomycin D delay death and affect bcl-2, bax, and Ice gene expression in astrocytes under in vitro ischemia.

An in vitro ischemia model was established and the effect of the metabolic inhibitors cycloheximide (CHX) and actinomycin D (ActD) on apoptosis in astrocytes under ischemia studied. CHX decreased by 75% the number of cells dying after 6 hr of ischemia compared with control cultures. TdT-mediated dUTP nick end labelling (TUNEL) staining of comparable cultures was reduced by 40%. ActD decreased cell death by 60% compared with controls. The number of TUNEL-positive cells was reduced by 38%. The nuclear shrinkage in TUNEL-positive astrocytes in control cultures did not occur in ActD-treated astrocytes, indicating that nuclear shrinkage and DNA fragmentation during apoptosis are two unrelated processes. Expression of bcl-2 (alpha and beta), bax, and Ice in astrocytes under similar ischemic conditions, as measured by quantitative reverse transcription-polymerase chain reaction, indicated that ischemia down-regulated bcl-2 (alpha and beta) and bax. Ice was initially down-regulated from 0 to 4 hr, before returning to control levels after 8 hr of ischemia. ActD decreased the expression of these genes. CHX reduced the expression of bcl-2 (alpha and beta) but increased bax and Ice expression. It is hypothesized that the balance of proapoptotic (Bad, Bax) and antiapoptotic (Bcl-2, Bcl-Xl) proteins determines apoptosis. The data suggest that the ratio of Bcl-2/Bad in astrocytes following ActD and CHX treatment does not decrease as much in untreated cells during ischemia. Our data indicate that it is the ratio of Bcl-2 family members that plays a critical role in determining ischemia-induced apoptosis. It is also important to note that ischemia-induced apoptosis involves the regulation of RNA and protein synthesis.

Animals↗
PubMed2001

Caspase activity in newt spermatogonial apoptosis induced by prolactin and cycloheximide.

We previously showed in vivo and in vitro, that among the spermatogenic stages of the newt, prolactin (PRL) induces apoptosis specifically in the penultimate stage of secondary spermatogonia. In the current report, we demonstrate in vitro that cycloheximide (CHX), an inhibitor of protein synthesis, induces morphological apoptotic changes similar to those caused by PRL, such as chromatin condensation and apoptotic body formation. Next, we found that Z-VAD-fmk, an inhibitor of various caspases, suppressed the apoptosis induced by PRL and CHX, but ICE inhibitor Ac-YVAD-CHO or caspase-3 inhibitor Ac-DEVD-CHO did not. As high caspase activity was present in extracts of testes treated with CHX, we suggest that an unidentified caspase induces the morphological changes of apoptosis in newt spermatogonia.

Amino Acid Chloromethyl Ketones↗
PubMed2006

The effect of 6-dimethylaminopurine (6-DMAP) and cycloheximide (CHX) on the development and chromosomal complement of sheep parthenogenetic and nuclear transfer embryos.

The effects of activation by 6-dimethylaminopurine (6-DMAP) and cycloheximide (CHX) on the development and chromosomal complement of sheep parthenogenetic and SCNT embryos were investigated. The results revealed that the blastocyst development of parthenogenetic embryos was significantly higher (P < 0.05) in 6-DMAP activated oocytes, compared to those activated with CHX (21.0 +/- 0.9 vs. 14.9 +/- 0.5, respectively). In contrast, the blastocyst frequencies did not significantly differ (P > 0.05) between the two activation treatment groups for SCNT embryos. The 6-DMAP or CHX treatment did not result in any significant difference in the blastocyst total cell number in either parthenote or SCNT embryos. The chromosomal analysis revealed that all the parthenogenetic embryos (100.0%) derived from 6-DMAP treatment, were chromosomally abnormal whereas in CHX-treated embryos, it was significantly lowered (93.6%, P < 0.05). Conversely, the proportions of chromosomally abnormal SCNT embryos did not significantly differ (P > 0.05) among the 6-DMAP and CHX- treated embryo groups (60.0% vs. 56.2%, respectively). This study demonstrated that oocyte activation agents such as DMAP and CHX have differing effects on meiotic or mitotic nuclei. The study also highlighted the feasibility of using bovine X and Y chromosome specific painting probes in sheep embryos.

Adenine↗
PubMed1980

Acute and persistent ultrastructural changes in rat liver after a single dose of 2-acetylaminofluorene: effect of co-administration of cycloheximide.

Electron microscope studies have been made of rat hepatic cell morphology, 24 hr, 48 hr and 24 weeks after a single intragastric dose of 2-acetylaminofluorene (2-AFF), alone or together with a single s.c. dose of cycloheximide (CHM). CHM prevents the acute perinuclear glycogen pooling, peripheral displacement of cytoplasmic organelles and nuclear shrinkage induced by 2-AAF. However, the induction by 2-AAF of changes in the granular endoplasmic reticulum, mitochondria and bile canaliculi is enhanced by co-administration of CHM. These changes persist for at least 24 weeks and are similar to those induced during 2-AAF hepatocarcinogenesis and observed in hepatocellular tumours. In view of the similar results obtained in previous studies with the azocarcinogen, 3'-methyl-4-dimethylaminoazobenzene, the possibility is discussed that these persistent changes might be associated with the initiation phase of neoplastic induction.

2-Acetylaminofluorene↗
PubMed1981

Teratogenesis of retinoic acid in rats: susceptible stages and suppression of retinoic acid-induced limb malformations by cycloheximide.

The susceptible stages and the malformation pattern produced by excess retinoic acid were investigated in rat fetuses. Retinoic acid (120 mg/kg body weight, suspended in rape oil) was administered orally to pregnant females on one of the first 20 days of gestation. Fetuses were examined for external and, after visualization of the skeleton with alizarin red, for skeletal malformations on the 21st day of gestation. Retinoic acid was highly embryolethal when administered on days 9 and 10 of gestation (96.2 and 100% resorptions). The earliest teratogenic effect of retinoic acid was noted on the 9th day of gestation. Severe multiple defects were produced by retinoic acid administration on days 9 and 11 of gestation, but more specific malformations involving the axial skeleton, the fore- and hindlimbs, and cleft palate resulted from treatment on days 12-18 of gestation. Cycloheximide, and inhibitor of protein synthesis, reduced the incidence of limb defects induced by retinoic acid. This result indicates that the teratogenic effect of retinoic acid on limb morphogenesis may be dependent upon continuous protein synthesis and is compatible with the view that vitamin A may act like a hormone.

Abnormalities, Drug-Induced↗
PubMed2002

The SCR1 gene from Schwanniomyces occidentalis encodes a highly hydrophobic polypeptide, which confers ribosomal resistance to cycloheximide.

In Saccharomyces cerevisiae, the SCR1 gene from Schwanniomyces occidentalis is known to induce ribosomal resistance to cycloheximide (cyh). A 2.8 kb DNA fragment encoding this gene was sequenced. Its EMBL Accession No. is AJ419770. It disclosed a putative tRNA(Asn) (GUU) sequence located downstream of an open reading frame (ORF) of 1641 nucleotides. This ORF was shown to correspond to SCR1. It would encode a highly hydrophobic polypeptide (SCR1) with 12 transmembrane domains. SCR1 is highly similar to a variety of yeast proteins of the multidrug-resistance (MDR) family. However, SCR1 only conferred resistance to cyh but not to benomyl or methotrexate. The cyh-resistance phenotype induced by SCR1 was confirmed in several S. cerevisiae strains that expressed this gene to reside at the ribosomal level. In contrast, a beta-galacosidase-tagged SCR1 was found to be integrated in the endoplasmic reticulum (ER). It is proposed that the ribosomes of yeast cells expressing SCR1 undergo a conformational change during their interaction with the ER, which lowers their affinity for cyh-binding. If so, these findings would disclose a novel ribosomal resistance mechanism.

Amino Acid Sequence↗