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PubMed1984

Effects of actinomycin D and cycloheximide on the increase in tyrosinase activity of hamster amelanotic melanoma cells in vitro.

Tyrosinase activity in the Ab hamster amelanotic melanoma cells cultured in serum-free Eagle's MEM increased 3 times after 6 h of primary cell culture. This increase was inhibited completely by cycloheximide, while actinomycin D had no effect on this process. After 24 h of culture in MEM with calf serum, further increase of the tyrosinase activity was inhibited by both cycloheximide and actinomycin D. The data presented may indicate that the increase of tyrosinase activity in the primary cell culture of the Ab melanoma is due initially to the unblocking of translation and later to the activation of transcription of the gene controlling the enzyme.

Animals↗
PubMed1975

Inhibition of Newcastle disease virus-induced fever in rabbits by cycloheximide.

Pretreatment with cycloheximide prevents virus-induced fever in rabbits. Compared to the febrile control animals, CH-pretreated afebrile animals exhibit similar concentrations of endogenous pyrogen in the blood and of prostaglandins of the E-group and adenosine 3', 5'-cycle monophosphate in the cerebrospinal fluid. The fever response seems to involve one or several additional so far unknown mediators which are sensitive to cycloheximide.

Animals↗
PubMed1994

Retinoic acid modulation of mucin mRNA in rat tracheal explants: response to actinomycin D, cycloheximide, signal transduction effectors and antisense oligodeoxynucleotide.

Factors affecting the retinoic acid modulated expression of mucin mRNA in rat tracheal cultures were studied. Actinomycin D had no effect on mucin mRNA in cultures grown with retinoic acid (RA+). The usual precipitous drop in mucin mRNA in cultures lacking retinoic acid (RA-) was prevented by actinomycin D. Cycloheximide also had no effect on mucin mRNA in RA+ cultures, but, like actinomycin D, it prevented the precipitous drop in mucin mRNA in RA- cultures. cAMP agonists had some marginal effects on the mucin mRNA, but none as dramatic as those noted by actinomycin D and cycloheximide in the RA- cultures. An antisense oligomer (18 bases) to rat mucin cDNA inhibited the mucin mRNA expression in RA+ cultures.

Animals↗
PubMed1990

Cathepsin B secretion by rabbit articular chondrocytes: modulation by cycloheximide and glycosaminoglycans.

Rabbit articular chondrocytes in monolayer culture are modulated away from their differentiated state and undergo morphological and biochemical changes. One of the characteristics of the modulated state is an abnormally high production of the cysteine endopeptidase cathepsin B. Addition to chondrocyte cultures of the protein biosynthesis inhibitor, cycloheximide, resulted in a concentration-dependent reduction of cathepsin B secretion, which was fully restored after removal of cycloheximide. Glycosaminoglycans added to the culture medium of modulated chondrocytes partially reduced the rate of secretion of cathepsin B, this effect being dependent on their structure, the degree of sulfation, and concentration. The age of the chondrocytes and the duration of the treatment also influenced this response. The switching off of cathepsin B release was apparently best favored by a high concentration of negatively charged sulfate groups attached to a polymeric glycosaminoglycan chain; this simulates the natural environment of the chondrocytes in articular cartilage.

Animals↗
PubMed1995

Potentiation of the respiratory burst of human neutrophils by cycloheximide: regulation of reactive oxidant production by a protein(s) with rapid turnover?

Incubation of human neutrophils with the protein biosynthesis inhibitor cycloheximide for > or = 90 min results in a decreased ability to generate reactive oxidants during the respiratory burst. This implies that active protein biosynthesis is required to sustain the ability of these cells to generate reactive oxidants. However, short term incubation of neutrophils (40-60 min) with either cycloheximide or puromycin results in a significant increase in oxidase activity stimulated by either fMet-Leu-Phe (> 60%) or by leukotriene B4 (> 30%). However, after incubation for 40-60 min with these inhibitors of protein biosynthesis, the respiratory burst stimulated by PMA was unaffected whilst that stimulated by the particulate stimuli opsonised zymosan or latex beads was significantly inhibited. The enhanced oxidase activity stimulated by the soluble agonists was not explained by changes in receptor expression, alterations in intracellular Ca2+ levels or by enhanced degranulation. These results suggest that oxidase activity stimulated by soluble agonists in neutrophils is normally regulated by a short-lived, actively-synthesised protein(s).

Amino Acid Sequence↗
PubMed1984

The effect of cycloheximide on nuclear uH2A content.

The effect of intraperitonal cycloheximide administration on acid-soluble rat liver chromatin proteins has been investigated by electrophoresis in acetic acid-urea polyacrylamide gels. A nonhistone protein, which migrates between oxidized histone H3 and histone H1 has been found to be increased in amount following cycloheximide treatment. This protein seems to be identical with semihistone protein H24 (uH2A). A possible relationship of uH2A to the inhibition of rRNA synthesis is discussed.

Animals↗
PubMed1976

Exocrine pancreatic enzymes in cycloheximide treated rats.

Cycloheximide, even in a dose of 0.25 mg/kg administered s.c. to rats stimulated by pancreozymin and secretin, inhibited lipase activity in pancreatic juice. Lipase activity in serum of control animals was inhibited by cycloheximide. The secretion of trypsin and chymotrypsin was also decreased.

Animals↗
PubMed1987

The effects of cycloheximide on Na+/H+ antiporter activity in cultured opossum kidney cells.

These studies examined the effects of cycloheximide on the Na+/H+ antiporter in cultured opossum kidney cells. The effects of cycloheximide on antiporter activity depended on the basal level of activity. These data suggest that the Na+/H+ antiporter may be regulated by several processes which are sensitive to protein synthesis inhibition.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

Gastric antisecretory activity of cycloheximide due to inhibition of protein synthesis.

Treatment of rats with cycloheximide 1 h before carbachol dose-dependently reduced the secretagogue-stimulated gastric acid secretion in pylorus ligated rats, and partially blocked carbachol- or histamine-induced activation of rat gastric (H+ + K+)-ATPase which includes translocation of reserve intracellular (H+ + K+)-ATPase into the apical membrane of the parietal cells and induction of a KCl pathway. Time-course studies showed that the drug was effective only when administered at least 30 min before the secretagogues. Puromycin showed the same effect as cycloheximide. Pulse labelling studies with [35S]methionine led to identification of two most actively synthesized polypeptides in rat gastric mucosa; the proteins of 38,000 and 14,000 molecular weight. The larger polypeptide was identified as rat pepsinogen. The identity of the smaller protein is not known yet. We suggest that synthesis of nascent polypeptide(s) is required for certain steps of the acid secretory process leading to the activation of the acid pump.

Adenosine Triphosphatases↗
PubMed1992

The effect of cycloheximide on natural and X-ray-induced cell death in the developing cerebral cortex.

Naturally occurring cell death in the cerebral cortex and subcortical white matter is increased after X-irradiation, and this process is curbed with cycloheximide, an inhibitor of protein synthesis. However, cycloheximide alone increases cell death during development, and this effect is dose-dependent. This suggests that, in both normal and experimentally-induced cortical cell death during development, different proteins are activated or inhibited, depending on the agent, the time of its application, and the previous metabolic or functional state of the cell.

Animals↗
PubMed1995

Carbamazepine induction of apoptosis in cultured cerebellar neurons: effects of N-methyl-D-aspartate, aurintricarboxylic acid and cycloheximide.

We have previously demonstrated that carbamazepine (CBZ) at concentrations above the therapeutic range is toxic to cultured cerebellar granule cells. Here, we ask whether the effect of CBZ involves neuronal apoptosis or necrosis. Treatment of cultured cerebellar granule cells with CBZ for 3 days resulted in a concentration-dependent fragmentation of DNA revealed as a laddered pattern in agarose gel electrophoresis, a phenomenon characteristic of apoptosis. Pretreatment of cells with N-methyl-D-aspartate (NMDA) blocked CBZ-induced DNA fragmentation and neurotoxicity as assayed by loss of mitochondrial activity with MTT or by [3H]ouabain binding to Na+/K(+)-ATPase. Aurintricarboxylic acid (ATA), a polyanionic dye, also markedly suppressed DNA fragmentation and cell death detected by morphological examination. A considerable level of DNA ladder formation was detected in untreated cells and this basal DNA fragmentation was also blocked by NMDA and ATA. Moreover, NMDA and ATA prevented CBZ-induced chromatin condensation as revealed by DNA binding with the fluorescent dye Hoechst 33258. Pretreatment of cells with cycloheximide, a protein synthesis inhibitor, prevented CBZ-induced cell death detected morphologically and attenuated CBZ-induced neurotoxicity assessed by mitochondrial activity and [3H]ouabain binding assays. Taken together, our results suggest that CBZ-induces death of cerebellar granule cells by an apoptotic process that is sensitive to NMDA, ATA and cycloheximide.

Animals↗
PubMed1996

Additive neuroprotective effects of dextrorphan and cycloheximide in rats subjected to transient focal cerebral ischemia.

Previous studies have implicated both excitotoxicity and apoptosis in the pathogenesis of cerebral infarction induced by focal ischemic insults. Here we tested the possibility that the NMDA antagonist, dextrorphan, and the protein synthesis inhibitor, cycloheximide, would produce additive protective effects in a rodent model of focal ischemia-reperfusion. Transient focal cerebral ischemia was induced by a 90 min period of ligation of the right middle cerebral artery and both common carotid arteries. Administration of either 30 mg/kg dextrorphan or 0.5 mg/kg cycloheximide, given i.p. 15 min before ischemia, reduced infarct volume by about 65%. When optimal concentrations of each drug were given together, infarct volume was reduced by 87% as measured 14 days later. These observations support the idea that both excitotoxicity, and apoptosis dependent on new protein synthesis, contribute to cerebral infarction after transient focal ischemia in the rat.

Animals↗
PubMed1977

Failure of cycloheximide to alter rate of recovery of temperature following acute DFP treatment.

Cycloheximide, 400 microgram intraventricularly 4 h after a 1 mg/kg i.m. injection of the irreversible anticholinesterase DFP, failed to alter the rate of recovery of temperature to normal. Tolerance to the hypothermic effects of DFP developed at the same rate in cycloheximide-treated rats. These findings suggest that neither recovery from the acute effects of DFP nor tolerance to its chronic effects depends on protein synthesis.

Animals↗
PubMed1992

Neutrophil infiltration into the ischaemic/reperfused rabbit isolated myocardium: effect of PF-5901 and cycloheximide.

The Langendorff-perfused rabbit heart preparation has been used to study the interaction of isolated rabbit neutrophils with regionally ischaemic myocardium. Short durations of regional ischaemia (10-60 min) and subsequent reperfusion (30 min) of the hearts with neutrophils resulted in a significant time-dependent accumulation of neutrophils (as assessed by myeloperoxidase activity) in the area at risk. Pre-activation of neutrophils with zymosan-activated serum prior to their infusion into the myocardium potentiated neutrophil accumulation in the area at risk. Pretreatment of the myocardium with a lipoxygenase inhibitor, PF-5901 (10 microM), or a de novo protein synthesis inhibitor, cycloheximide (10 microM), significantly reduced the accumulation of neutrophils in the ischaemic/reperfused myocardium. In contrast, pretreatment of neutrophils with cycloheximide (10 microM, for 15 min) prior to their infusion had no significant effect on neutrophil accumulation in the area at risk. The cyclooxygenase inhibitor, indomethacin (10 microM), had no effect on neutrophil accumulation in the area at risk following ischaemia and reperfusion. These results suggest the involvement of de novo protein synthesis and the lipoxygenase products in the infiltration of neutrophils following ischaemia and reperfusion in vitro.

Animals↗
PubMed1996

Systemic administration of dynorphin A-(1-13) markedly improves cycloheximide-induced amnesia in mice.

The effects of systemic or intracerebroventricular injection of dynorphin A-(1-13), a kappa-selective opioid receptor agonist, on cycloheximide-induced amnesia were investigated by using a step-down-type passive avoidance task in mice. The intracerebroventricular injection of dynorphin A-(1-13) (0.3-3 micrograms) before training significantly prolonged step-down latency. The systemic administration of dynorphin A-(1-13) (1, 3 and/or 10 mg/kg, i.p.) before training or retention tests markedly inhibited the cycloheximide (30 mg/kg, s.c.)-induced shortening of step-down latency, indicating antiamnesic effects of dynorphin A-(1-13). One and 3 mg/kg doses of ((+/-)trans-3, 4-dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, methanesulfonate hydrate (U-50,488H), another kappa-selective opioid receptor agonist, significantly inhibited the shortening. The anti-amnesic effects of dynorphin A-(1-13) (3 and 10 mg/kg, i.p.) were almost completely antagonized by intracerebroventricular administration of the quaternary derivative of the opioid receptor antagonist naltrexone methobromide (0.3 microgram), but not by systemic administration of the opioid receptor antagonist (1 mg/kg, s.c.), demonstrating central mediation of the anti-amnesic effects of dynorphin A-(1-13). Furthermore, the kappa-selective opioid receptor antagonist, nor-binaltorphimine (2 mg/kg, s.c.), almost completely antagonized the effects of dynorphin A-(1-13) (3 and 10 mg/kg, i.p.). These results suggest that dynorphin A-(1-13) produces anti-amnesic effects through the blood-brain barrier.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1978

Cycloheximide-induced mitotic delay in Physarum polycephalum.

Cycloheximide pulses applied to Physarum polycephalum surface plasmodia delay mitosis. Pulses applied in G2 cause a delay of mitosis which is linearly dependent on the phase in the cell cycle at which the pulse is applied. A 30 min pulse of 10 micrograms/ml cycloheximide starting in G2 at time t after mitosis induces an excess delay (delay in excess of pulse duration) of the next mitosis of (0.55) t-1.3 h. The excess delays induced by 7 h pulses during G2 are at most 1 h larger. Pulses applied less than 30 min before mitosis induce only small delays.

Cycloheximide↗