Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cycloheximide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1973

Measles virus ribonucleic acid and protein synthesis: effects of 6-azauridine and cycloheximide on viral replication.

Cycloheximide and 6-azauridine were employed to study the time course of measles virus protein and nucleic acid syntheses in AV3 cells. Synthesis of ribonucleic acid (RNA) essential for infectivity was first detected at 6 hr and increased concurrently with the formation of essential protein. Maximum levels of virus-specific RNA and protein were present by 18 hr, a time when only 5% of progeny virus was detected. Essential RNA and protein syntheses preceded the formation of infectious virus by at least 10 to 12 hr. The time course of RNA and protein syntheses essential for the formation of complement-fixing (CF) antigen and salt-dependent agglutinin (SDA) was also determined. RNA synthesis essential for the formation of SDA was first detected at 2 hr and was present maximally by 6 hr, whereas SDA-protein increased concurrently with the protein essential for infectivity. This suggested that the last protein essential for infectivity may be SDA. RNA synthesis essential for the formation of CF antigen was first detected at 4 hr, while CF-protein increased at 5 hr and preceded SDA-protein and protein essential for infectivity by approximately 3 hr. Reversal of inhibition of protein synthesis by cycloheximide indicated that early protein synthesis (1 to 3 hr) was required for the formation of infectious virus. The data suggest that the relatively long eclipse period observed with measles virus is related to a long maturation period rather than to late formation of early proteins, viral RNA, or structural proteins.

Amnion↗
PubMed1977

Inhibitory effect of various cytostatics and cycloheximide on acute experimental pancreatitis in rats.

Cycloheximide, 5-azacytidine, and 4-methoxybenzoyl-beta-bromoarylate (Cytembena) block the development of experimental acute pancreatitis in rats when mediated by the administration of 5% bile solution into the pancreas in vivo. Six hours after drug treatment the pathological changes, evaluated macroscopically or using histological sections of the pancreas, were significantly decreased. The drugs affected the amount of abdominal fluid and lowered its lipase and amylase activity. The known inhibitory mechanism of the active drugs and the possible advantage of cycloheximide for clinical use are briefly mentioned.

Acrylates↗
PubMed1983

Comparison of chromosome associations in human lymphocytes arrested by colcemid, nocodazole, or cycloheximide.

The method of "generalized distances" was applied to compare the effects on homologous interchromosomal distances of colcemid, the routinely used tubulin inhibitor with the effects of two other metaphase arrestants: nocodazole, also a tubulin inhibitor and cycloheximide, an inhibitor of protein synthesis which preserves somatic association. More homologous pairs were associated in the cycloheximide treatment than in the other two procedures; however, while several chromosomes which tend to lie toward the center of the metaphase plate showed somatic association in the various treatments, we found no evidence for somatic association of the larger, more peripherally located chromosomes in human cells in any of our treatments (chromosome pair 7 excepted in the colcemid sample).

Benzimidazoles↗
PubMed1975

Adaptation to cycloheximide: in vitro studies with filamentous fungi.

Adaptation of numerous strains of filamentous fungi to cycloheximide was noted upon first transfer during serial exposure to the antibiotic. The extent of this adaptation varied in part with the species and strain of the microorganism. Exposure on subsequent transfers caused no change in the growth of any of the strains used. These results suggest that nonzoopathogens may be differentiated from zoopathogens on the basis of adaptation to cycloheximide and that such adaptation might also be found in other eucaryotes.

Adaptation, Biological↗
PubMed1978

Rat hepatic lysine-2-oxoglutarate reductase activity. Induction by lysine, glucagon and cycloheximide administration.

The activity of hepatic lysine-2-oxoglutarate reductase was determined in white female rats maintained on one of two dietary lysine levels (0.23 and 0.54% in diets A and B, respectively). The high dietary lysine increased the enzyme activity (p less than 0.05) twofold compared with the activity obtained with the diet A (67 vs. 27 mumol saccharopine/30 min/g liver protein). Repeated intraperitoneal injection of glucagon (259 microgram/100 g body weight/day) showed a short initial drop in the enzyme activity, followed by a marked rise, which remained above the basal level after withdrawal of the drug. Repeated injections of cycloheximide increased the enzyme activity, and the findings suggested that the apparent increase was due to the inhibition of the system responsible for the degradation of the enzyme. The individual free amino acids of the livers varied as a function of treatment. The ratio of E/N amino acids was found to be a good measure of the physiological condition of the animal, with the lowest value in animals treated with cycloheximide.

Amino Acids↗
PubMed1979

In vitro release of prolactin by thyrotropin-releasing hormone: influence of dopamine, thyroxine, and cycloheximide.

An acute incubation procedure, using explanted normal rat hemipituitaries pretreated with fresh plasma obtained from pituitary donor animals, was employed to further investigate the in vitro stimulation of prolactin (PRL release by thyrotropin-releasing hormone (TRH). Pretreatment with dopamine (0.1 microgram/ml) caused a 30-50% decrease in the amount of PRL released into incubation media; the inhibitory effect of dopamine was not reversed by treatment with 0.5-6.0 ng. TRH, although these TRH concentrations consistently stimulated PRL release from pituitaries not exposed to dopamine. Treatment with thyroxine (10(-6) to 10(-5) M) showed a competitive inhibition of thyrotropin release by TRH (0.5 ng), but was without effect on TRH-stimulated PRL release. Cycloheximide (100 microgram/ml) blocked a net increase in PRL levels. TRH, nevertheless, significantly increased PRL release in the presence of cycloheximide. The results indicate that neither dopamine nor thyroxine compete with TRH in causing PRL release, and that the TRH stimulation of PRL release is unrelated to ongoing levels of hormone synthesis.

Animals↗
PubMed1983

Age-related effect of cycloheximide on lipid peroxidation in rough and smooth microsomes of rat liver.

Cycloheximide, at a nonlethal dose of 2 mg/kg body weight, has different effects on microsomal in vivo lipid peroxidation in different age groups. In general, the antibiotic increases microsomal lipid peroxidation in newborn and 1-year-old rats, but decreases it in 15- and 75-day-old rats. Low doses of cycloheximide induces lipid peroxidation in vitro whereas higher doses cause inhibition. The degree of change differs in the two microsomal fractions. The sucklings are more susceptible to such a change than the older rats. In vivo lipid peroxidation in rat liver homogenate and rough and smooth microsomes declines as a function of age. Smooth microsomes show more lipid peroxidation than the rough in the different age groups.

Aging↗
PubMed1980

Parathyroid hormone acutely increases polyphosphoinositides of the rabbit kidney cortex by a cycloheximide-sensitive process.

Parathyroid hormone(PTH) rapidly increases the concentrations of diphosphoinositide and triphosphoinositide in rabbit kidney cortex. Cycloheximide pretreatment abolishes these effects of PTH. These findings are similar to those reported for adrenocorticotropin and cyclic AMP action in the adrenal cortex, and suggest a common mechanism. Cycloheximide-sensitive effects of PTH, e.g., phosphaturia, may require polyphosphoinositides and/or other phospholipids.

Animals↗
PubMed1981

Adrenocorticotropin and adenosine 3',5'-monophosphate stimulate de novo synthesis of adrenal phosphatidic acid by a cycloheximide-sensitive, CA++-dependent mechanism.

We tested further our postulate that enhanced de novo synthesis of phosphatidic acid is responsible for ACTH- and cAMP-induced increases in adrenal phospholipids in the phosphatidate polyphosphoinositide pathway. During incubation of adrenal sections or cells in vitro, ACTH and cAMP increased the concentrations of and incorporation of [3H]glycerol and [14C]palmitate into phosphatidylcholine and phosphatidylethanolamine, two major phospholipids which are derived from phosphatidic acid, but are extrinsic to the inositide pathway. Thus, it is unlikely that ACTH and cAMP increase inositide phospholipids at the expense of other phospholipids. Similar to previously reported effects on phosphatidic acid and inositide phospholipids, cycloheximide blocked the effects of ACTH and cAMP on phosphatidylcholine and phosphatidylethanolamine. In addition, Ca++ was required for these effects, as well as for cAMP-induced increases in phosphatidic acid, inositide phospholipids, and steroidogenesis. Our findings strongly suggest that ACTH, via cAMP, stimulates de novo phosphatidate synthesis by a cycloheximide-sensitive, Ca++-dependent process, and this stimulation causes a rapid generalized increase in adrenal phospholipids. Moreover, the increased incorporation of labeled glycerol and palmitate into phospholipids suggests that ACTH and cAMP may stimulate the glycerol-3'-PO4 acyltransferase reaction. This stimulatory effect may play a central role in the steroidogenic and trophic actions of ACTH and cAMP.

Adrenal Glands↗
PubMed1984

Effects of cycloheximide, alpha-amanitin, and alpha-difluoromethylornithine on thyrotropin-induced increases in the micrococcal nuclease sensitivity of thyroid nuclear chromatin.

Treatment of calf thyroid slices with TSH increases the nuclease sensitivity of nuclear chromatin, i.e. the amount of DNA released from nuclei by mild digestion with DNase I and micrococcal nuclease. Cycloheximide and alpha-amanitin were used to investigate the roles played by protein and RNA synthesis in mediating this effect of TSH; alpha-difluoromethylornithine, an irreversible inhibitor of ornithine decarboxylase, was used to investigate the possible involvement of polyamines. Calf thyroid slices were incubated with or without TSH (50 mU/ml) for 5 h, in the presence or absence of inhibitors. Nuclei were then prepared, subjected to mild digestion with micrococcal nuclease, and centrifuged at 1200 X g. The amount of DNA in 1200 X g supernatants was increased by TSH; this was inhibited by cycloheximide (100 micrograms/ml) and alpha-amanitin (4 micrograms/ml) when these agents were present throughout incubations with TSH. In contrast, alpha-amanitin failed to inhibit the TSH effect when it was added to incubations 30 min or 2 h after the addition of TSH. These results indicate that RNA and protein synthesis play a part in mediating the effect of TSH on the micrococcal nuclease sensitivity of chromatin, and that the RNA synthesis involved takes place within the first 30 min of exposure of thyroid slices to TSH. alpha-Difluoromethylornithine (5 mM) inhibited the TSH-dependent development of micrococcal nuclease sensitivity; however, it also inhibited nuclease digestion when it was added directly to nuclei prepared from fresh thyroid tissue. This observation should serve as a warning against uncritical acceptance of the notion that all effects of alpha-difluoromethylornithine are the result of inhibition of ornithine decarboxylase.

Amanitins↗
PubMed1991

Regulation of proenkephalin A messenger ribonucleic acid levels in normal B lymphocytes: specific inhibition by glucocorticoid hormones and superinduction by cycloheximide.

Proenkephalin A (PEA) encodes a group of small peptides known to function as neurotransmitters, neuromodulators, and neurohormones in the nervous and neuroendocrine systems. This gene has been shown to be expressed in lymphoid cells, supporting the concept of bidirectional communication between the immune system and the central nervous system. In the present study, we investigated the effect of steroids and the inhibition of protein and RNA syntheses on the regulation of PEA expression in normal rat B cells. The transient expression of PEA messenger (m) RNA levels occurring normally in B cells was markedly inhibited by the presence of either 50 nM prednisolone or dexamethasone, both of which are glucocorticoids; other steroids, such as testosterone or the steroid-inactive metabolite androsterone, were ineffective. In the presence of cycloheximide, a protein synthesis inhibitor, PEA mRNA was superinduced by a factor of 15-fold. Sorting by flow cytometry of cycloheximide-treated cells followed by in situ hybridization analysis revealed that the expression of PEA mRNA was exclusively confined to a small fraction of B cells. These results indicate that the mechanisms regulating PEA gene expression in B cells differ from those previously described in cells of the neuroendocrine and the nervous systems.

Animals↗
PubMed1984

Blockade by anti-glucocorticoids, actinomycin D and cycloheximide of the anti-inflammatory action of some Kampohozai (Chinese traditional medicines) against serotonin.

Blockade by anti-glucocorticoids, progesterone and 17 alpha-methyltestosterone, a messenger ribonucleic acid (m-RNA) synthesis inhibitor, actinomycin D, and a protein synthesis inhibitor, cycloheximide, of the anti-exudative action of five kinds of Kampohozai (Daisaikoto, Shosaikoto, Saikokeishito, Daiobotanpito and Tokakujokito) were studied to investigate mode of the anti-inflammatory action of those Kampohozai. The inflammatory lesion was provoked by injection of serotonin (0.3 micrograms) in the Tyrode solution (5 microliter) in subplantar region of the hind paw of mice. The above anti-glucocorticoids and the m-RNA and protein synthesis inhibitors suppressed the anti-inflammatory effects of Daisaikoto and Shosaikoto dose-dependently. The action of Saikokeishito was suppressed weakly by treatment with progesterone or 17 alpha-methyltestosterone, but not blocked by treatment with actinomycin D or cycloheximide. On the other hand, Daiobotanpito and Tokakujokito were not blocked by treatment with those four inhibitors. These results suggest that mechanism of anti-inflammatory action of Daisaikoto and Shosaikoto is similar to that of glucocorticoid but Daiobotanpito and Tokakujokito exert anti-inflammatory effects through some other mechanisms.

Animals↗
PubMed1991

The effect of tacrine (THA) on cycloheximide- and basal forebrain lesion-induced memory deficit in rats.

The effects of 9-amino-1,2,3,4-tetrahydroacridine (tacrine), an active acetylcholinesterase inhibitor, on cycloheximide- and basal forebrain (BF) lesion-induced memory deficit in the water maze and passive avoidance task were investigated. While cycloheximide (1.5 mg/kg, s.c.) produced amnesia in the passive avoidance task, chronic administration of tacrine (1, 3 and 10 mg/kg, once a day for 1 week) improved the amnesia. BF lesion produced amnesia in both the water maze and passive avoidance tasks. Chronic tacrine (0.1-3 mg/kg, passive avoidance task, or 0.3 mg/kg, water maze task, once a day for 1 week) improved BF lesion-induced amnesia in the passive avoidance and water maze tasks. These results suggest that tacrine may be useful for senile dementia.

Administration, Oral↗
PubMedDate not supplied

Transport and processing of ribosomal RNA in plant cells after treatment with cycloheximide.

In freely suspended cells of parsley (Petroselinum crispum) protein synthesis is inhibited nearly totally by 5 mug/ml cycloheximide within 10 min. This very low dose has a slight effect on the rRNA synthesis too. During an incubation period of 60 min with [32P] orthophosphate in the presence of the inhibitor (5 mug/ml) at least 65-70% mature rRNA are synthesized compared with the control. After 120 min the synthesis is progressively reduced to 60-65%, and after 240 min to 30-40%. Cycloheximide causes a delay of the prn addition to the 2.3 X 10(6) daltons RNA, normally detectable in pulse experiments, two further precursor molecules do emerge which undernormal circumstances apparently are shortlived. Their molecular weights are 2.0 X 10(6) and 0.9 X 10(6) daltons. The pulse-chase technique and cell fractionation into nuclear and ribosomal parts enables us to demonstrate a rapid transfer of labelled 18S and 25S RNA during a 15 min chase treatment to the mature cytoplasmic ribosomes. Under these conditions no differential transport of the two components takes place. The cells possess a pool of proteins. Therefore the formation of RNP-particles or ribosomes respectively and the transport from the nucleus to the cytoplasm are indipendent from protein synthesis for some time.

Biological Transport, Active↗
PubMed1995

Acute changes in biliary excretion of reverse triiodothyronine in rats after insulin-induced hypoglycemia: effect of glucose, verapamil, cycloheximide and actinomycin D.

Biliary excretion of reverse triiodothyronine (rT3) was estimated in rats during hypoglycemia induced by a 10-min infusion of 1 U of insulin (INS) and for the following 5 h. During that period an increase in biliary rT3 was found. This was seen also during the infusion of exogenous glucagon (10 micrograms in 1.2 ml of saline per 1 h for 5 h) given independently of INS. The infusion of glucose (1 g/kg per 50 min or 2 g/kg per 110 min) following INS infusion delayed the increase in rT3. The increase in rT3 was prevented by actinomycin D (1 mg/kg) when injected before (90 min), but not after (30 min) INS, and also by cycloheximide (2.5 mg/kg) injected immediately before INS. The same dose of cycloheximide also prevented a similar increase of rT3 during the infusion of exogenous glucagon. Verapamil (5 mg/kg divided into five doses per 4 h) blunted the increase of rT3. These data indicate that following INS injection counter-regulatory hormones may be responsible for the increased production of rT3; this altered metabolic activity apparently is dependent on protein synthesis.

Animals↗
PubMed1979

Effects of cycloheximide on the uterine refractory state induced by 'nidatory' oestrogen in rats.

After priming with oestradiol, ovariectomized rats were given 6 days of progesterone treatment in which two doses of 50 ng oestradiol were given on Days 3 and 6. This basic treatment allows the oestradiol-induced (1st injection) disappearance of uterine sensitivity to decidual stimuli to occur. Cycloheximide could not mimic oestrogen action in the production of the uterine refractory state. However, a high dose (500 micrograms per animal) of this inhibitor given with the first injection of oestradiol allowed the uterus to remain in a neutral state and to respond to decidual induction after the second dose of oestradiol. By delaying the injection of cycloheximide after the first oestrogen treatment, protein synthesis requisite to the occurrence of uterine refractoriness would not take place within 12 h after the 'nidatory' oestrogen injection.

Animals↗
PubMed1979

Effect of cycloheximide on the ovine corpus luteum: the role of granules in the secretion of progesterone.

Cycloheximide (3 mg/h) was infused into the corpus luteum of the sheep via a side branch of the ovarian artery. The concentration of progesterone in the peripheral plasma and the luteal tissue decreased after the infusion. Ultrastructural studies showed that cycloheximide caused inhibition of the formation and secretion of densely stained granules in the luteal cells. The results provide further evidence that progesterone bound to protein is secreted by the luteal cell in the form of granules.

Animals↗
PubMed1986

Effect of cycloheximide on nuclear maturation of pig and mouse oocytes.

Culture of mouse oocytes in medium with 1 or 100 micrograms cycloheximide/ml did not prevent germinal vesicle breakdown (GVBD). In contrast, GVBD in pig oocytes was absolutely blocked at concentrations of 1, 5, 10, 50 and 100 micrograms cycloheximide/ml, respectively. The inhibition of GVBD was not influenced by the presence or absence of cumulus cells and it was fully reversible. When cycloheximide treatment (5 micrograms/ml) was given after preincubation for 6, 12 and 16 h, GVBD occurred in 15, 46 and 75% of oocytes, respectively. It is concluded that proteins important for GVBD of pig oocytes were present in sufficient amounts at about 12 h of culture. The fusion of pig oocytes in metaphase I to oocytes with an intact germinal vesicle revealed that cycloheximide did not inhibit GVBD induced by maturing ooplasm. Therefore, induction of prematurely condensed chromosomes by the maturing ooplasm did not require protein synthesis. However, continuous protein synthesis was necessary to maintain metaphase I and prematurely condensed chromosomes in a typical configuration.

Animals↗