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At least 19 recordsLinked to original sources
PubMed1987

The effects of the protein synthesis inhibitor anisomycin on the febrile responses to intracerebroventricular injections of bacterial pyrogen, arachidonic acid and prostaglandin E2.

1. Anisomycin (15 mg/kg) was administered s.c. to cats at ambient temperatures of 5 degrees C, 20 degrees C and 38 degrees C. It produced biphasic effects on body temperature at 5 degrees C and 20 degrees C, an initial fall in temperature followed by a rise in body temperature, and a rise in body temperature of long latency at 38 degrees C. 2. Anisomycin (15 mg/kg) attenuated the hyperthermic responses to centrally injected PGE2 (1 microgram) at all ambient temperatures studied and also completely abolished the hyperthermic response to arachidonic acid (100 ng i.c.v.) at 20 degrees C. 3. Shigella dysenteriae (100 ng i.c.v.) raised the body temperature of cats by increasing heat production and reducing heat loss at 5 degrees C and 20 degrees C, and by increasing heat conservation at 38 degrees C. Anisomycin (15 mg/kg s.c.) pretreatment did not affect the temperature responses to the pyrogen at 20 degrees C and 38 degrees C, but did reduce the responses to Shigella dysenteriae (100 ng and 1 microgram i.c.v.) at 5 degrees C. 4. Anisomycin (15 mg/kg s.c.) was administered to cats, 90 min after the injection of Shigella dysenteriae (100 ng i.c.v.), at 20 degrees C at the onset of hyperthermia in control experiments. Under these conditions, no hyperthermia was observed over a 2 h period following anisomycin injection. 5. It is concluded that anisomycin interferes with pyrogen induced fever by acting at a site after PGE2 in the pathway to fever.

Animals↗
PubMed1992

Phase response curve to anisomycin in tau mutant hamsters.

Administration of the protein synthesis inhibitor, anisomycin, to wild type hamsters produces phase shifts in their circadian rhythms that have similarities to shifts produced by non-photic behavioral stimulation. A mutation that shortens the period of rhythms in hamsters results in altered responsiveness to non-photic input. However, responses of the mutants to anisomycin are unaffected: their phase response curve (PRC) for anisomycin is similar to that of wild types. This suggests that 1) anisomycin is not acting on mechanisms specifically involved in non-photic behavioral phase shifting, and 2) the mutation affects the non-photic input pathway or the pacemaker itself at a point that is upstream from anisomycin's site of action.

Animals↗
PubMed1989

The protein synthesis inhibitor, anisomycin, causes exacerbation of the iminodipropionitrile-induced spasmodic dyskinetic syndrome in rats.

The effects of anisomycin on dyskinetic head movements, circling, and locomotor activity were investigated in the IDPN-induced syndrome. Intracerebroventricular (ICV) injections of anisomycin in conjunction with IDPN caused exacerbation of all aspects of the syndrome, although circling and vertical head dyskinesias (retrocollis) were the most affected. Animals treated with only anisomycin showed persistent retrocollis but not laterocollis or circling. Biochemical studies confirmed the increases in the concentration of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) previously observed in the striata of IDPN-treated rats two weeks after stopping administration of the drug. Rats treated with anisomycin alone also showed significant increases in striatal 5-HT and 5-HIAA concentrations which were somewhat higher on the side of the ICV infusions. Coadministration of IDPN and anisomycin did not cause any further increases in 5-HT or 5-HIAA. These results suggest that inhibition of protein synthesis by IDPN may be one of the processes involved in the development of the persistent dyskinetic syndrome.

Animals↗
PubMed1978

Effects of anisomycin and CNS stimulants on brain catecholamine synthesis.

Mice were injected with anisomycin, an inhibitor of cerebral protein synthesis; d-amphetamine, strychnine, or caffeine was administered 30 min later. Fifteen min before sacrifice at 1 or 2 hr after injection of anisomycin, 3H-tyrosine was injected intravenously, and catecholamine synthesis rates were estimated by measurement of the specific activity of 3H-tyrosine and the accumulation of 3H-norepinephrine and 3H-dopamine. Anisomycin decreased synthesis rates of catecholamines, but this effect was not significantly affected by any of the CNS stimulants. These results suggest that the recently reported reversal of anisomycin-induced amnesia by these stimulants is not due to an attenuation of brain catecholamine synthesis inhibition.

Animals↗
PubMed1975

Simultaneous ribosomal resistance to trichodermin and anisomycin in Saccharomyces cerevisiae mutants.

A spontaneous mutant of Saccharomyces cerevisiae resistant to trichodermin has been isolated. It displays cross resistance both in vivo and in vitro to a number of sesquiterpene antibiotics (fusarenon X, trichothecin and verrucarin A) and to the chemically unrelated antibiotic anisomycin. The mutation conferring resistance to anisomycin and trichodermin is expressed in the 60-S subunit of the yeast 80-S ribosome. Mutant ribosomes bind [-14C]trichodermin much less efficiently than wild type ribosomes, suggesting that resistance may be due, at least in part, to this property. However, both types of ribosomes bind [-3H] anisomycin equally. These results suggest that anisomycin and trichodermin have different binding sites on the 60-S subunit of eukaryotic ribosomes, even though previous results have shown that both antibiotics bind to mutually exclusive sites.

Anti-Bacterial Agents↗
PubMed1990

Comparison of the in vitro activities of quassinoids with activity against Plasmodium falciparum, anisomycin and some other inhibitors of eukaryotic protein synthesis.

Using the inhibition of incorporation of [3H]hypoxanthine as an index of viability of malaria parasites, it was shown that a chloroquine-sensitive strain of Plasmodium falciparum (T9-96) and a chloroquine-resistant strain (K1) did not differ in their sensitivities to the quassinoids ailanthinone, bruceantin and chaparrin. Similarly, there were no differences between the strains in their sensitivities to the protein synthesis inhibitors anisomycin, deacetylanisomycin, cephalotaxine, homoharringtonine, cycloheximide, puromycin and puromycin aminonucleoside. The IC50 values derived for ailanthinone and bruceantin, cycloheximide, homoharringtonine and puromycin were in the nanomolar range, whereas those for the anisomycins, cephalotaxine and the aminonucleoside of puromycin were micromolar or greater. Those drugs tested which contain an ester moiety (ailanthinone, bruceantin, anisomycin, homoharringtonine) were more active than the related drugs (chaparrin, deacetylanisomycin, cephalotaxine) that do not. Cross-resistance to inhibitors of protein synthesis appeared not to accompany resistance to chloroquine.

Animals↗
PubMedDate not supplied

Fever produced by intrahypothalamic pyrogen: effect of protein synthesis inhibition by anisomycin.

In the unrestrained cat, the inhibition of protein synthesis by anisomycin, given either subcutaneously (5.0--25.0 mg/kg) or directly into the anterior hypothalamic, preoptic area (1.0--25.0 micrograms) impaired the development of a bacterial fever. S. typhosa infused intravenously (1:10 dilution in 1 ml) or into AH/POA (1.0 microliter) evoked an intense fever which was either significantly delayed or prevented by anisomycin. Conversely, anisomycin failed to affect the typical hyperthermia evoked by 100 ng PGE2 or 1.0--7.0 micrograms 5-HT similarly infused into AH/POA. These data demonstrate that an intermediary humoral factor of unknown nature is required in the hyperthermic effector pathway underlying the febrile response.

Animals↗
PubMed1977

Effect of anisomycin on the cellular level of native ribosomal subunits.

Treatment of Ehrlich ascites cells with anisomycin induces an almost threefold increase in the level of native 60S ribosomal subunits. This increase is not the result of an increase in rate of synthesis or transport of these subunits but is caused by a defect in the joining of the 60S subunits to the smaller initiation complex to form an 80S complex. Experimental evidence for such a blocking of the "joining reaction" could be found in the formation of "half-mer"-type oligosomes and by the release of extra 40S subunits when these oligosomes were treated with ribonuclease. Cycloheximide, an inhibitor of the translocation reaction, and inhibitors of the initiation prevent the increase of native 60S subunits induced by anisomycin. Our results imply that the increse of 60S subunits induced by anisomycin may be helpful in estimating the amount of initiating mRNAs in the cell.

Animals↗
PubMed1978

Memory: modification of anisomycin-induced amnesia by stimulants and depressants.

Mice were trained in a passive (foot shock)avoidance task. When administered after training, the stimulants caffeine or nicotine blocked amnesia for the task that had been produced by injections of the protein synthesis inhibitor anisomycin given prior to training. With foot shock at a higher intensity, anisomycin did not produce amnesia by itself, but the administration of the depressants chloral hydrate or sodium phenobarbital after training did cause amnesia. Stimulants and depressants did not have an appreciable influence on the overall degree of protein synthesis inhibition produced by anisomycin. The results support the hypothesis that arousal after training is an important factor in the conversion of short-term to long-term memory.

Animals↗
PubMed1992

MK-801, but not anisomycin, inhibits the induction of tolerance to ischemia in the gerbil hippocampus.

We examined whether MK-801, an N-methyl-D-aspartate (NMDA)-receptor antagonist, or anisomycin, a reversible protein synthesis inhibitor, inhibits the induction of ischemic tolerance following preconditioning with sublethal ischemia in gerbil hippocampus. Preconditioning with 2 min of ischemia, which induced heat shock protein-72 immunoreactivity, prevented hippocampal CA1 neuronal damage following 3 min of ischemia produced 3 days later. MK-801, but not anisomycin, inhibited the induction of tolerance although the heat shock protein synthesis was reduced in both groups. The present result suggests that NMDA receptor activation, causing stress response, induces the ischemic tolerance.

Animals↗
PubMed1991

A mutation in the large subunit ribosomal RNA gene of Tetrahymena confers anisomycin resistance and cold sensitivity.

Anisomycin, an antibiotic that specifically inhibits the peptidyl transfer function of eukaryotic ribosomes, has been used to select resistant mutants in Tetrahymena thermophila. A mutation conferring anisomycin resistance (an-r) has been localized to a 1.2-kb fragment of the large subunit ribosomal RNA (rRNA) gene by transformation via microinjection. A single base pair change was detected within this region. Nine independently isolated an-r mutants had the same base pair change. T. thermophila strains that are homozygous for this mutation are cold sensitive, unable to mate and grossly abnormal in cell morphology.

Animals↗
PubMed1976

Effects of anisomycin on brain protein synthesis and passive avoidance learning in newborn chicks.

The effects of anisomycin (ANM) on newborn chicks have been studied with respect to brain protein synthesis, growth, EEG, toxicity, and several passive avoidance learning tasks. It was found that intracerebral ANM (80 nmol) gave a maximum inhibition of brain protein synthesis of 30%, while a combination of subcutaneous (10 mumol; 53 mg/kg) plus intracerebral (80 nmol; 21 mug) ANM inhibited by 91% in the first 2 hr and by 75% in the subsequent 2 hr period. Cycloheximide (CXM) also in combined injections at the same doses as ANM, inhibited by 97% in the 4 hr that followed injection. However, all the CXM-injected chicks were dead by 18 hr, while the lethality of ANM did not differ from that of saline. ANM also did not affect EEG measured at 1, 3, 5, or 24 hr following the subcutaneous plus intracerebral injections, nor did ANM affect body or brain growth curves or brain protein accretion. In the learning experiments, animals were initially trained to peck at water-coated metal spheres (type A learning) or at water imbibed birdseed (types B and C learning) in less than 1 sec, and were exposed to the same lures treated with the aversant methylanthranilate (MeA) one day later on one occasion (types A and B learning) or exposed twice (type C learning) and tested for learning retention one day later. Learning criterion was set as failure to peck at the lure during the first 20 sec of presentation. If ANM was injected 1 hr prior to MeA exposure, large and highly significant memory deficits were found during the retention test, as compared with saline injected controls. No effect of ANM was seen, however, if it was injected one day after learning, indicating that it did not interfere with retrieval mechanisms. ANM also decreased the external manifestations of fear or displeasure that chicks express during retention testing. Such manifestations have a high correlation with pecking suppression (r = 0.88, P less than 0.001).

Amino Acids↗
PubMed1977

Anisomycin sensitive mutants of Physarum polycephalum isolated by cyst selection.

The haploid myxamoebae of Physarum polycephalum reversibly differentiate to form dormant microcysts under conditions of starvation. The thin-walled cysts can be selective recovered from a cell suspension which has been treated with the surfactant Triton X-100 to lyse amoeboid forms. Excystment, which is initiated by suspension in liquid medium, is inhibited by antibiotics which block protein synthesis. Cysts of drug resistant mutants excyst rapidly in media containing sufficient antibiotic to maintain drug sensitive strains in the encysted state. The selective survival of non-excysted cells following Triton X-100 treatment has been employed to enrich for drug sensitive mutants. Several anisomycin sensitive mutants have been isolated, one of which has been analysed genetically. The possible applications of this mutant enrichment technique are discussed.

Anisomycin↗
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↗
PubMed1975

Quantitative binding of antibiotics to ribosomes from a yeast mutant altered on the peptidyl-transferase center.

Quantitative binding studies of [G-3H]anisomycin and [acetyl-14C]trichodermin to sensitive and resistant 80-S ribosomes from yeasts are described in this work. A single mutation, most probably affecting the ribosome peptidyl transferase centre, appears to have pleiotropic effects on the ribosome leading to resistance to trichodermin and anisomycin and to an increased sensitivity to sparsomycin. Resistance to trichodermin is due to a reduced affinity of ribosomes from the mutant for the antibiotic. Ribosomes from the sensitive strain (Y 1661 bind [acetyl-14C]trichodermin with a dissociation constant of 0.99 muM while those from the resistant one (TR1) bind [acetyl-14C]trichodermin with a dissociation constant of 15.4 muM. Similar results are obtained when the binding of [acetyl-14C]trichodermin to Y 166 and TR1 60-S subunits is studied. The mutant TR1 is also resistant to anisomycin. Although trichodermin and anisomycin bind to the ribosome at mutually exclusive sites, the higher affinity binding of [G-3H]anisomycin that is responsible for the inhibition of the peptidyl transferase center is practically identical for Y 166 and TR1 ribosomes. Therefore, the mutation in the ribosome leading to resistance to trichodermin and anisomycin decreases the affinity for trichodermin but not for anisomycin. Trichodermin, trichothecin and fusarenon X inhibit the binding of [G-3H]anisomycin to TR1 ribosomes to a lower extent than to Y 166 ribosomes, suggesting that the resistance of TR1 ribosomes to the effects of trichothecin and fusarenon X is caused by a decrease in the affinity of the ribosomes for these drugs, as was seen with trichodermin. On the other hand, verrucarin A inhibits [G-3H]anisomycin binding to Y 166 and TR1 ribosomes to a similar extent and therefore its affinity for the ribosome does not appear to be affected by the mutation leading to resistance. Trichothecin, trichodermin and fusarenon X appear to have a common binding site on the 60-S ribosomal subunits, which overlaps or is closely linked to the binding sites of anisomycin and verrucarin A.

Acyltransferases↗