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Biomedical subjects

E Bedows

Publications and source records attributed to E Bedows.

33 records · Page 2Linked to original sources
PubMed1986

Inhibition of herpes simplex virus type 1 replication by halothane.

Halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) inhibited herpes simplex virus type 1 (HSV-1) replication, although HSV-1 DNA was synthesized at normal levels in Vero cells. Viral capsids and extracellular virions were inhibited, and HSV-1 protein synthesis decreased by 50%, although no specific HSV-1 protein failed to be synthesized. Hyperbaric pressure failed to reverse the halothane-induced inhibition of HSV-1 replication.

Capsid↗
PubMed1985

Hyperbaric pressure of 51 atmospheres is without effect on the depression of oxygen uptake in kidney tissue culture produced by halothane.

Although anesthetized animals are awakened when subjected to increased pressure, compression does not result in antagonism of all phenomena associated with these drugs. It has recently been demonstrated that halothane's inhibition of respiration of isolated rat liver mitochondria is not reversed by hydraulic compression to 51 atmospheres. In order to determine whether this phenomenon can be extrapolated to the whole cell, we have investigated the effect of hydraulic compression of intact renal cells equilibrated with halothane, and conclude that pressure does not overcome the inhibitory effect of this anesthetic.

Animals↗
PubMed1984

Effect of halothane on the replication of animal viruses.

Five RNA- and two DNA-containing viruses were propagated in Vero cells and tested for their ability to replicate in the presence of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane), a commonly used inhalational anesthetic. Halothane did not affect poliovirus replication at any anesthetic concentration tested, but all other viruses were either partially or totally inhibited by clinical doses of the anesthetic. Replication of Sendai virus, simian virus 40, vesicular stomatitis virus, and herpes simplex virus type 1 were moderately inhibited by halothane exposure. At concentrations of 2.2% (vol/vol) halothane, peak virus titers were reduced by ca. 2 orders of magnitude for vesicular stomatitis virus and simian virus 40, 3.5 orders of magnitude for Sendai virus, and 4 orders of magnitude for herpes simplex virus. Newcastle disease virus and measles virus were the most susceptible to exposure to halothane. Total inhibition of the replication of these viruses occurred at 1.6 to 2.0% halothane. All of the viruses whose replication was susceptible to the action of halothane were inhibited in a concentration-dependent manner. Furthermore, with the exception of simian virus 40, the inhibition of the replication of all viruses was reversible after halothane removal, although total recovery of virus synthesis was not observed unless the culture medium was changed or the pH was adjusted after anesthetic removal.

Animals↗
PubMed1984

Effect of general anesthetics and pressure on aerobic metabolism of monkey kidney cells.

The authors examined the inhibition of aerobic metabolism in monkey kidney cell cultures exposed to halothane, enflurane, and isoflurane. The ability of hyperbaric pressure to reverse the halothane-induced metabolic inhibition also was examined. Incubation of two monkey kidney cell lines for 24 h with clinically equipotent concentrations (2.6 MAC) of halothane, enflurane, or isoflurane vapors increased the concentration of lactate in the media by 126 to 244% relative to nonexposed control cultures. The increased rate of lactate accumulation was proportional to the concentration of halothane and was accompanied by a decrease in media pH. Removal of halothane restored the normal rate of lactate production. Hyperbaric pressures of 25, 50, and 100 atmospheres did not alter the halothane-stimulated rate of lactate production relative to non-anesthetic-treated controls, although pressure alone did depress the rate of lactate accumulation in all cultures. The stimulation of lactate production likely reflects the known ability of halothane to inhibit mitochondrial respiration. The failure of pressure to reverse the stimulation of lactate production by halothane suggests that inhibition of mitochondrial metabolism cannot be reversed by pressure.

Aerobiosis↗
PubMed1983

Alterations in influenza virus pulmonary pathology induced by diethyl ether, halothane, enflurane, and pentobarbital anesthesia in mice.

Three-week-old CD-1 mice infected with the PR-8 (mouse-adapted) strain of influenza virus while exposed to enflurane demonstrated a decrease in virus titers from the lungs of infected animals, less abnormality of lung histology, and an increase in survival in animals as compared with those receiving the other anesthetics tested. Greater than 90% mortality occurred in groups of mice which inhaled aerosolized virus and received no anesthesia, pentobarbital, diethyl ether, or halothane anesthesia 96 h following infection. Infected mice anesthetized with enflurane 96 h post-infection had significantly lower mortality rate (68%) when compared with the other groups. Halothane-anesthetized mice receiving intranasal influenza virus during anesthesia demonstrated increased survival and a delay in the mean day of death when compared with animals receiving either diethyl ether of pentobarbital anesthesia. Animals receiving enflurane during virus inoculation had an even lower mortality rate and a later mean day of death when compared with infected animals receiving day of the other three anesthetics. Examination of lungs from animals infected during anesthesia demonstrated influenza virus titers significantly less in the animals that received enflurane anesthesia when compared with the other groups. Histologic sections of lungs revealed extensive spread of the disease process into the alveoli and interstitium of the lungs of animals infected while receiving pentobarbital or diethyl ether anesthesia. Animals infected during halothane demonstrated pathologic characteristics similar to pentobarbital- and diethyl-ether-treated groups; however, the changes were not as extensive. Mice infected during exposure to enflurane revealed only a mild bronchopneumonia.

Anesthesia↗
PubMed1983

Pressure reversal of halothane's antiviral effect.

The authors have studied the effects that hyperbaric pressure and halothane had on measles virus replication. Two per cent halothane at one atmosphere of air (ATA) reduced the number of infectious measles virus particles produced in cultured Vero cells by greater than four orders of magnitude (P less than 0.001) relative to virus produced in untreated cultures at 1 ATA. The same concentration of halothane at 100 ATA still reduced the amount of virus synthesized but only by 1 1/2 orders of magnitude (P less than 0.01) as compared with control cultures. Pressure (100 ATA) alone reduced virus production insignificantly. Thus, it appears that the antiviral effects of halothane on measles virus replication in cultured Vero cells is reversible at least partially by pressure.

Animals↗
PubMed1983

Fate of microfilaments in vero cells infected with measles virus and herpes simplex virus type 1.

In herpes simplex virus type 1-infected Vero cells, reorganization of microfilaments was observed approximately 4 h postinfection. Conversion of F (filamentous) actin to G (globular) actin, as assessed by a DNase I inhibition assay, was continuous over the next 12 to 16 h, at which time a level of G actin of about twice that observed in uninfected cells was measured. Fluorescent localization of F actin, using 7-nitrobenz-2-oxa-1,3-diazole (NBD)-phallacidin, demonstrated that microfilament fibers began to diminish at about 16 to 18 h postinfection, roughly corresponding to the time that G actin levels peaked and virus-induced cytopathology was first observable. In measles virus-infected cells, no such disassembly of microfilaments occurred. Rather, there was a modest decrease in G actin levels. Fluorescent localization of F actin showed that measles virus-infected Vero cells maintained a complex microfilament network characterized by fibers which spanned the entire length of the newly formed giant cells. Disruption of microfilaments with cytochalasin B, which inhibits measles virus-specific cytopathology, was not inhibitory to measles virus production at high multiplicities of infection (MOI) but was progressively inhibitory as the MOI was lowered. The carbobenzoxy tripeptide SV-4814, which inhibits the ability of Vero cells to fuse after measles virus infection, like cytochalasin B, inhibited measles virus production at low MOI but not at high MOI. Thus, it appears that agents which affect the ability of Vero cells to fuse after measles virus infection may be inhibitory to virus production and that the actin network is essential to this process.

Actins↗
PubMed1982

Enrichment of measles virus-like RNA in the nucleocapsid fraction isolated from subacute sclerosing panencephalitis brains.

A procedure has been developed which facilitates the detection of measles virus RNA sequences in human brains. The procedure involves isolating subviral components (nucleocapsids) from brain tissues prior to RNA purification, followed by hybridization of these RNAs to cDNA synthesized from measles virus 50 S RNA template. Using these techniques we were able to obtain an RNA fraction which was manyfold enriched in measles virus-specific RNA, relative to unfractionated subacute sclerosing panencephalitis (SSPE) brain RNAs 70-100% of the measles virus-specific RNA present these SSPE brain samples were recovered in this enriched fraction.

Base Sequence↗
PubMed1981

Inhibiting effects of enflurane and isoflurane anesthesia on measles virus replication: comparison with halothane.

Replication of measles virus in BSC cells was studied in the presence of enflurane (2-chloro-1,1,2-trifluoroethyl difluoromethyl ether), a commonly used volatile anesthetic agent, and its isomer, isoflurane (1-chloro-2,2,2-trifluoroethyl difluoromethyl ether). At clinical concentrations of the anesthetics (up to 4%), cell division was retarded, whereas only minimal toxic cellular effects were observed. The appearance of progeny virus from the cell cultures exposed to these anesthetics was decreased in a dose-related manner. Incorporation of [(3)H]uridine into measles virus nucleocapsids also decreased progressively with increasing anesthetic concentrations. In comparing the inhibition of measles virus replication in the presence of halothane (2-bromo-2-chloro,1,1,1-trifluoroethane), enflurane, or isoflurane, it was found that both inhibition of the appearance of infectious virus at 48 h postinfection and incorporation of [(3)H]uridine into measles virus nucleocapsids were proportional to the anesthetic concentrations. An equivalent degree of effect was produced by anesthetically equivalent concentrations of the three anesthetics (minimal alveolar concentration) but not by absolute concentrations. In addition, recovery of infectious virus synthesis from the inhibition encountered during exposure of infected BSC cells to halothane or isoflurane was also investigated. In cultures exposed to halothane or enflurane, recovery of infectious virus synthesis was rapid and complete. Recovery of virus synthesis was slower after isoflurane removal and did not reach the peak control titers of infected cultures not exposed to the anesthetic. Treatment with halothane resulted in the formation of a preponderance of slowly sedimenting virus nucleocapsid particles which contained less than full-length ribonucleic acids after anesthetic removal. Neither enflurane nor isoflurane treatment of BSC cultures resulted in the formation of significant levels of these slowly sedimenting particles with short genomes after anesthetic removal.

Capsid↗
PubMed1981

Host cell factors involved in the production of slowly sedimenting nucleocapsids in measles virus-infected cells.

A decrease in the sedimentation rates of the measles virus nucleocapsid, and the RNA contained within, were observed during acute measles virus infection when the growth conditions of Vero cells were altered. The change in sedimentation rates of virus nucleocapsids in these experiments was apparently due to the physiological state of the cell and was independent of the history of the measles virus used for infection since: (i) the same virus stock was used to infect cells from which nucleocapsids were prepared, (ii) nucleocapsid sedimentation rates were rapid when Vero cells freshly revived from liquid nitrogen were infected, but nucleocapsid profiles showed no decrease in the amount of slowly sedimenting material using the same cells and changing the virus preparation used for infection. Frequent cell splittings and numerous medium changes were among the growth factors which appeared to correlate to slowly sedimenting particle production. Changes in the amount of self-complementarity of the measles virus RNA were also observed under these conditions.

Animals↗
PubMed1980

Anesthetic action and virus replication: inhibition of measles virus replication in cells exposed to halothane.

Replication of measles virus in BSC cells was studied in the presence of halothane, a commonly used volatile anesthetic. At clinical concentrations of the anesthetic, appearance of progeny virus was decreased in a dose-related manner. This inhibition was reversible as the removal of halothane allowed virus replication to be resumed. Studies attempting to elucidate the mechanism of action of the anesthetic inhibition of virus replication revealed that halothane did not directly inactivate the virus particle or prevent viral adsorption to the cell. Infectious virus and nucleocapsid production were decreased or stopped, depending on the anesthetic dosage used. Direct immunofluorescent staining for measles virus antigen was negative in cells treated at the higher concentrations of halothane. Recovery of nucleocapsid production started within a few hours after removal of halothane. Furthermore, the combined inhibitory effects on viral ribonucleic acid synthesis of 5-azacytidine and halothane were additive. This evidence suggests that inhibition of measles virus replication occurs at or before ribonucleic acid synthesis.

Anesthesia↗
PubMed1977

L cell DNA ligase joins RNA to DNA on a DNA template.

L cell DNA ligase catalyzes a covalent linkage between 5'-hosphoryl oligodeoxyribonucleotides and 3'-hydroxyl oligoribonucleotides on a complementary polydeoxyribonucleotide template. This reaction occurs to a substantially lesser extent than does the sealing of DNA to DNA. The joining of [5'32P]d(pA)12-18 to (Ap)11A on poly[d(T)] or of [5'-32P]d(pG)12-18 to 5'-hydroxyl, 3'-hydroxyl oligo(I) ON POLY[D(C)] was demonstrated by the formation of alkaline phosphatase resistant radioactivity. The 32P of the hybrid reaction products became sensitive to the action of alkaline phosphatase after treatment with alkali. Furthermore, hydrolysis of the products of the linkage of [5'-32P]d(pG)12-18 to 5'-hydroxyl, 3'-hydroxyl oligo(I) on poly[d(C)] with micrococcal nuclease and spleen phosphodiesterase resulted in the formation of [3'-32P]IMP. Attempts to seal [5'-32p[-(pA)12 to d(Ap)11-17A on poly[d(T) or [5'-32P]oligo(pI) to d(Gp)11-17G on poly[d(C)] were unsuccessful.

DNA↗
PubMed1975

T4-induced RNA ligase joins single-stranded oligoribonucleotides.

RNA ligase isolated from Escherichia coli infected with bacteriophage T4 will catalyze the formation of an intermolecular 3' leads to 5' phosphodiester linkage between an oligoribonucleotide with a free 3'-hydroxyl and another oligoribonucleotide with a 5'-phosphate. Upon reaction with (Ap)5C, nearly quantitative conversion of the hexamer [5'-32P]p(Up)5U to the dodecamer (Ap)5C[3' leads to 5'-32P]p(Up)5U was observed. The product was identified by its mobility on RPC-5 column chromatography, its resistance to alkaline phosphatase, and the appearance of the expected radiolabeled products on hydrolysis with alkali, ribonuclease A, snake venom phosphodiesterase, and spleen phosphodiesterase. The coupling of other pairs of single-stranded oligoribonucleotides has also been demonstrated. The intermolecular joining reaction is probably mechanistically similar to the intramolecular cyclization activity previously reported for Tr RNA ligase. It is expected that this enzyme will be useful for the synthesis of RNA fragments of defined sequence.

Chromatography, Gel↗
PubMedDate not supplied

An investigation of the antiviral activity of Podophyllum peltatum.

The antiviral activity of an aqueous extract of Podophyllum peltatum was investigated. The extract was fractionated by reversed-phase chromatography, and podophyllotoxin was found to be the most active component in inhibiting the replication of measles and herpes simplex type I viruses. beta-Peltatin and desoxypodophyllotoxin produced marginal antiviral effects, while alpha-peltatin and picropodophyllotoxin were inactive at the levels tested.

Animals↗