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PubMed1976

XC cell fusion by murine leukemia viruses: fusion from without.

Concentrated murine leukemia virus (MuLV) or MuLV producing cells induce XC cell fusion within an hour leading to syncytia formation. While MuLV inactivated by UV irradiation, beta-propiolactone or hydroxylamine treatment still caused cell fusion, Bromelin- or trypsin treated MuLV was no longer able to fuse XC cells. Though sonicated MuLV induced no XC cell fusion, it interfered with cell fusion as caused by untreated MuLV. XC cells infected by diluted MuLV of a titer lower than 1 X 10(5) PFU/ml formed no syncytia although they produced MuLV. The cell fusion mechanism is discussed.

Animals↗
PubMed1976

Significance of treatment interval and DNA repair in the enhancement of viral transformation by chemical carcinogens and mutagens.

Treatment of Syrian hamster embryo cells with diverse classes of chemical carcinogens enhanced transformation by a carcinogenic simian adenovirus, SA7. Optimal enhancement was a function of time of chemical addition in relation to time of virus addition and cell transfer. Aflatoxin B1 (AFB1) and the polycyclic hydorcarbons, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (MCA), and 7,12-dimethylbenz(a)anthracene (DMBA) enhanced SA7 transformation when added prior to virus, but inhibited transformation when added after virus absorption and cell transfer. The enhancement of SA7 transformation was maximal when cytosine arabinoside, caffeine and 6-acetoxy-benzo(a)pyrene (6-ac-B(a)P) were added after virus, but minimal when added before virus. A third class of chemicals, including beta-propiolactone (beta-PL), methyl methanesulfonate (MMS), N-acetoxy-2-acetylaminofluorene (Ac-AAF), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and methylazoxymethanol acetate (MAM-ac), enhanced SA7 transformation added before, or after, virus inoculation and cell transfer. All chemicals which induced changes in DNA sedimentation in alkaline sucrose gradients and unscheduled DNA (repair) synthesis in hamster cells, increased the frequency of SA7 transformation. However, several chemicals such as dibenz(a,h)anthracene (DB(a,h)A), benzo(e)pyrene (B(e)P), cytosine arabinoside, and caffeine enhanced SA7 transformation but did not induce DNA sedimentation changes or repair. Chemicals that cause DNA damage, which can be repaired by hamster cells, may enhance viral transformation by providing additional sites for integration of viral DNA during the repair process. Chemicals that apparently do not induce DNA repair synthesis may enhance viral transformation by incorporation of viral DNA into gaps in cell DNA at sites of unrepaired damage during scheduled DNA synthesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

In vitro Dimroth rearrangement of 1-(2-carboxyethyl) adenine to N6-(2-carboxyethyl)adenine in single-stranded calf thymus DNA.

The new adduct N6-(2-carboxyethyl)adenine (N6-CEA) was prepared from 1-(2-carboxyethyl)adenine (1-CEA) by base catalyzed (Dimroth) rearrangement of 1-CEA. The structure of N6-CEA was assigned on the basis of UV spectra and electron impact and isobutane chemical ionization mass spectra. When the carcinogen beta-propiolactone was reacted in vitro with calf thymus DNA, 1-CEA but not N6-CEA was detected on paper chromatograms following acid hydrolysis of the DNA. When BPL-reacted single-stranded DNA was incubated at pH 11.7 (37 degrees C, 18 h) prior to acid hydrolysis, it was found that 1-CEA was completely converted to N6-CEA in DNA by Dimroth rearrangement, whereas no conversion occurred at pH 7.5. The extent of Dimroth rearrangement at various pHs and temperatures was determined for 1-CEA, 1-methyladenine (1-MeA), 1-(2-carboxyethyl)-deoxyadenosine-5'-monophosphoric acid (1-CEdAdo5'P) and the phosphodiester 5'-O-(2-carboxyethyl)phosphono-1-(2-carboxyethyl)deoxyadenosine (1-CE-Ado-5'-P-CE).

Adenine↗
PubMed1983

Inhibition of unscheduled DNA synthesis in human lymphocytes by chemical carcinogens.

Freshly isolated human peripheral lymphocytes were treated with an alkylating agent immediately after collection and subsequently treated with UV radiation. This system was used because it represents a method for assaying damage in cells immediately after their removal from the host. The amount of UV-induced repair was measured as unscheduled DNA synthesis (UDS) by incorporation of [3H]deoxythymidine into the cellular DNA. The alkylating agents beta-propiolactone (BPL) and methyl methane-sulfonate (MMS) inhibited UDS at concentrations of 0.08 mM and 0.6 mM, respectively. Lower concentrations had no effect. Lymphocytes allowed to remain in culture medium after treatment with the alkylating agents did not recover the ability to perform UV-induced UDS even when cells were irradiated 48 h after carcinogen treatment. The decrease in UV-induced UDS resulting from alkylating agent treatment could not be attributed to cell death.

Carcinogens↗
PubMed1984

In vitro alkylation of calf thymus DNA by acrylonitrile. Isolation of cyanoethyl-adducts of guanine and thymine and carboxyethyl-adducts of adenine and cytosine.

Reaction of the rodent carcinogen acrylonitrile (AN) at pH 5.0 and/or pH 7.0 for 10 and/or 40 days with 2'-deoxyadenosine (dAdo), 2'-deoxycytidine (dCyd), 2'-deoxyguanosine (dGuo), 2'-deoxyinosine (dIno), N6-methyl-2'-deoxyadenosine (N6-Me-dAdo) and thymidine (dThd) resulted in the formation of cyanoethyl and carboxyethyl adducts. Adducts were not detected after 4 h. The adducts isolated were 1-(2-carboxyethyl)-dAdo (1-CE-dAdo), N6-CE-dAdo, 3-CE-dCyd, 7-(2-cyanoethyl)-Gua (7-CNE-Gua), 7,9-bis-CNE-Gua, imidazole ring-opened 7,9-bis-CNE-Gua, 1-CNE-dIno, 1-CE-N6-Me-dAdo and 3-CNE-dThd. Structures were assigned on the basis of UV spectra and electron impact (EI), chemical ionization (CI), desorption chemical ionization (DCI) and Californium-252 fission fragment ionization mass spectra. Evidence is presented which strongly suggests that N6-CE-dAdo was formed by Dimroth rearrangement of 1-CE-dAdo during the reaction between AN and dAdo. The carboxyethyl adducts resulted from initial cyanoethylation (by Michael addition) at a ring nitrogen adjacent to an exocyclic nitrogen atom followed by rapid hydrolysis of the nitrile moiety to a carboxylic acid. It was postulated that the facile hydrolysis is an autocatalyzed reaction resulting from the formation of a cyclic intermediate between nitrile carbon and exocyclic nitrogen. AN was reacted with calf thymus DNA (pH 7.0, 37 degrees C, 40 days) and the relative amounts of adducts isolated were 1-CE-Ade (26%), N6-CE-Ade (8%), 3-CE-Cyt (1%), 7-CNE-Gua (26%), 7,9-bis-CNE-Gua (4%), imidazole ring-opened 7,9-bis-CNE-Gua (19%) and 3-CNE-Thy (16%). Thus a carcinogen once adducted to a base in DNA was shown to be subsequently modified resulting in a mixed pattern of cyanoethylated and carboxyethylated AN-DNA adducts. Three of the adducts (1-CE-Ade, N6-CE-Ade and 3-CE-Cyt) were identical to adducts previously reported by us to be formed following in vitro reaction of the carcinogen beta-propiolactone (BPL) and calf thymus DNA. The results demonstrate that AN can directly alkylate DNA in vitro at a physiological pH and temperature.

Acrylonitrile↗
PubMed1988

A simple and rapid method for preparation of HIV-expressing targets for functional assays.

Standardized samples of target cells expressing viral antigen are necessary to perform reproducible and comparable functional assays for immune responses to human immunodeficiency virus (HIV-1). HIV-infected cultured cell lines show wide variability in the number of HIV-expressing cells and in the amount of viral antigen per cell. They, as well as cells coated with the infectious virus, are a biohazard. 0.015% v/v beta-propiolactone (BPL) in buffered solution at pH 7.5 inactivates the infectivity of HIV but retains its antigenicity. BPL-inactivated HIV easily binds to T4 receptor bearing T-lymphocytes in a 30 min incubation at 22 degrees C. The process of adsorption is dose-dependent and results in a standardized and reproducible sample of target cells. Applications for the method are demonstrated and include: (1) preparation of target cells for assay of antibody-dependent cellular cytotoxicity (ADCC), and (2) characterization of antisera to HIV for their capacity to block HIV binding to cells.

Antibodies, Viral↗
PubMed1975

Influence of N2 or O2 on two alkylating agents in Neurospora crassa.

Previous studies have indicated that the alkylating agent, 2-methoxy-6-chloro-9-(3-[ethyl-2-chloroethyl]aminopropylamino)acridine dihydrochloride (ICR-170), induces much more killing and mutation in conidia of Neurospora crassa treated in an atmosphere of N2 than in an atmosphere of O2. It was desirable to determine if a similar effect--more killing and mutation in N2 than in O2--could be observed with two other known alkylating agents, beta-propiolactone (BPL) and ethyl methanesulfonate (EMS), in the same test system. Conidia of a heterokaryotic strain of N. crassa were bubbled with N2 or O2 during treatment with BPL or EMS. Forward-mutation was measured in the ad-3 region by a direct method. The results indicate that N2 or O2 do not influence the lethal and mutagenic activities of BPL or EMS during treatment of conidia. Hence the influence of N2 or O2 on the lethal and mutagenic activites of ICR-170 is different from the influence of these gases on BPL or EMS using the ad-3 test system in N. crassa.

Alkylating Agents↗
PubMed1976

The resistance of Micrococcus radiodurans to killing and mutation by agents which damage DNA.

The resistance of Micrococcus radiodurans to the lethal and mutagenic action of ultraviolet (UV) light, ionising (gamma) radiation, mitomycin C (MTC), nitrous acid (NA), hydroxylamine (HA), N-methyl-N'-nitro-N-nitrosoguanidine (NG), ethylmethanesulphonate (EMS) and beta-propiolactone (betaPL) has been compared with that of Escherichia coli B/r. M. radiodurans was much more resistant than E. coli B/r to the lethal effects of UV light (by a factor of 33), gamma-radiation (55), NG (15) and NA (62), showed intermediate resistance to MTC (4) and HA (7), but was sensitive to EMS (1) and betaPL (2). M. radiodurans was very resistant to mutagens producing damage which can be repaired by a recombination system, indicating that it possesses an extremely efficient recombination repair mechanism. Both species were equally sensitive to mutation to trimethoprim resistance by NG, but M. radiodurans was more resistant than E. coli B/R to the other mutagens tests, being non-mutable by UV light, gamma-radiation, MTC and HA, and only slightly sensitive to mutation by NA, EMS and betaPL. The resistance of M. radiodurans to mutation by UV-light, gamma-radiation and MTC is consistent with an hypothesis that recombination repair in M. radiodurans is accurate since these mutagens may depend on an "error-prone" recombination system for their mutagenic effect in E. coli B/r. However, because M. radiodurans is also resistant to mutagens such as HA and EMS, which are mutagenic in E. coli in the absence of an "error-prone" system, we propose that all the mutagens tested may have a common mode of action in E. coli B/r, but that this mutagenic pathway is missing in M. radiodurans.

Escherichia coli↗
PubMed1991

Protection of chickens from lethal influenza virus infection by influenza A/chicken/Pennsylvania/1/83 virus: characterization of the protective effect.

The influenza A/chicken/Pennsylvania/1/83 (H5N2) virus is the first known example of an influenza virus isolated from a natural infection which contained primarily defective interfering particles (T. M. Chambers and R. G. Webster, J. Virol. 61, 1517-1523, 1987). In chickens, coinoculation of this virus together with the closely related but highly virulent influenza A/chicken/Pennsylvania/1370/83 virus results in reduced mortality compared to virulent virus infection alone (Bean et al., J. Virol. 54, 151-160, 1985). The biological basis of this protective effect has not been established. Protective activity required greater than or equal to 100-fold excess input of protecting virus over virulent virus, functioned effectively during the first generations of virulent virus multiplication, and also functioned against an antigenically heterologous (H7N7) virulent influenza virus. Protection was correlated with the complete inhibition of virulent virus spread to the brain of infected chickens. Plaque-purified chicken/Pennsylvania/1/83 virus depleted of defective interfering particles, and beta-propiolactone-inactivated virus, had no protective effect. These characteristics are consistent with the hypothesis that protection was the result of defective interfering particle-mediated interference with virulent virus multiplication within the respiratory tract of the chicken.

Animals↗
PubMed1989

In vivo micronucleus test using mouse hepatocytes.

The bone-marrow micronucleus (BMM) test is highly specific for clastogenic effects but its sensitivity is determined to a great extent by the substances tested, particularly by their metabolism. Some compounds, such as unstable mutagens or those which generate short-lived metabolites, are not detected in this test because the metabolites produced in the liver do not reach the bone marrow. In an attempt to provide qualitative and quantitative assessments of chromosomal mutations produced in vivo by genotoxic agents not detected in the mouse BMM test, a mouse-liver micronucleus test, adapted from Tates model, was developed. The animals were treated twice, with an interval of 24 h between treatments, and then subjected to partial hepatectomy (PH) 24 h after the second treatment in order to induce mitotic stimulation. The incidence of micronucleated hepatocytes was determined 96 h after PH. The test was evaluated with 5 procarcinogens, each with a complex metabolic pattern: dimethylnitrosamine (DMN), diethylnitrosamine (DEN), 1,1-dimethylhydrazine (1,1-DMH), 4-aminophenol (4-APOL), 4-aminobiphenyl (4-ABPYL) and one direct unstable mutagen, beta-propiolactone (BPL). All these compounds are negative in the mouse BMM test but caused a major increase in the incidence of micronuclei in mouse hepatocytes. This test is simple and can be readily compared with the BMM test. Furthermore, it offers a better assessment of the impact of a compound at the chromosomal level in a metabolically competent cell and can therefore be used for the evaluation of the genotoxic activity of compounds with complex metabolic pathways.

Aminobiphenyl Compounds↗
PubMed1993

Lack of predictivity of bone marrow micronucleus test versus testis micronucleus test: comparison with four carcinogens.

In vivo somatic chromosome mutation tests are usually carried out using the bone marrow micronucleus test in the mouse. This test is also considered predictive for the study of clastogenic effects in germ cells. However, it has been reported that the sensitivity of the bone marrow micronucleus test is insufficient to detect unstable compounds or short-lived metabolites and the use of target cells with metabolic activity (hepatocytes) has been questioned. In order to analyze in vivo micronucleus induction in cells with metabolic enzyme activity, we compared the sensitivity of somatic and germ cells to four carcinogens in the bone marrow and spermatid micronucleus test in the mouse. Three procarcinogens with a complex metabolic pattern (dimethylnitrosamine, diethylnitrosamine and 1,1-dimethylhydrazine) and one direct unstable mutagen (beta-propiolactone) were tested. All four carcinogens were not detected by the bone marrow micronucleus test but were detected in the mouse spermatid micronucleus test in which they induced clear clastogenic effects, as was the case in a previous study in liver micronucleus test. In conclusion, this study demonstrates that the bone marrow micronucleus test is not sufficient for the prediction of a clastogenic hazard in germ cells. In addition to a second in vivo test in an organ with metabolic enzymes, i.e., the liver, the spermatid micronucleus test can be performed when a specific risk to the testis is likely.

Animals↗
PubMed1984

A rapid method for the inactivation of virus infectivity prior to assay for interferons.

Virus infectivity in samples of culture medium or suspensions of animal tissue which are required for interferon assay can be rapidly and conveniently inactivated by overnight incubation with beta-propiolactone (BPL). As BPL hydrolyses spontaneously samples can be assayed with no further treatment. BPL does not affect the interfering activity of alpha, beta or gamma mouse interferons.

Animals↗
PubMed1990

Preparation of noninfectious hepatitis A virus hemagglutinin for detecting hemagglutination inhibition antibodies.

Hepatitis A virus (HAV) harvested from infected MRC-5 cells can hemagglutinate various species of erythrocytes at acid pH (Eckels et al., 1989). Further studies revealed that the majority of the hemagglutinin (HA) in MRC-5 and BS-C-1 cells was cell-associated. A simplified procedure for preparing HAV-HA consisted of collecting infected cells in phosphate-buffered saline followed by three cycles of freeze-thawing and sonication. The fluids were clarified and stored at 4 degrees C. The analysis of HA by rate-zonal sucrose gradient centrifugation indicated that the majority of HA co-migrated with infectious virus. Complete inactivation of infectious HAV with 0.03% beta-propiolactone (BPL) did not affect HA activity, while inactivation with 0.05% formalin caused a 16-fold reduction in titer. There was no difference in HAI antibody titers when BPL-treated HA was compared to untreated HA in the hemagglutination inhibition (HAI) test.

Animals↗
PubMed1982

Influenza virus: an NMR study of mechanisms involved in infection.

High resolution 1H-NMR spectroscopy has been used to study the infection of chicken embryo fibroblasts by influenza virus. Marked changes in the NMR spectrum occur when infectious influenza virus is introduced into the fibroblasts and these changes appear to depend upon the presence of active neuraminidase (EC 3.2.1.18). A crude preparation of neuraminidase from Vibrio cholerae is able to effect similar changes. Only minor spectral changes are observed in the absence of culture medium or when the viral genome material is inactivated by beta-propiolactone. Similarly, little change is seen in the NMR spectrum when amantadine, which is thought to inhibit uncoating of the virus inside the cell, or actinomycin D, which inhibits cellular nucleic acid metabolism, are incubated with fibroblasts prior to the addition of virus. The results suggest that neuraminidase, in co-operation with a factor in the infectious process, initiates a cellular event which can be monitored by NMR. The nature of this cellular mechanism is unknown, but further studies are under way to determine its importance in viral infection.

Amantadine↗
PubMedDate not supplied

Sensitivity of carcinogen-treated DNA to inactivation by ultraviolet radiation.

The DNA of bacteriophage SPO2c12 was treated with methylmethane sulfonate (MMS), beta-propiolactone (BPL), 2-anthramine (AA) or benzo[a]pyrene (BP) and then exposed to 254-nm radiation. Competent Bacillus subtilis host cells were transfected with DNA subjected to the carcinogen-UV treatment or with DNA treated with carcinogen only. Survival curves were obtained for loss of plaque-forming ability as a function of UV dose. The UV sensitivity of DNA treated with MMS, BPL or AA was not significantly different from that of untreated DNA. The results indicate that in competent B. subtilis the pathways for repair of alkylating agent damage and for repair of UV damage are probably different.

Bacillus subtilis↗
PubMed1987

Characterization of a double avirulent mutant of rabies virus and its potency as a vaccine, live or inactivated.

A strain bearing two mutations which abolish the virulence for adult animals after intracerebral or intramuscular inoculation has been constructed from the CVS strain of rabies virus. This apathogenic phenotype is stable after three successive passages of the double mutant in suckling mice brain. Trials of vaccination performed on mice in parallel with the double mutant and CVS both inactivated with beta-propiolactone indicate that the mutant is at least as efficient as CVS. This strain has also been found to be efficient as a live virus vaccine.

Animals↗
PubMed1991

Principles of selective inactivation of viral genome. VII. Some peculiarities in determination of viral suspension infectivity during inactivation by chemical agents.

When the infectivity of the influenza virus is determined by means of titration on chicken embryos, calculating the infection titre according to Reed and Muench, the course of inactivation with beta-propiolactone shows an anomaly - the fraction of infected embryos in a batch initially increases and then decreases as the degree of dilution of the virus-containing sample is increased. This anomaly occurs because a slight dilution lowers the agent concentration insufficiently so that inactivation goes on after the dilution of the sample before and/or after the inoculation of the solution into the embryo. The anomaly can be avoided either by neutralizing or removing the agent prior to titration or by starting titration from high dilutions.

Animals↗
PubMed1995

A multistep procedure for the chemical inactivation of human immunodeficiency virus for use as an experimental vaccine.

The kinetics of inactivation of four different strains of HIV-1 (RF, MN, SF2 and IIIB) by beta-propiolactone (BPL) and binary ethylenimine (BEI) were studied under various conditions. The conditions that would be required for the reduction of virus infectivity by at least 10(20) TCID50 ml-1 were estimated on the basis of the experimental rates of inactivation obtained. A multiple step procedure including treatment with 0.2% BPL, 0.05% sodium cholate, 10 mM BEI and 0.02% formaldehyde was designed to inactivate HIV-1 for use as an experimental vaccine. Complete inactivation of virus infectivity was confirmed by prolonged cell culture. The experimental vaccine preparation was analysed for the presence of HIV-1 proviral DNA utilizing the polymerase chain reaction. After treatment with both BPL and BEI proviral DNA was detected in one of four samples using primers encoding a 244 bp segment of the pol region of the viral genome. Proviral DNA could not be detected in any of the four samples using primers encoding segments of > 400 bp in the gag and reverse transcriptase region.

AIDS Vaccines↗