Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00249 (Mutagen)
 5,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal mouse sera contain naturally occurring antibodies that are cytotoxic in the presence of rabbit complement for NB1, a cell line derived from a neuroblastoma adrenal metastasis of a spontaneous ovarian teratoma. The anti-NB1 antibodies can be specifically removed from normal mouse sera by absorption of the sera with homogenized brain tissue of mouse, rat, guinea pig, chicken, and man and by homogenized kidney tissue of mouse and man. The antigen recognized by anti-NB1 naturally occurring autoantibodies, designated mouse brain antigen-2 (MBA-2), is not present on other normal tissues or tumor cell lines tested. MBA-2 is distinct from previously described mouse brain antigens.
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PMID:Interspecies brain antigen detected by naturally occurring mouse anti-brain autoantibody. 4 48

Commercially prepared antibody conjugates that are now available allow extensive application of direct immunofluorescence for diagnosing herpetic infections. Five of these conjugates--Microbiological Associates bivalent herpes antiserum (MBA-bivalent), MBA anti-herpes types 1 (MBA-1) and 2 (MBA-2), and Flow Laboratories anti-herpes types 1 (Flow-1) and 2 (Flow-2)--were compared for antibody titer, diagnostic accuracy, and nonspecific background staining on known infected tissue. Four of these were tested simultaneously on 75 clinical specimens. No attempt was made to differentiate between herpes simplex virus type 1 or type 2 infections. All antisera were comparable in titer and exhibited fluorescence with both herpes simplex virus types 1 and 2 antigens. The most significant difference was excessive nonspecific staining consistently seen with the MBA-2 conjugate. Overall, Flow-2 and MBA-bivalent antisera were preferable.
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PMID:Clinical evaluation of commercial conjugates for direct immunofluorescence of herpes simplex virus. 7 46

We have surveyed the clastogenic potential of 12 different groups of stains and dyes totalling 48 compounds. We observed that 18 compounds induced significant increase in chromosome damage. Most of them were also found to be mutagenic, carcinogenic, or toxic in other reported studies. However, no significant studies were reported on six of them. It is concluded that these agents are potentially harzardous and should be studied further in detail.
Environ Mutagen 1979
PMID:Studies on the clastogenic effects of biologic stains and dyes. 9 47

Mutagen-induced intergenic and interallelic recombination as well as forward mutation were studied in one and the same strain of S. cerevisiae. In nontoxic dose ranges, the induction of mutants and recombinants was parallel after treatment with ethyl methanesulfonate (EMS), methyl methanesulfonate (MMS), N-methyl-N'-nitro-M-nitrosoguanidine (MNNG), triethylene melamine (TEM), 4-nitroquinoline 1-oxide (4-NQO), sodium nitrite (NaNO2), and 1-fluoro-2,4-dinitrobenzene (2,4-DNFB). Acridine orange (AO) after treatment without light induced recombinants, but reduced the frequency of spontaneous mutations. In combination with TEM, AO exerted the same effect, i.e., reduced its mutagenic effect and enhanced its recombinogenic effect. 4,5,6-Trichloro-2-(2,4-dichlorophenoxy) phenol (Cl5-predioxin) induced mutants and intergenic recombinants, but specifically reduced the spontaneous frequency of interallelic recombinants. In combination with TEM, it enhanced its mutagenic and intergenic recombinogenic effects but reduced its interallelic recombinogenic effect. The main conclusions of the present study, that is 1. Essentially similar lesions can lead to different genetic consequences, and 2. Induction of mutation and recombination are jointly correlated, i.e., suppression of mutations leads to an enhancement of recombinations, while suppression of recombinations leads to an enhancement of mutations, are used to set up a speculative concept for mutation and recombination induction in the diploid yeast cell during mitosis.
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PMID:Evidence that induction and suppression of mutations and recombinations by chemical mutagens in S. cerevisiae during mitosis are jointly correlated. 10 36

Drosophila melanogaster males from a Basc stock were mutagenized with either X-rays, ethyl methanesulfonate (EMS), or nitrogen mustard (HN2). Groups of identically treated males were crossed to different types of female. Sex-linked recessive lethals were scored as a genetic end point. The females used were homozygous for X-chromosomal mutations (mus(1)101D1, mus(1)104D1, mei-9 or mei-41D5) which lead to defective DNA repair and which increase the mutagen sensitivity of larvae. Females from a white stock with normal DNA repair capacities served as controls. The premutational lesions induced in mature sperm are only processed after insemination by the maternal enzyme systems present in the oocytes. Differences in the efficiency of the processing of lesions can lead to maternal effects on the frequency of mutations recovered from mutagenized sperm. It was found that, with the exception of mus(1)104D1, all mutants analysed significantly modify the mutation fixation of one or more types of premutational lesions. The most drastic effect is found with the mus(1)101D1 stock in which HN2-induced DNA cross-links do not lead to sex-linked recessive lethals. It is assumed that mus(1)101D1 is defective in an early step of DNA cross-link repair. Our first set of data clearly demonstrates that the study of maternal effects in Drosophila is an efficient tool to analyse the in vivo function of repair mutations on chemically induced mutagenesis.
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PMID:Mutagen-sensitive mutants in Drosophila melanogaster: effects on premutational damage. 11 70

Drosophila melanogaster males were exposed to gaseous 1, 2-dibromoethane at concentrations lower than those used in aerosol treatments of suspected mutagens by other investigators. Premeiotic stages appear to be more sensitive than postmeiotic stages to gaseous mutagens. At an exposure of 125 ppm . hr, significant numbers of mutations were induced in spermatids, spermatocytes, and spermatogonia. Since this exposure increased the mutation rate in spermatogonial stages by a factor of 20--40 over the spontaneous rate, it appears that the lowest detectable exposures may be much lower than 125 ppm . hr for 1, 2-dibromoethane.
Environ Mutagen 1979
PMID:Sensitivity of Drosophila melanogaster to low concentrations of the gaseous 1, 2-dibromoethane: I. acute exposures. 12 76

Adult males of 20 different stocks of Drosophila melanogaster, including 16 with various X-linked mutagen-sensitive mutations, were tested for sensitivity to the lethal action of methyl methane sulfonate (MMS) in a continuous feeding experiment. It was impossible to establish a correlation between MMS-toxicity in adults and MMS-toxicity in larvae. In addition, experiments to examine the fertility of MMS-treated flies of four mutagen-sensitive strains and one wild-type strain were performed. These experiments demonstrated that the spermatogonia of mei-9L1 and mei-41D5 in larvae and in adults are more sensitive to MMS than the spermatogonia of the wild-type strain or the other two mutagen-sensitive strains.
Environ Mutagen 1979
PMID:Lack of correlation between MMS-toxicity in larvae and in adults of mutagen-sensitive mutants of Drosophila melanogaster. 12 77

Differences greater than 6,000-fold in the mutagenic potency of three nitrosamides that are methylating agents [N-methyl-N-nitrosourea (MNU), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-nitrosocarbaryl (NC)] could be accounted for in part by differences in their uptake into the Haemophilus influenzae cells. Uptake was roughly correlated with the octanol/water partition coefficient. The most potent mutagen, NC, was concentrated by the cells. The least potent, MNU, was essentially excluded from the bacteria. Uptake was a linear function of concentration, whereas induction of novobiocin-resistant mutations followed higher-order kinetics. The effective dose of chemical to the bacteria (number of molecules taken up) under conditions of mutagenesis could be calculated.
Environ Mutagen 1979
PMID:Mutagenicity of nitrosocarbaryl and other methylating nitrosamides as related to uptake in Haemophilus influenzae. 12 78

Drosophila melanogaster males were exposed to homogeneous magnetic fields of intensities of 13,000 to 37,000 Gauss as eggs, larvae, pupae and as adults. Sex linked recessive lethals were scored in chromosomes exposed as spermatozoa, spermatids and as spermatocytes. There was no indication of enhanced mutation induction by the magnetic fields.
Environ Mutagen 1979
PMID:Genetic effects of strong magnetic fields in Drosophila melanogaster: I. Homogeneous fields ranging from 13,000 to 37,000 Gauss. 12 79

Rats treated with di(2-chloroethyl)methylamine (HN2), N-methyl-N-nitrosourea (MNUA) and N-ethyl-N-nitrosourea (ENUA) excrete significantly larger amounts of deoxycytidine (dC) and thymidine in their urine 0-24 h after treatment. Ethyl methanesulphonate (EMS) and dimethylnitrosamine (DMN) gave negative results in this respect but all five alkylating agents increased the excretion of 1-methyl-nicotinamide (1-meNmd). In addition, a larger quantity of 7-methylguanine (7MG) and uric acid was excreted after DMN treatment. 1,4-Dimethanesulphonoxybutane (myleran), 2,2-dichlorovinyl dimethyl phosphate (dichlorvos), 5-fluorouracil (5FU), cytosine arabinoside (araC), 2-acetylaminofluorene (AAF) and 7-bromomethylbenz-[a]anthracene (7-BrMBA) gave negative results.
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PMID:Increased urinary excretion of nucleic acid and nicotinamide derivatives by rats after treatment with alkylating agents. 12 32


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