Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protease inhibitor was isolated and purified from pigeon pea Cajanus capan. By using gel filtration analysis the inhibitor was found to have an Mr of 18,200. It inhibits trypsin competitively with a specific inhibitor constant Ki of 1.53 x 10(-7) M. The purified inhibitor produced a marked reduction in aflatoxin B1-induced beta-galactosidase activity in Escherichia coli PQ37. This reduction is independent of whether the protease inhibitor was added to the reaction medium prior to or after aflatoxin B1 activation. The observed reduction may therefore be a result of the inhibitor's activity on the RecA protease produced in response to aflatoxin B1-induced DNA damage in the bacteria.
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PMID:Isolation and partial characterization of pigeon pea protease inhibitor: its effect on the genotoxic action of aflatoxin B1. 157 83

A simple and sensitive procedure for the determination of cytochrome P-450 (P-450)-mediated activation of chemical procarcinogens and promutagens to DNA-damaging products has been developed using a method measuring the expression of the umu gene in Salmonella typhimurium TA1535/pSK1002, which is based upon the initial procedures as described by Oda et al. [Mutation Res. 147, 219 (1985)]. The chemicals examined were a variety of potent carcinogenic and mutagenic compounds including heterocyclic aromatic amines, aromatic amines, polycyclic aromatic hydrocarbons and aflatoxin B1. These chemicals were incubated with rat liver microsomes or a reconstituted monooxygenase system containing three forms of purified P-450 in the presence of a bacterial tester strain, and the induced-umu gene expression was determined by measuring the beta-galactosidase activity produced by fusion gene in the cells. The activity was increased linearly for at least 2 hr with an initial lag time of 30 min and was dependent on the concentrations of P-450 in the reaction mixture. Thus, the metabolic activation of these compounds by P-450 could be compared on a basis of the specific beta-galactosidase activity/min/nmol P-450. Among three forms of P-450, two isozymes induced by 3-methylcholanthrene were found to be more active in catalyzing the metabolic activation of most of the chemicals examined than a form of P-450 which is induced by phenobarbital. Data also showed that a high spin form of P-450 isolated from 3-methylcholanthrene-treated rats had a profound role in the activation of procarcinogens and promutagens. This conclusion was based on the results of catalytic activities by three forms of P-450 in a reconstituted monooxygenase system, and on the effects of specific antibodies against these P-450s on the reactions catalyzed by liver microsomes.
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PMID:Cytochrome P-450-mediated activation of procarcinogens and promutagens to DNA-damaging products by measuring expression of umu gene in Salmonella typhimurium TA1535/pSK1002. 329 69

The umu test system is a newly developed method to evaluate genotoxic activities of a wide variety of environmental carcinogens and mutagens (Oda et al., 1985). In the present study, we further examined the abilities of 151 chemicals to induce umu gene expression in Salmonella typhimurium TA1535/pSK1002. Among the chemicals examined, 72 compounds induced umu gene expression, which could be defined on a basis of increased beta-galactosidase activity by 2-fold over the background level. The potent genotoxic compounds without metabolic activation were adriamycin, bleomycin, daunorubicin, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene, N-ethyl-N'-nitro-N-nitrosoguanidine, furylfuramide, methyl methanesulfonate, N-methyl-N'-nitro-N-nitrosoguanidine, mitomycin C, 1-nitropyrene and 4-nitroquino-line-1-oxide. In the presence of S9, aflatoxin B1, 2-aminoanthracene, Glu-P-1, IQ, MeIQ, MeIQx, Trp-P-1 and Trp-P-2 also induced umu gene expression markedly. Several chemicals such as 2-acetylaminofluorene, 9-aminoacridine, azobenzene, benzanthracene, benzidine, diethyl nitrosamine, 1-nitronaphthalene, paraquat, potassium dichromate and sodium nitrite were weakly genotoxic and the induction by these compounds could be detected only when the incubation time was prolonged from 2 h to 5 h. Data are also presented that some of the chemicals such as dimethyl sulfoxide, m-dioxan, 5-fluorouracil and paraquat, which have been reported to be non-mutagenic in Ames/Salmonella assay, were found to be active in inducing umu gene expression, while the known mutagenic compounds including acrylonitrile, 4,4'-dinitrobiphenyl, furfural, methylene chloride, 1-naphthylamine, sodium azide, o-tolidine and o-toluidine were non-genotoxic in the present assay system.
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PMID:SOS-inducing activity of chemical carcinogens and mutagens in Salmonella typhimurium TA1535/pSK1002: examination with 151 chemicals. 331 33

The genotoxic activity of 11 mycotoxins was investigated in Escherichia coli K 12. The induction of the SOS function sfi A whose level of expression is monitored by means of a sfi A::lac Z operon fusion was assayed by measuring the beta-galactosidase activity in the PQ 37 strain. Most of these fungal metabolites did not induce SOS response in this bacterial test. Only aflatoxicol, a reduced metabolite of aflatoxin B1 was well detected as an SOS inducer if metabolic activation was performed. Patulin, penicillic acid and viomellein are only weak inducing agents. The other fungal compounds tested failed to demonstrate a positive SOS inducing activity. Relationship between SOS chromotest, mutagenicity to Salmonella typhimurium and in vivo carcinogenicity was discussed.
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PMID:Genotoxic activity of some mycotoxins using the SOS chromotest. 331 61

Comparison between about 80 strains of Aspergillus flavus, belonging to the series flavus and oryzae, obtained from international collections but also isolated from French or African substrates revealed the following observations: 1. Cultural and morphological characteristics of toxicogenic and atoxicogenic strains of A. flavus are similar. However, the former produce a diffusible yellow pigment in 83% of isolates. 2. The two groups of conidiospores have the same resistance to UV irradiation (254 nm, 5 and 10 min). All the strains are equally sensitive to 4 antifungal antibiotics: nystatine, ketoconazole, clotrimazole and amphotericine. 3. A difference was seen in the capacity to produce enzymes as alpha-galactosidase, beta-galactosidase and beta-glucosidase, implicated in the glucid metabolism. The specific hydrolytic activity has been confirmed by the characterization of a large amount of beta-galactosidase and by a diauxic growth on glucose medium supplemented by lactose. Possible relationship between these characters and aflatoxin B1 production by A. flavus strains is discussed.
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PMID:[Morphological characteristics and physiological properties of aflatoxin B1 producing and non-producing Aspergillus flavus strains]. 393 61

A new method for the detection and quantitation of aflatoxin B1 in liquids is described. The method is based on the SOS Chromotest, in which damage caused by aflatoxin B1 to the DNA of suitably engineered E. coli induces beta-galactosidase. Aflatoxin B1 developing in orange juice inoculated with spores of Aspergillus parasiticus is detectable equally well by TLC as by the SOS-Chromotest.
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PMID:Detection and quantitation of aflatoxin B1 in orange juice by SOS-Chromotest. 393 7

The effects of repeated intraperitoneal administration of aflatoxin B1 on the peripheral and central nervous systems of rats were investigated. Biochemical markers of neurotoxicity were monitored in nervous tissues following aflatoxin B1 dosage and after the cessation of aflatoxin B1 administration. Aflatoxin B1 increased the activities of beta-glucuronidase and beta-galactosidase in the central and peripheral nervous systems. Repeated exposure of rats to aflatoxin B1 also activated Na+ K+-ATPase and inhibited Mg2+-ATPase. Nervous tissue levels of DNA and total protein increased while the concentrations of RNA and phospholipid were depressed by aflatoxin B1. The alterations in these parameters were specific for each of the tissues examined during the recovery of the rats. The findings indicate that the repeated administration of aflatoxin B1 to rats results in degeneration in the central and peripheral nervous systems that may be related to the overt toxicity observed following aflatoxin administration.
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PMID:The neurotoxicity of aflatoxin B1 in the rat. 613 86

The methodology for the production of monoclonal antibodies to chemical carcinogen-modified DNA has been improved to provide high yields of hybridomas, using guanine-imidazole ring-opened aflatoxin B1-modified DNA as an example (iro-AFB1 DNA). The percentage of immunised mice which responded to iro-AFB1 DNA-protein immunisation and the number of specific hybridomas produced was dependent on the level of modification of DNA. One in three BALB/c mice had detectable (but low) antibody titre when 0.3% modified iro-AFB1 DNA was used and this yielded 2 specific hybridomas, whereas all mice responded at reasonable titres and 6 specific hybridomas were obtained when 3% modified iro-AFB1 DNA was used. Other factors found to improve the number and titre of mice responding to immunisation and the yield of hybridomas were: KLH greater than BSA as carrier protein, C57 BL/6 X BALB/c F1 greater than BALB/c mice for antibody production, fusion success and ascites growth. The conditions limiting the sensitivity and reproducibility of an enzyme-linked immunosorbent assay (ELISA) using these monoclonal antibodies with beta-galactosidase-linked sheep F(ab')2 anti-mouse IgG as the second antibody were also tested. Present experience with AFB1 and other carcinogens indicates that these methods should be applicable to the production of monoclonal antibodies to DNA modified by a wide variety of chemical carcinogens.
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PMID:Improved conditions for the production of monoclonal antibodies to carcinogen-modified DNA, for use in enzyme-linked immunosorbent assays (ELISA). 640 64

The induction of the gene RNR3 was investigated in yeast Saccharomyces cerevisiae using RNR31 lacZ fusion. Gene induction was monitored by measuring beta-galactosidase activity. Various drugs that cause DNA damage effectively induced RNR3 expression; alkylating agents (cisplatin, mitomycin C and N-methyl-N'-nitro-N-nitrosoguanidine), a radical producer (bleomycin), and an intercalator (actinomycin D) induced RNR3. When yeast expressing rat CYP1A1 was exposed to 2-aminofluorene, a concentration-dependent induction of RNR3 was observed. Aflatoxin B1 also induced the expression of RNR3 in the same yeast strain concomitant with inhibition of cell growth. In control yeast, no induction of RNR3 was observed upon exposure to 2-aminofluorene or aflatoxin B1. Exposure to 2-acetylaminofluorene or benzo[a]pyrene did not lead to induction of RNR3 in yeast expressing CYP1A1. These results indicate that DNA damage by chemicals related to carcinogenesis induces RNR3, and that activation of these procarcinogens was required for DNA damage-dependent induction of RNR3.
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PMID:Induction in the gene RNR3 in Saccharomyces cerevisiae upon exposure to different agents related to carcinogenesis. 750 73

We studied the antimutagenic effects of urine on the SOS-inducing activity of mutagenic substances by using a novel test system (umu-test) for detecting DNA damaging agents, which uses a new tester strain (Salmonella typhimurium TA1535/pSK1002). The SOS-inducing activity of chemicals was detected in terms of the level of umu operon expression by measuring beta-galactosidase activity. We first examined the effects of various amounts of urine on SOS responses caused by mitomycin C (MMC). As a result, the urine suppressed beta-galactosidase activity of MMC dose-dependently. A urine concentration of 50 microliters/ml in the medium also suppressed 89.9% of SOS response induced by 0.1 microgram/ml of PEP, 75.6% of that induced by 0.02 microgram/ml of AF2 and 60.9% of that induced by 0.1 microgram/ml of AFB1. In addition, a urine concentration of 50 microliters/ml in the medium also suppressed 85.6% of SOS response by 5 J/m2 of UV irradiation. The observed suppression seemed to be directly related to the SOS responses at a cellular level, rather than to interaction between urine and mutagens, because the urine suppressed SOS responses induced not only by various mutagens but also by UV irradiation. These results suggest that urine works as a strong antimutagen against UV and chemical substances.
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PMID:Suppressive effects of urine on the SOS responses induced by UV and chemical mutagens. 801 82


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