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)

Fluoranthene, a non-carcinogenic polycyclic aromatic hydrocarbon, inactivates Escherichia coli cells in the presence of near-ultraviolet light (NUV; 300-400 nm). E coli cells carrying defects in the uvrA6 or katF genes are sensitized to inactivation by the simultaneous treatment with fluoranthene and NUV, suggesting that DNA is a target and that hydrogen peroxide is generated. Haemophilus influenzae transforming DNA can be inactivated by the simultaneous treatment with fluoranthene and NUV confirming DNA as a target. Using the photooxidation of imidazole and histidine as probes, fluoranthene was found to generate singlet oxygen in organic and aqueous media. In water, it participated in electron transfer reactions, reducing nitro blue tetrazolium as well as ferricytochrome C. This reduction took place both in the presence of air, where superoxide anion was formed, and under argon. Simultaneous treatment with fluoranthene and NUV was incapable of inducing histidine-independent mutations. Simultaneous treatment with fluoranthene and NUV was incapable of inducing the uvrA gene product as evidenced by the absence of the induction of beta-galactosidase in an E coli operon fusion strain [uvrA215::Mud(Ap,lac)].
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PMID:Phototoxic effects of fluoranthene, a polycyclic aromatic hydrocarbon, on bacterial species. 282 96

Mu dX phage was used to isolate three gene fusions to the lacZ gene (soi::lacZ; soi for superoxide radical inducible) that were induced by treatment with superoxide radical anion generators such as paraquat and plumbagin. The induction of beta-galactosidase in these fusion strains with the superoxide radical generating agents required aerobic metabolism. Hyperoxygenation (i.e., bubbling of cultures with oxygen gas) also induced the fusions. On the other hand, hydrogen peroxide did not induce the fusions at concentrations that are known to invoke an adaptive response. Introduction of oxyR, htpR, or recA mutations did not affect the induction. Two of the fusion strains exhibited increased sensitivity to paraquat but not to hydrogen peroxide. The third fusion strain showed no increased sensitivity to either agent. All three fusions were located in the 45- to 61-min region of the Escherichia coli chromosome.
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PMID:Isolation of gene fusions (soi::lacZ) inducible by oxidative stress in Escherichia coli. 283 46

Escherichia coli produces two distinct species of catalase, hydroperoxidases I and II, which differ in kinetic properties and regulation. To further examine catalase regulation, a lacZ fusion was placed into one of the genes that is involved in catalase synthesis. Transductional mapping revealed the fusion to be either allelic with or very close to katE, a locus which together with katF controls the synthesis of the aerobically inducible hydroperoxidase (hydroperoxidase II). katE was expressed under anaerobic conditions at levels that were approximately one-fourth of those found in aerobically grown cells and was found to be induced to higher levels in early-stationary-phase cells relative to levels of exponentially growing cells under both anaerobic and aerobic conditions. katE was fully expressed in air and was not further induced when the growth medium was sparged with 100% oxygen. Expression of katE was unaffected by the addition of hydrogen peroxide or by the presence of additional lesions in oxyR or sodA, indicating that it is not part of the oxyR regulon. When katF::Tn10 was introduced into a katE::lacZ strain, beta-galactosidase synthesis was largely eliminated and was no longer inducible, suggesting that katF is a positive regulator of katE expression.
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PMID:Transcriptional regulation of katE in Escherichia coli K-12. 304 91

The Mu dl (ApR lac) bacteriophage was used to generate mutants of Escherichia coli which were defective in formate hydrogenlyase. Three mutants were chosen for further analysis: they lacked hydrogenase (hydrogen: benzyl viologen oxidoreductase) activity, but produced normal levels of fumarate reductase activity and two- to three-fold reduced levels of benzyl viologen (BV)-dependent formate dehydrogenase activity. Two of them (hydC) were shown to contain about 4-fold reduced amounts of formate hydrogenlyase and fumarate-dependent H2 uptake activities. The third one (hydD) was totally devoid of both activities. Their insertion sites were located at 77 min on the E. coli map. Subdivision of these mutants into two classes was subsequently based on the restoration capacity of hydrogenase activity with high concentration of nickel in the growth media. Addition of 500 microM NiCl2 led to a complete recovery of hydrogenase activity, and to the concomitant restoration of normal BV-linked formate dehydrogenase, formate hydrogenlyase and fumarate-dependent H2 uptake activities in the hydC mutants. The hydD mutant was insensitive to the effect of nickel. Expression of the lac operon in hydC and hydD mutants was induced by anaerobiosis. It was not increased by the addition of formate under anaerobic conditions. The presence of nitrate resulted in slightly reduced beta-galactosidase activities in the hydC mutants, whereas those found in the hydD mutant reached only one third of the level obtained in its absence. Fumarate had no effect on both classes. Moreover, in contrast to the hydD locus, the hydC::Mu dl fusions were found to be dependent upon the positive control exerted by the nirR gene product and were totally repressed by an excess of nickel. In addition, the low levels of overall hydrogenase-dependent activities found in a nirR strain were also relieved by the presence of nickel. Our results strongly suggest that the pleiotropic regulatory gene nirR is essential for the expression of a gene (hydC) involved in either transport or processing of nickel in the cell, whose alteration leads to a loss of hydrogenase activity.
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PMID:Genetic and physiological characterization of new Escherichia coli mutants impaired in hydrogenase activity. 308 8

Enhanced digestion of yogurt by lactose-intolerant individuals is believed to be due to inherent beta-galactosidase (lactase) in the culture organisms that aids in the hydrolysis of ingested lactose. However, sweet acidophilus milk, which contains lactase-rich organisms, does not enhance lactose digestion. Using breath-hydrogen measurements to indicate malabsorption in 14 human subjects, we compared utilization of: milk, yogurt, heated yogurt, yogurt plus lactose, heated yogurt plus lactase, sweet acidophilus milk (SAM), and SAM made with sonicated cells. Results indicate that both the reduction of lactose during fermentation and the presence of indigenous bacterial lactase are responsible for the increased ability to tolerate lactose in yogurt. Improved utilization of SAM by sonication suggests that intracellular lactase is not available during digestion and that sonication releases the lactase activity from the cells.
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PMID:Modification of sweet acidophilus milk to improve utilization by lactose-intolerant persons. 310 15

We examined the efficiency of two beta-galactosidase preparations--one derived from the yeast, Kluyveromyces lactis (Lactaid), the other derived from the fungus, Aspergillus oryzae (Takamine)--to assist the in vivo digestion of lactose consumed by healthy Guatemalan preschool children. Milk prehydrolyzed by in vitro incubation with enzymes was used as the standard of reference, and the degree of incomplete digestion of lactose from 240 mL of milk was determined using the hydrogen breath test. In in vivo dose-response studies, both 3,250 neutral lactose units of Lactaid and 6,635 food and chemical codex lactose units of Takamine completely eliminated excess H2 excretion in a small sample of lactose-maldigesting subjects. When evaluated in a controlled, clinical trial setting, the same dose of Lactaid added directly to the milk at consumption produced an 82% relative reduction in H2 excretion, whereas Takamine was equally as effective as the prehydrolyzed milk. Thus, intraluminal conditions and gastrointestinal transit in the preschool child support the effective assisted digestion of milk lactose in an efficient manner and with the same enzyme to milk ratios as observed previously in adults.
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PMID:Effective reduction of lactose maldigestion in preschool children by direct addition of beta-galactosidases to milk at mealtime. 310 27

Lactose digestion from and tolerance to flavored and frozen yogurts, ice cream, and ice milk were evaluated (20 g lactose/meal) in lactase-deficient subjects by use of breath hydrogen techniques. Unflavored yogurt caused significantly less hydrogen production than milk (37 vs 185 delta ppm X h, n = 9). Flavored yogurt was intermediate (77 delta ppm X h). Subjects were free of symptoms after consuming flavored and unflavored yogurts. Of seven commercial yogurts tested, all contained significant levels of microbial beta-galactosidase (beta-gal). In addition, eight subjects were fed meals of milk, ice milk, ice cream, and frozen yogurts with and without cultures containing high levels of beta-gal. Peak hydrogen excretion after consumption of frozen yogurt with high beta-gal was less than one-half of that observed after the other five test meals and intolerance symptoms were absent. Tolerance to frozen yogurt, produced under usual commercial procedures, was found to be similar to that of ice milk and ice cream.
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PMID:Lactose digestion from flavored and frozen yogurts, ice milk, and ice cream by lactase-deficient persons. 311 36

Alveolar macrophages from patients with active pulmonary sarcoidosis have been shown to secrete several factors, such as interleukin-1 and alveolar macrophage-derived growth factor. We examined alveolar macrophages from nonsmoking patients with sarcoidosis undergoing bronchoalveolar lavage (BAL) for evaluation of disease activity. We compared these cells with macrophages from smoking and nonsmoking control patients. The amount of hydrogen peroxide released by the macrophages either spontaneously or after stimulation by phorbol myristate acetate was measured. The alveolar macrophages from smokers spontaneously released hydrogen peroxide, as we previously observed. The macrophages from the patients with sarcoidosis also released detectable amounts of hydrogen peroxide, but the macrophages from the non-smokers did not. Alveolar macrophages from all three groups released hydrogen peroxide when stimulated with phorbol myristate acetate. The macrophages from all three groups were examined for the presence on the surface membrane of beta-galactosidase, an enzyme that appears on the surface of older, activated macrophages. The macrophages in the BAL fluid of the patients with sarcoidosis had less beta-galactosidase staining than did those from the smokers, although they released comparable amounts of hydrogen peroxide. These findings suggest that alveolar macrophages in the BAL fluid of patients with sarcoidosis are younger, more monocyte-like, and activated by various factors, including gamma-interferon.
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PMID:Spontaneous hydrogen peroxide release from alveolar macrophages of patients with active sarcoidosis: comparison with cigarette smokers. 312 8

A gene coding for a Bowman-Birk-type proteinase inhibitor was synthesized chemically, cloned and expressed in Escherichia coli as a fusion protein with a beta-galactosidase fragment. The corresponding mutant inhibitor, carrying a P1 = Arg16 instead of Lys and an Ile27 instead of Met was obtained after cyanogen bromide cleavage, refolding and affinity chromatography on trypsin-Sepharose. Dissociation constants of complexes with trypsin of this mutant and wild-type Bowman-Birk inhibitor are identical within experimental error. This is explained by differential patterns of hydrogen bonds between side-chains of Arg or Lys in proteinase inhibitors and the primary specificity pocket of trypsin.
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PMID:Chemical synthesis, molecular cloning and expression of gene coding for a Bowman-Birk-type proteinase inhibitor. 329 96

The gene pheV from Escherichia coli, coding for tRNAPhe and carried on a plasmid, has been mutagenised with hydroxylamine. Mutants in the structural gene have been identified using two criteria: (i) de-attenuation of beta-galactosidase expression, while under the control of the attenuator region of the pheS,T operon by means of an operon fusion; (ii) loss of ability to complement thermosensitivity of a mutant Phe-tRNA synthetase. Mutants showing de-attenuation were sequenced and two nucleotide changes identified: G44----A44 (found five times) and m7G46----A46 (found once). Sequencing of mutants that lost complementation identified two further tRNA mutants, C2---U2 and G15----A15; the mutant m7G46----A46 was also re-isolated by this criterion. Three of the mutants involve bases implicated in tertiary rather than secondary structure hydrogen bonding. One hypothesis for the mechanism of de-attenuation is that mutant tRNAPhe molecules compete with the wild-type tRNAPhe on the ribosome but are inefficient at some step in the elongation process.
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PMID:Functional mutants of phenylalanine transfer RNA from Escherichia coli. 389 9


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