Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased use of the biocidal compound tri-n-butyltin (TBT) in antifouling paints has prompted research aimed at determining the mechanism for TBT toxicity. Past investigations indicate that the primary cellular target for TBT is the cell membrane. Erythrocyte suspensions treated with TBT concentrations 2 greater than or equal to 5 microM undergo hemolysis described by a sigmoidal kinetic pattern. Transformation of cell shape from discocyte to echinocyte occurs at TBT concentrations greater than or equal to 0.1 microM, indicating that the compound enters the outer membrane bilayer. TBT at concentrations greater than or equal to 10 microM forms electron-dense aggregates that are intercalated within plasma membranes as viewed in ultrathin sections by transmission electron microscopy. Qualitative X-ray microanalysis of these aggregates confirms the presence of tin. The size of these structures can be modified by either 10 mM cyanide or 2,3-dimercaptopropanol (British Anti-Lewisite, BAL). Adding 10 mM cyanide to hemolytic TBT concentrations resulted in a synergistic stimulation of hemolysis attributable to high cyanide anion concentrations in or near the cell membrane. The elevated cyanide anion levels are thought to contribute to membrane lysis. The lipophilic dimercapto compounds BAL, dithiothreitol, and 2,3-dimercaptosuccinate are effective inhibitors of TBT-induced lysis. Water-soluble 2,3-dimercapto-1-propane sulfonate, a BAL analog, was largely ineffective as an inhibitor. The detailed molecular mechanism for TBT-induced membrane lysis is not yet clear. Cellular ATP depletion could be induced by TBT as well as by delipidation of anionic phospholipids or even formation of tributylstannylperoxy radicals, resulting in lipid peroxidation.
Toxicology 1987 Dec 01
PMID:tri-n-Butyltin: a membrane toxicant. 282 77

Condensation of the Grignard reagent derive from 2-[4-(allyloxy)phenyl]ethyl bromide (4b) with 7 alpha-acetyl-6,14-endo-ethenotetrahydrothebaine (5) furnished the (R) tertiary carbinol, 7, which upon methoxymercuration followed by treatment with the KBr gave the bromomercurio compound 10 (Hybromet). The corresponding N-cyclopropylmethyl analogue, 11, was prepared also. The bromomercurio compound, 1, and the mercaptobenzothiazole derivative, 3, gave allyl phenyl ether when treated with BAL at room temperature. Similar treatment of 10 with BAL gave 7 in high yield. Binding studies using rat brain homogenates indicated that 7, 13, and 14 have moderately high affinities for mu rather than delta binding sites. Although much weaker, 10 showed preferential mu binding also. These results along with the fact that 10 reacted smoothly with sulfhydryl groups suggest that Hybromet would be a suitable ligand for use in affinity chromatography.
J Med Chem 1985 Dec
PMID:Hybromet: a ligand for purifying opioid receptors. 299 8

The germ-line micronuclear genome of the ciliate Tetrahymena thermophila contains approximately 10(2) chromosome-internal blocks of tandemly repeated C4A2 sequences (mic C4A2). This repeated sequence is the telomeric sequence in the somatic macronucleus. Each of six cloned micC4A2 was found to be adjacent to a conserved 30 bp sequence, which we propose is the terminal inverted repeat of a family of DNA elements (the Tel-1 family). This 30 bp sequence contains a site for the infrequently cutting restriction enzyme Bst XI, which allows full-length Tel-1 elements to be cut out of the micronuclear genome. BAL 31 exonuclease digestion of Bst XI-cut micronuclear DNA showed the majority of micC4A2 blocks to be associated with the ends of the Tel-1 family. We propose that Tel-1 elements are transposable and suggest a novel mechanism to account for the origin of micC4A2, in which telomeric repeats are added to the ends of free linear forms of the transposable elements prior to reintegration.
Cell 1985 Dec
PMID:The internally located telomeric sequences in the germ-line chromosomes of Tetrahymena are at the ends of transposon-like elements. 300 Jun 13

A functional bacteriophage T4 dam+ gene, which specifies a DNA [adenine-N6]methyltransferase (Dam), was cloned on a 1.8-kb HindIII fragment [Schlagman and Hattman, Gene 22 (1983) 139-156]. Sequence analysis [Macdonald and Mosig, EMBO J. 3 (1984) 2863-2871] revealed two overlapping in-phase open reading frames (ORFs). The 5' proximal ORF initiates translation at an AUG and encodes a 30-kDa polypeptide, whereas the downstream ORF initiates translation at a GUG and encodes a 26-kDa polypeptide. Analysis of BAL 31 deletions in our original dam+ clone has verified that at least one of these overlapping ORFs, in fact, encodes T4 Dam. To investigate where T4 Dam translation is initiated, we have constructed plasmids in which a tac or lambda PL promoter is placed 5' to either the longer ORF or just the shorter ORF. Only clones which contain a promoter in front of the longer ORF produce active T4 Dam. This indicates that the 26-kDa polypeptide alone cannot be T4 Dam. Additional experiments suggest that only the 30-kDa polypeptide is required for enzyme activity and that the shorter ORF is not translated in plasmid-carrying cells. We also present evidence that T4 Dam is capable of methylating 5'-GATC-3', GATm5C, and GAThmC sequences; non-canonical sites (e.g., GACC) are also methylated, but much less efficiently.
Gene 1988 Dec 20
PMID:The DNA [adenine-N6]methyltransferase (Dam) of bacteriophage T4. 307 68

To further study the role of arachidonic acid metabolites in the development of hyperoxic lung injury and the function of PMNs and/or alveolar macrophages in facilitating this role, we exposed adult rabbits to greater than 95% O2 or air for 24, 40, 48, or 65 hours. At the end of each study, bronchoalveolar lavage [BAL] of the left lung was performed, and the right lung was inflated and fixed for light and electron microscopy. PGE2, 6-keto-PGF1 alpha and thromboxane B2 were measured by RIA in arterial and venous plasma at the beginning and end of each study and in BAL fluid obtained at sacrifice. Production of these three PGs by BAL cells placed in cell culture was also measured. Significant hyperoxic lung injury did not develop until 65 hours, as evidenced by significant increase in BAL total protein and percent PMNs, and by morphologic findings. At 40 hours, however, BAL fluid PGE2 and 6-keto-PGF1 alpha increased and BAL cell production of all 3 PGs was significantly increased (p less than .05). In summary, the early PG increases observed in these studies may directly contribute to the development of hyperoxic lung injury or, rather, may be representative of a generalized increase in all arachidonic acid metabolites, including the lipoxygenase pathway. The increase in BAL cell PG production and increased PG concentrations in BAL fluid prior to any increase in BAL PMNs suggest that the AM may be the source of the early arachidonic acid metabolite increase in response to hyperoxia.
Prostaglandins Leukot Med 1986 Dec
PMID:The early involvement of pulmonary prostaglandins in hyperoxic lung injury. 310 36

Some genetic and biochemical properties of the tetracycline resistance element of the Staphylococcus aureus plasmid pT181 have been studied. Resequencing of a portion of the tetracycline resistance gene (tet) showed the presence of a single open reading frame of 1,299 nucleotides capable of encoding a polypeptide of 433 amino acids. Analysis of BAL 31 nuclease-generated deletion mutants of the tet gene showed the presence of two complementation groups within this region. Northern blot hybridizations demonstrated that the tet gene encodes a single mRNA, and its initiation site has been mapped by S1 nuclease protection experiments. We also identified an approximately 52,000-dalton tetracycline-inducible polypeptide in Bacillus subtilis minicells carrying pT181. Induction of the tet gene by tetracycline resulted in a 4-fold increase in the levels of TET mRNA and at least a 15-fold increase in the amount of TET protein in B. subtilis minicells.
J Bacteriol 1988 Dec
PMID:Characterization of the tetracycline resistance gene of plasmid pT181 of Staphylococcus aureus. 314 48

The relative abilities of approximately 20 chelating agents to act as antagonists for acute and chronic lead poisoning have been examined in the mouse. The acute LD50 for lead acetate trihydrate was determined and found to be 135.3 mg Pb/kg for i.p. injection with a 95% confidence interval of 87.1-210.3 mg Pb/kg. The relative efficacy of chelating agents to reduce liver, kidney, spleen, bone and brain levels of lead was determined. The movement of lead from the liver to the bone was followed during the first 7 days post injection and was found to result in appreciable changes in the lead levels of these organs from day to day during this entire period. Of the compounds examined, the ones which were most effective in mobilizing lead under various conditions included meso-2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercaptopropane-1-sulfonate (DPMS), disodium calcium ethylene-diaminetetraacetate (Na2CaEDTA), trisodium zinc triethylenetetraminehexa-acetate, dicalcium ethylenediaminetetra(methylenephosphonate) (Ca2EDTPO) and diethyl dimercaptosuccinate (DEMSA) and 2,3-dimercapto-1-propanol (BAL).
Toxicology 1988 Dec 30
PMID:Comparative mobilization of lead by chelating agents. 321 88

We monitored arterial oxygen saturation (StcO2) continuously using the OHMEDA Biox 3700 oximeter. We studied seven patients undergoing a 100 ml bronchoalveolar lavage (BAL-100), seven patients undergoing a 200 ml bronchoalveolar lavage (BAL-200), and seven patients during diagnostic fibreoptic bronchoscopy alone. Immediately following insertion of the bronchoscope a brief increase in StcO2 level (0.3-0.5%) was seen, followed by a gradual decline, never exceeding 2-5% during the diagnostic bronchoscopy. Introduction of lavage fluid into a segmental bronchus always produced a further decline in StcO2. In the BAL-100 group the fall did not exceed 7%, whereas in the BAL-200 group a fall of up to 15% from the baseline level was observed. Return to initial values was seen in most of the patients within 10 min following completion of the procedure. Only in those patients with the most profound StcO2 fall was this period increased, up to 30 min.
Eur Respir J 1988 Dec
PMID:Effect of different volumes of BAL fluid on arterial oxygen saturation. 322 90

Macrolide antibiotics are concentrated by phagocytic cells in vitro. We studied the in-vivo uptake of josamycin by alveolar macrophages recovered by broncho alveolar lavage performed in patients 3 h after ingestion of 1 g of the drug. Simultaneous determination of the antibiotic levels was performed on the BAL supernatant and the serum and the results compared to those obtained by incubating alveolar macrophages and blood polymorphonuclears at 2 and 8 mg/l. Josamycin concentration was measured using a high pressure liquid chromatography method. Results show that intracellular josamycin levels in vivo are similar to those observed in vitro. Accumulation of the drug also occurs in BAL fluid (reaching about a 100-fold the serum concentration). Pulmonary and serum levels are significantly correlated.
J Antimicrob Chemother 1988 Dec
PMID:Josamycin pulmonary penetration determined by broncho-alveolar lavage in man. 324 40

When garlic (Allium sativum) was administered to rat per os simultaneously with cadmium, methylmercury and phenylmercury to detect the protective effect against the heavy metal poisoning, accumulation of heavy metals in liver, kidneys, bone and testes were decreased, and histopathological damages and the inhibition of serum alkaline phosphatase activities by heavy metals were reduced. Such effect of garlic was not shown in the 1.7% garlic treated group and most remarkable in the 6.7% garlic treated group. The protective effect of garlic was superior to those of 2,3 dimercapto-1-propanol (BAL) and D-penicillamine (PEN), and nearly similar to those of 2,3-dimercaptosuccinic acid (DMSA) and N-acetyl-DL-penicillamine (APEN), the current remedies, while garlic was not effective as a curative agent for heavy metal poisoning. The excretion of cadmium was enhanced, more through feces than urine by garlic but the effect to the urinary excretion of cadmium was not significant comparing with DMSA or APEN when cadmium was ip injected in the first 3 days during the 12 days of oral administration of DMSA, APEN or garlic.
J Korean Med Sci 1987 Dec
PMID:A study on the effect of garlic to the heavy metal poisoning of rat. 326 78


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