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)

Infection of Pseudomonas BAL-31 with the lipid-containing bacteriophage PM2 resulted in no detectable change in the rate of phosphatidylglycerol (PG) or phosphatidylethanolamine (PE) biosynthesis. An increase in the PG content of infected cultures was not seen until the cultures began to lyse, and this increase was in fact only a relative increase resulting from the extensive turnover of PE at the onset of culture lysis. Turnover studies revealed that the glycerol, phosphorus fatty acid, and ethanolamine moieties of PE turned over simultaneously at the time of lysis, and therefore made it unlikely that there was a PE to PG conversion during the latent period of the phage. The lipid found in the bacteriophage did not reflect a preferential selection for lipid synthesized before or after infection, but in fact reflected the composition of the host membrane at the time the phage were assembled. The use of a modified medium that allowed the cultivation of Pseudomonas BAL-31 as a prototroph and resulted in reliable lysis times of infected cultures led us to the conclusion that PM2 infection effects little change in host phospholipid metabolism, and that there is sufficient PG in the host cytoplasmic membrane to account for a full burst of phage. As a result of the reliable lysis times that we have achieved, we concluded that certain metabolic events, i.e., PE turnover, are lytic phenomena and must not be confused with events relevant to the biosynthesis and maturation of the phage.
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PMID:Phospholipid metabolism in Pseudomonas BAL-31 infected with lipid-containing bacteriophage PM2. 95 79

Qualitative and quantitative analysis was performed on phospholipids isolated from bronchoalveolar lavage fluid during the development of pulmonary fibrosis in the rat. A single transtracheal injection of 2.0 units of bleomycin was administered to rats to induce lung injury. Animals were killed at 0, 3, 7, 14, 30, and 120 days after bleomycin treatment. Total lipid phosphorus in BAL from animals given bleomycin increased from 1.6 mumol/lung in normal animals to 3.2 mumol/lung at 14 and 30 days. The increase in phospholipids was primarily in phosphatidylcholine with minor increases in phosphatidylinositol and phosphatidylethanolamine. These quantitative changes were accompanied by qualitative changes that included an increase in the percentage of total phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylinositol. In contrast, the percentage of phosphatidylglycerol was significantly reduced. Plasma phospholipid analysis indicated that these alterations were not due to plasma contamination. The functional significance of the phospholipid changes was assessed by comparing air- and saline-filled compliance measurements at similar times after bleomycin. Abnormal compliance measurements were observed at 3, 7, and 14 days after bleomycin. At 3 and 7 days the predominant compliance defect was at the air-liquid interface; however, at 14 days, when phospholipids were significantly elevated, the defect was primarily due to tissue components.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation of changes in pulmonary surfactant phospholipids with compliance in bleomycin-induced pulmonary fibrosis in the rat. 244 Mar 55

Phosphatidylethanolamine is the only phosphatide present in purified bacteriophage PM2 when obtained from bacteria grown and infected in minimal medium. The growth cycle of bacteriophage PM2 shows the basic general features described for virulent bacteriophages. PM2 infection of Pseudomonas BAL-31 causes a pronounced increase in deoxyribonucleic acid synthesis, but no detectable effect on the incorporation of phosphorus into lipid. When (32)P-prelabeled bacteria are infected with PM2, the specific activity of the phosphatide phosphorus in the virus is almost the same as that in the host bacteria labeled before infection. It is concluded that the viral phosphatide is not synthesized de novo after infection, but it probably is derived from preexisting cellular phosphatidylethanolamine.
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PMID:Origin of phospholipid in bacteriophage PM2. 570 22

Experiments were carried out to determine the long-term effect of instillation of 500 mg of generic bituminous, anthracite, quartz, or titanium dioxide (TiO2) dust on the composition of pulmonary surfactant. Dust was instilled in the caudal lobe of the right lungs of female pigtailed macaque monkeys (Macaca nemestrina). The composition of surfactant isolated from cell-free bronchoalveolar lavage (CF-BAL) samples obtained from right lungs (dust exposed) at various times over the following year was compared with that of surfactant isolated from CF-BAL from left lungs (dust free). Little change was seen in the amount of surfactant-associated lipid phosphorus as a result of exposure to dust. Exposure to quartz, anthracite, or TiO2 dust induced a significant increase in the total amount of protein in the surfactant-enriched fraction. The relative amount of specific proteins was also altered: surfactant-associated protein A decreased, and the amount of the heavy and light chains of immunoglobulin molecules (identified by NH2-terminal amino acid sequence analysis) increased. These changes were visible more than a year after instillation of quartz and at least 3 months after instillation of anthracite dust. Despite variation in the responses of the individual animals, the changes observed might serve as an indicator of the severity of the effect of exposure of the lung to mineral dust and/or to pathogens.
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PMID:Long-term effects of instilled mineral dusts on pulmonary surfactant isolated from monkeys. 761 61

Pulmonary alveolar microlithiasis is characterized by the presence in pulmonary alveolus of round shaped little bodies containing concentric calcareous lamellas. The incidence is similar in all continents, in both sexes and it is higher in age brackets between 20 and 50 years. The disease is prevalent among family units. Clinical reports may suggest the hypothesis that the disease may be hereditary. Pathogenetic hypotheses may indicate that a reduced lung mucociliary function leading to an excess of alveolar mucus may induce the formation of alveolar microliths by mucus condensation. Microliths may appear either confined in particular areas of the lung or widespread. Chemically, microliths consist of large amounts of calcium and phosphorus and, in reference to histology, they consist of calcareous concentric lamellas which are placed around an amorphous or granular central nucleus. The dissociation between definite X-ray pattern of lungs and relative poor clinical symptoms is the most common characteristics of the disease. However, a certain degree of dyspnea with a productive cough may occur together with a sporadic hemoptysis and thoracic pains. X-ray pattern of the lung reveals dissemination of radio-opaque nodules which may make lungs appear to be sprinkled with sand. The evolutive course of the disease leads to pulmonary insufficiency which is related to the increase of number of microliths in several areas of lungs. The inability to identify clear etiological and pathogenetic elements makes difficult therapeutic approach which is palliative such as the use of diphosphonate, steroids and therapeutic BAL.
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PMID:Pulmonary alveolar microlithiasis: an overview of clinical and pathological features together with possible therapies. 1456 Oct 14