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:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 Rats received a total of 18 mg/kg cis-dichlorodiammineplatinum (II) (CDDP) intravenously and were treated concomitantly with calcium-disodium ethylenediaminetetraacetic acid (CaNa2EDTA), 2,3-dimercaptopropanol (BAL), deferoxamine, 2,3-dimercaptosuccinic acid (DMS) or vehicle. In comparison to controls, renal platinum concentration was significantly reduced in the DMS and deferoxamine-treated groups. However, significant deterioration occurred in the deferoxamine-treated group. The hepatic platinum concentration was unaffected by the chelating agents. 2 Following a dose of 6 mg/kg CDDP intravenously, eight days of treatment with DMS, 50 mg/kg daily, had no effect on renal platinum excretion, while treatment with 100 or 200 mg/kg daily reduced renal platinum concentration by 50%. 3 In order to determine whether DMS could prevent the nephrotoxicity of CDDP, rats were given 6 mg/kg CDDP intravenously, followed by a four day course of DMS treatment at doses of 0, 50, 100 or 200 mg/kg daily begun 3 h after the CDDP dose. DMS failed to prevent renal toxicity as indicated by weight loss, serum creatinine concentration, renal histology, and the urinary excretion of N-acetyl-beta-glucosaminidase, a renal tubular enzyme.
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PMID:The effect of heavy metal chelators on the renal accumulation of platinum after cis-dichlorodiammineplatinum II administration to the rat. 626 16

The aim of this study was to evaluate whether markers of collagen synthesis, hyaluronan (HA) and procollagen type III aminoterminal peptide (PIIINP) in bronchoalveolar lavage fluid (BALF) and serum (S) were correlated to paraclinical markers of disease activity (S-ACE, S-IgG S-IgA S-calcium, chest X-ray (CXR) profusion score, pulmonary function tests (FEV1, FVC, TLC, DLCO)) in pulmonary sarcoidosis. The material comprised 48 patients with biopsy proven sarcoidosis (35 male, 13 female, median age 31 years) and 24 controls (16 male, 8 female, median age 60 years). BAL was performed in the right middle lobe with 250 ml saline. Patients had higher BALF-HA, mean 88 +/- 13 (SEM) micrograms/l, than controls, 39 +/- 2 micrograms/l (p < 0.01), higher BALF-albumin, 121 +/- 13 mg/l, than controls 58 +/- 4 mg/l (p < 0.01), and higher BALF/S-HA ratio, 3.35 +/- 0.51, than controls, 1.23 +/- 0.60 (p < 0.01). There were no significant differences for S-HA, BALF-PIIINP, or S-PIIINP. In patients significant correlations were found between BALF-HA, S-HA, and BALF-albumin; between S-HA and S-ACE; between BALF/S-HA and BALF-albumin; between CXR profusion score and S-HA, S-ACE, S-IgG, S-IgA, FEV1, FVC, TLC and DLCO. The results indicate that measurement of S-HA, BALF-HA, and BALF-albumin may be of value in the monitoring of disease in pulmonary sarcoidosis.
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PMID:Hyaluronan and procollagen type III aminoterminal peptide in serum and bronchoalveolar lavage fluid in patients with pulmonary sarcoidosis. 761 74

Role of CD45 in B cell antigen receptor (BcR)-mediated signaling events in mature B cells was examined using BAL-17 and its CD45-negative clones. In the CD45-negative clones, BcR stimulation induced tyrosine phosphorylation almost identical to the parental cells, with a few exceptions of reduced phosphorylation, especially of a protein of about 60 kDa. BcR-induced calcium responses were reduced in the CD45-negative clones, but the kinetics were similar to the parent. BcR stimulation led to growth inhibition in the parental cells, but signals for growth inhibition were completely blocked in the CD45-negative clones. Interestingly, the same stimulation induced low, but significant levels of apoptosis both in the parent and in the CD45-negative clones. Thus, in mature BAL-17 cells, CD45 subtly mediate early signaling events (tyrosine phosphorylation and Ca2+ mobilization), and is absolutely required for the signaling pathway leading to growth regulation, but has limited effects on apoptosis.
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PMID:Antigen receptor-initiated growth inhibition is blocked in CD45-loss variants of a mature B lymphoma, with limited effects on apoptosis. 766 90

Chelating agents such as calcium disodium ethylenediaminetetraacetate (EDTA), 2,3-dimercaptopropanol (BAL), or D-penicillamine (D-PA) have been widely used for the past 4 decades as antidotes for the treatment of acute and chronic metal poisoning. In recent years, meso-2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercapto-1-propanesulfonate (DMPS) and sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) have also shown to be effective to prevent against toxicity induced by a number of heavy metals. The purpose of the present article was to review the protective activity of various chelating agents against the embryotoxic and teratogenic effects of well-known developmental toxicants (arsenic, cadmium, lead, mercury, uranium, and vanadium). DMSA and DMPS were found to be effective in alleviating arsenate- and arsenite-induced teratogenesis, whereas BAL afforded only some protection against arsenic-induced embryo/fetal toxicity. Also, DMSA, DMPS, and Tiopronin were effective in ameliorating methyl mercury-induced developmental toxicity. Although the embryotoxic and teratogenic effects of vanadate were significantly reduced by Tiron, no significant amelioration of uranium-induced embryotoxicity was observed after treatment with this chelator.
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PMID:Prevention by chelating agents of metal-induced developmental toxicity. 779 20

To elucidate the pathogenesis of sarcoidosis, we mainly investigated the surface molecules including adhesion molecules on BAL T cells and the functions of BAL T cells such cytokine production, [Ca2+] mobilization, PKC expression. Results are following. Adhesion molecules were up-regulated on BAL T cells compared with peripheral T cells, but cytokine production was decreased via TcR stimulation through [Ca2+] mobilization was occurred. PKC isozyme alpha expression was decreased compared with peripheral blood T cells.
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PMID:[Specificity of surface antigen and function of BAL T cells]. 804 24

Some types of interstitial lung disease (ILD) are characterized by an abnormal proliferation and activation of lymphocytes in the alveolus and interstitium. Recent data have suggested that membrane signals on alveolar macrophages (AM) in normal lung play a crucial role in limiting lymphocyte activation by altering early events in receptor-mediated signal transduction in lymphocytes. In the current study fixed AM from normal volunteers and from patients with either sarcoidosis or idiopathic pulmonary fibrosis were compared for the ability to inhibit CD3-mediated increases in intracellular calcium concentration [(Ca2+)i]. All normal AM inhibited CD3-mediated increases in (Ca2+)i, whereas seven of 10 ILD AM were permissive of this early event in T-lymphocyte activation. Patients with ILD and permissive AM displayed significantly greater mean BAL lymphocytes than did those with suppressive AM (42 versus 12%, respectively). The inhibitory effect of normal AM could be partially duplicated by incubation of lymphocytes with surfactant (SF) obtained from normal lungs. Analysis of one SF component, SF protein A, in normal and in ILD AM membranes disclosed reduced SF protein A in ILD AM. These results demonstrate alterations in AM in patients with ILD and a lymphocytic alveolitis that renders AM permissive for early events in T-cell activation.
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PMID:Effect of interstitial lung disease macrophages on T-cell signal transduction. 811 82

The effects of Ag binding on B cell development and activation are mediated by intracellular signals initiated by the B cell AgR. In this report, we show that the B cell AgR regulates the production of inositol phospholipids involved in two different signal transduction pathways, the phosphatidylinositol 3-kinase (PtdIns 3-kinase) pathway and the phospholipase C (PLC) pathway. Phosphatidylinositol 3-phosphate (PtdIns3P), phosphatidylinositol 3,4-bisphosphate [PtdIns(3,4)P2], and phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P3] are produced by PtdIns 3-kinase, an enzyme that appears to be an essential component of tyrosine kinase-mediated signaling. Both PtdIns(3,4)P2 and PtdIns(3,4,5)P3 are likely to function as second messengers in vivo because they can activate the zeta isoform of protein kinase C (PKC) in vitro. We show that cross-linking of the B cell AgR with anti-Ig antibodies caused a five- to sixfold increase in the levels of PtdIns(3,4)P2 in both the mature B cell line BAL 17 and the immature B cell line WEHI-231. PtdIns(3,4)P2 levels increased within 15 s of anti-Ig addition and remained elevated for at least 5 min. AgR cross-linking also caused a slower increase in PtdIns3P levels (approximately 50% over control) and a small, transient increase in PtdIns(3,4,5)P3 levels. Thus, the B cell AgR activates the PtdIns 3-kinase pathway. The other inositol phospholipid signaling pathway involves PLC, which cleaves phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2], yielding second messengers that increase intracellular calcium and activate other isoforms of PKC. We analyzed the effects of AgR signaling on PtdIns(4,5)P2 and its precursor, phosphatidylinositol 4-phosphate (PtdIns4P). Consistent with its ability to activate PLC, AgR ligation decreased the levels of PtdIns(4,5)P2. In contrast, AgR cross-linking increased the levels of PtdIns4P. Increased synthesis of PtdIns4P followed by phosphorylation at the D-5 position may prevent depletion of PtdIns(4,5)P2. Thus, signaling by the B cell AgR increases the levels of PtdIns 4-kinase products and PtdIns 3-kinase products. The simplest interpretation of our results is that the B cell AgR activates both PtdIns 3-kinase and PtdIns 4-kinase.
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PMID:Both phosphatidylinositol 3-kinase and phosphatidylinositol 4-kinase products are increased by antigen receptor signaling in B cells. 825 4

WEHI-231 is a murine B cell lymphoma that has been used extensively as a model for the immature stage B cell and its functional response to Ag receptor cross-linking as a model for immature B cell tolerance. This cell line expresses sIgM, CD5, and FcR gamma, but lacks the B cell-specific isoform of CD45 (B220). This study demonstrates for the first time that WEHI-231, in contrast to classically defined immature B cells, expresses delta on its surface. Analysis of delta on WEHI-231 revealed structural differences with respect to that on BAL-17 or primary splenic B cells. Although the m.w. of delta on the latter two B cell populations was similar, delta on WEHI-231 manifested a marked increase in its apparent m.w. deduced by SDS-PAGE. This difference was found to be due primarily to differential N-linked glycosylation. Signal transduction through the endogenous sIgD on WEHI-231 was investigated. In contrast to cross-linking of sIgM, cross-linking of the endogenous surface IgD on WEHI-231 was unable to generate a negative growth response in these cells. This inability may be due to uncoupling from normal surface Ig signaling pathways. The signaling properties of the endogenous sIgD on WEHI-231 differ from that on primary B cells and other sIgD-expressing cell lines. Whereas sIgD on splenic B lymphocytes or the mature B cell line BAL-17 is coupled to inositol phospholipid hydrolysis and calcium mobilization, cross-linking of sIgD on WEHI-231 failed to elicit these events, although induced changes in tyrosine phosphorylation were observed. Thus, endogenous expression of surface IgD on WEHI-231 is inconsistent with its representing the classically defined immature stage B cell. The structural and signaling differences associated with delta on these cells suggest the potential for developmentally regulated delta function and model for study of sIgD signal transduction.
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PMID:Endogenous expression of delta on the surface of WEHI-231. Characterization of its expression and signaling properties. 840 28

We have described recently the prevention of apoptosis by CD2-soluble CD48 interaction on antigen B cell receptor occupancy. Here, we show that CD2 ligation is also able to interfere with B cell receptor-independent apoptosis pathways such as spontaneous death in spleen B cells or serum deprivation and hydrogen peroxide exposure in the BAL-17 cell line. In all cases, CD2 ligation induces a signal that prevents the downregulation of Bcl-2 expression. The specific CD2 signal pathway involved in this phenomenon is still unknown. As reported, CD2 did not appear to induce Ca2+ mobilization, phosphatidylinositol turnover, or PKC translocation in B cells. Nevertheless, we show that CD2 receptor ligation is coupled to the tyrosine phosphorylation pathway in B cells. These observations indicate that CD2 is functionally able to trigger at least an early signal that could play a role in apoptosis blockage B cells in addition to the adhesion one. The results suggest the participation of cellular membrane receptors other that CD40 in apoptosis rescue, not only in the antigen-dependent but also in the antigen-independent phases of B cell lymphopoiesis.
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PMID:CD2 ligation abrogates antigen-independent apoptosis in B cells. 866 Aug 37

Amifostine, a chemo- and radioprotective agent developed as adjunctive therapy for malignancies, induces hypotension after approximately 20% of patient administrations. This study examines the molecular mechanisms underlying hypotension induced by amifostine. Amifostine and its metabolite, WR-1065, induced dose-dependent hypotension in anesthetized rats that was not blocked by N(G)-methyl L arginine (L-NAME), an NO synthase inhibitor. WR-1065 but not amifostine induced concentration-dependent relaxation of isolated rat aortic rings in an endothelium-independent fashion. Relaxation was not associated with increases in cGMP or cAMP and could not be blocked by L-NAME or indomethacin. Similarly, neither amifostine or WR-1065 activated adenylyl, particulate guanylyl, or soluble guanylyl cyclases. WR-1065 relaxed rat aortic rings precontracted with norepinepherine, suggesting alpha-adrenergic blocking activity. However, neither amifostine nor WR-1065 altered the ability of prazosin or phentolamine to bind to alpha-adrenergic receptors. Further, WR-1065 had no effect on receptor-mediated increases in intracellular calcium in BAL 17 murine B lymphocytes in vitro. Thus, hypotension after administration of amifostine is mediated by WR-1065 and appears to result from direct relaxation of vascular smooth muscle. Smooth muscle relaxation induced by WR-1065 is not related to production of nitric oxide, prostaglandins, or cyclic nucleotides; alpha-adrenergic receptor antagonism; or interference with receptor-dependent increases in intracellular calcium. Administration of ephedrine, an efficacious adrenergic agonist, attenuated hypotension induced by amifostine in anesthetized rats and may be useful in alleviating hypotension associated with amifostine administration in patients.
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PMID:Hypotensive mechanisms of amifostine. 872 52


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