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Query: UMLS:C0242706 (hyperoxia)
5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microvascular cells are most vulnerable to direct oxygen damage. Using an in vitro model system we have investigated the effect of elevated oxygen on the proliferation, morphology, and integrity of microvascular endothelial cells (EC) and pericytes. Cultivation of these cells at oxygen concentrations of 40% for 1 wk resulted in the inhibition of EC proliferation but had no effect on the growth of the pericytes. Similarly, hyperoxia induced a dramatic change in the shape of the EC, increasing their spread area by close to six-fold. Under the same conditions, the spread area of the pericytes was unaffected. To understand the effect of the hyperoxic treatment on the cells, the integrity of various membrane systems was assessed. 51Chromium release was used to monitor plasma membrane integrity. There was no difference in chromium release by EC and pericytes over the 7 d of growth under normoxic and hyperoxic conditions. Mitochondrial integrity was examined by staining the cells with Rhodamine 123, which is selectively accumulated by the mitochondria. The staining pattern of the mitochondria of both EC and pericytes was altered by growth in the elevated oxygen. Finally, the lysosomes were visualized using acridine orange. The acridine orange staining pattern revealed enlarged and perinuclear lysosomes in the EC but no change in the pericyte lysosomal staining pattern. Thus, the cells of the microvasculature seem to be differentially affected by hyperoxia, a fact that may be significant in the etiology of reperfusion injury, ischemic disease, and pathologies associated with prematurity.
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PMID:Effects of hyperoxia on microvascular cells in vitro. 243 58

Chlorpyrifos (Dursban) is an organophosphate insecticide widely used mainly for control of mosquito larvae. This study used the dominant freshwater leech Nephelopsis obscura as a representative aquatic invertebrate to test toxicity of chlorpyrifos on a nontarget species. RNA synthesis in neurons of the cerebral ganglion, epithelial cells of the intestine, and the tegument of small immature (50-70 mg) and large mature (300-400 mg) N. obscura was examined histochemically with acridine orange fluorochrome after exposure to chlorpyrifos in concentrations of 16, 32, 64, 128, and 144 ppb for as long as 6 weeks. The maximum environmental concentration of this insecticide in lake water, when used properly, is 4.25 ppb. There was no mortality, and no behavioral changes were observed in experimental animals, except for transient curling and cutaneous mucus secretion at the highest concentrations of chlorpyrifos. No pathological changes were observed in the intensity of RNA fluorescence or in the distribution of RNA within the cytoplasm of neurons or epithelial cells in any specimens, unlike N. obscura exposed to anoxia, hyperoxia, or salinity. Chlorpyrifos in the concentrations studied does not appear to adversely affect nucleic acid metabolism in N. obscura.
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PMID:Unimpaired RNA synthesis in neurons and epithelial cells in a freshwater leech exposed to the organophosphate insecticide chlorpyrifos. 247 46

When confluent calf pulmonary arterial endothelial monolayers cultured on polycarbonate micropore membranes were exposed to hyperoxia (95% O2) for 3 days, endothelial cells became enlarged, and their permeability to 125I-labeled albumin was markedly increased. Similar changes were not observed when endothelial monolayers were exposed to hyperoxia for 1 or 2 days. Cell counting and acridine orange staining of endothelial monolayers revealed that the hyperoxia-induced increase in albumin permeability was not associated with a denuding injury or loss of cells from the monolayers. Vimentin filament staining of O2-exposed monolayers showed thickening of the perinuclear vimentin coil in some cells. Rhodamine-phalloidin staining demonstrated that hyperoxia caused a progressive alteration in the actin distribution. Two days after O2 exposure, peripheral actin bands became thinner, whereas the number of cytoplasmic stress fibers was increased. Three days after O2 exposure, peripheral actin bands of most cells were disrupted or absent. Because peripheral actin bands play an important role in maintaining the integrity of endothelial monolayers, disruption of peripheral bands by hyperoxia may in part be responsible for the observed change in permeability.
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PMID:Hyperoxia causes increased albumin permeability of cultured endothelial monolayers. 336 37

To test whether the possibly enhanced sensitivity of aged cells to oxidative stress may depend on their content of ceroid/lipofuscin, AG-1518 human fibroblasts with various amounts of the pigment accumulated due to prolonged cultivation under normobaric hyperoxia were exposed to acute oxidative stress (2.5 microM naphthazarin, 15 min) and then returned to standard culture conditions. Twenty-four hours after the naphthazarin treatment, 37% of the cells were still vital, whereas others had undergone oxidative stress-induced apoptosis with ensuing postapoptotic necrosis. The average amount of ceroid/lipofuscin within the surviving cells was only about half of that of the initial population of cells, as measured before the naphthazarin exposure. This finding suggests that ceroid/lipofuscin-rich cells have an increased sensitivity to oxidative stress. The ceroid/lipofuscin quantity strongly positively correlated with the size of the acidic compartment (as evaluated by uptake of the weakly basic lysosomotropic fluorochrome acridine orange) and with its content of the lysosomal protease cathepsin D, as assayed by immunocytochemistry. We hypothesize that the enhanced sensitivity of ceroid/lipofuscin-loaded cells to oxidative stress may be caused by the increased amounts of lysosomal enzymes, known as mediators of oxidative damage, and/or by catalysis of intralysosomal oxidative reactions by lipofuscin-associated iron.
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PMID:Ceroid/lipofuscin-loaded human fibroblasts show increased susceptibility to oxidative stress. 1057 36

TB/C3 hybridoma cells were transected with either pEF-MClneopA or pEF bcl2-MClneopA vectors to produce a control cell line (TB/C3 pEF) and a cell line that overexpresses the "antiapoptotic" human bcl-2 protein (TB/C3 bcl2). Flow cytometry analysis of intracellular bcl-2 protein levels enabled near on-line monitoring of the stability of bcl-2 expression in the absence of drug selection. It was possible to maintain spontaneous selection of cells with the overexpression of bcl-2 protein during semicontinuous cultures at very low dilution rates, where cells were subjected to the selective conditions of nutrient limitation and high toxic metabolite concentrations. Interestingly, cells that overexpressed bcl-2 were adapted to suspension culture conditions significantly faster than control cells. Dual fluorescence staining with acridine orange and propidium iodide allowed for discrimination between viable, apoptotic, secondary necrotic, and necrotic cells, respectively. Compared with the usual trypan blue method of establishing culture viability, dual staining demonstrated that under stressful conditions a significant proportion of cells that excluded trypan blue were also undergoing cell death through apoptosis. In batch cultures the overexpression of bcl-2 more than doubled the membrane intact (MI) cell productive period (the integral of Ml cell density with respect to culture time) and increased the monoclonal antibody (mAb) production by approximately 40% when compared with the control cell line. The overexpression of bcl-2 protein also significantly extended the cell integrity and viability by the suppression of apoptosis in conditions of hypoxia, hyperoxia, glutamine deprivation, glucose deprivation, and serum limitation. The suppression of apoptosis in anaerobic conditions suggests that bcl-2 exerts its antiapoptotic activity by a mechanism that does not involve an oxidative reactive pathway. In conditions of excess thymidine, which suppressed cell proliferation, Ml cell density and specific mAb productivity were further enhanced by the overexpression of bcl-2, which suggests the possibility of accomplishing a controlled proliferation in immortalized cell lines without invoking cell death. Cell size and intracellular mAb were increased for TB/C3 bcl2 cells compared with TB/C3 pEF control cells when analyzed by flow cytometry.
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PMID:Prevention of hybridoma cell death by bcl-2 during suboptimal culture conditions. 1863 67