scholarly journals Induction of superoxide dismutase by oxygen in neonatal rat lung.

1977 ◽  
Vol 252 (10) ◽  
pp. 3509-3514 ◽  
Author(s):  
J B Stevens ◽  
A P Autor
Keyword(s):  
Superoxide Dismutase ◽  
Neonatal Rat ◽  
Rat Lung

Neuroprotection against hypoxia-ischemia in neonatal rat brain by novel superoxide dismutase mimetics

2003 ◽  
Vol 346 (1-2) ◽  
pp. 41-44 ◽  
Author(s):  
Katsuyoshi Shimizu ◽  
Nishadi Rajapakse ◽  
Takashi Horiguchi ◽  
R.Mark Payne ◽  
David W. Busija
Keyword(s):  
Superoxide Dismutase ◽  
Rat Brain ◽  
Neonatal Rat ◽  
Hypoxia Ischemia ◽  
Superoxide Dismutase Mimetics ◽  
Neonatal Rat Brain

Cytokines increase rat lung antioxidant enzymes during exposure to hyperoxia

1989 ◽  
Vol 66 (2) ◽  
pp. 1003-1007 ◽  
Author(s):  
C. W. White ◽  
P. Ghezzi ◽  
S. McMahon ◽  
C. A. Dinarello ◽  
J. E. Repine
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Antioxidant Enzyme Activities ◽  
Rat Lung ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Necrosis Factor

Pretreatment with the combination of tumor necrosis factor/cachectin (TNF/C) and interleukin 1 (IL-1) increased glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), glutathione peroxidase (GPX), catalase (CAT), and superoxide dismutase (SOD) activities in lungs of rats continuously exposed to hyperoxia for 72 h, a time when all untreated rats had already died. Pretreatment with TNF/C and IL-1 also increased, albeit slightly, lung G6PDH and GR activities of rats exposed to hyperoxia for 4 or 16 h. By comparison, no differences occurred in lung antioxidant enzyme activities of TNF/C and IL-1- or saline-pretreated rats exposed to hyperoxia for 36 or 52 h; the latter is a time just before untreated rats began to succumb during exposure to hyperoxia. The results raise the possibility that TNF/C and IL-1 treatment can increase lung antioxidant enzyme activities and that increased lung antioxidant enzymes may contribute to the increased survival of TNF/C and IL-1-pretreated rats in hyperoxia for greater than 72 h.

A novel epithelial cell from neonatal rat lung: isolation and differentiated phenotype

1990 ◽  
Vol 259 (6) ◽  
pp. L415-L425 ◽  
Author(s):  
P. E. Roberts ◽  
D. M. Phillips ◽  
J. P. Mather
Keyword(s):  
Epithelial Cell ◽  
Molecular Mechanisms ◽  
Basal Medium ◽  
Fold Increase ◽  
Cell Types ◽  
Cell Number ◽  
Neonatal Rat ◽  
Rat Lung ◽  
Cell Type

A novel epithelial cell from normal neonatal rat lung has been isolated, established, and maintained for multiple passages in the absence of serum, without undergoing crisis or senescence. By careful manipulation of the nutrition/hormonal microenvironment, we have been able to select, from a heterogeneous population, a single epithelial cell type that can maintain highly differentiated features in vitro. This cell type has characteristics of bronchiolar epithelial cells. A clonal line, RL-65, has been selected and observed for greater than 2 yr in continuous culture. It has been characterized by ultrastructural, morphological, and biochemical criteria. The basal medium for this cell line is Ham's F12/Dulbecco's modified Eagle's (DME) medium plus insulin (1 micrograms/ml), human transferrin (10 micrograms/ml), ethanolamine (10(-4) M), phosphoethanolamine (10(-4) M), selenium (2.5 x 10(-8) M), hydrocortisone (2.5 x 10(-7) M), and forskolin (5 microM). The addition of 150 micrograms/ml of bovine pituitary extract to the defined basal medium stimulates a greater than 10-fold increase in cell number and a 50- to 100-fold increase in thymidine incorporation. The addition of retinoic acid results in further enhancement of cell growth and complete inhibition of keratinization. We have demonstrated a strategy that may be applicable to isolating other cell types from the lung and maintaining their differentiated characteristics for long-term culture in vitro. Such a culture system promises to be a useful model in which to study cellular events associated with differentiation and proliferation in the lung and to better understand the molecular mechanisms involved in these events.

Detection of chondroitin sulfates and decorin in developing fetal and neonatal rat lung

2002 ◽  
Vol 282 (3) ◽  
pp. L484-L490 ◽  
Author(s):  
Yiqiong Wang ◽  
Kaori Sakamoto ◽  
Jody Khosla ◽  
Philip L. Sannes
Keyword(s):  
Extracellular Matrix ◽  
Chondroitin Sulfate ◽  
Wide Distribution ◽  
Neonatal Rat ◽  
Chondroitin Sulfate Proteoglycan ◽  
Sulfate Proteoglycan ◽  
Rat Lung ◽  
Adult Rats ◽  
Chondroitin Sulfates ◽  
Monospecific Antibodies

Chondroitin sulfates and their related proteoglycans are components of extracellular matrix that act as key determinants of growth and differentiation characteristics of developing lungs. Changes in their immunohistochemical distribution during progressive organ maturation were examined with monospecific antibodies to chondroitin sulfate, a nonbasement membrane chondroitin sulfate proteoglycan, and the specific chondroitin sulfate-containing proteoglycan decorin in whole fetuses and lungs from newborn and adult rats. Alveolar and airway extracellular matrix immunostained heavily in the prenatal rat for both chondroitin sulfate and chondroitin sulfate proteoglycan, whereas decorin was confined to developing airways and vessels. These sites retained their respective levels of reactivity with all antibodies through 1–10 days postnatal but thereafter became progressively more diminished and focal in alveolar regions. The heavy staining seen early in development was interpreted to reflect a significant and wide distribution of chondroitin sulfates, chondroitin sulfate proteoglycans, and decorin in rapidly growing tissues, whereas the reduced and more focal reactivity observed at later time points coincided with known focal patterns of localization of fibrillar elements of the extracellular matrix and a more differentiated state.

Rosiglitazone, a peroxisome proliferator-activated receptor-γ agonist, prevents hyperoxia-induced neonatal rat lung injury in vivo

2006 ◽  
Vol 41 (6) ◽  
pp. 558-569 ◽  
Author(s):  
Virender K. Rehan ◽  
Ying Wang ◽  
Sanjay Patel ◽  
Jamie Santos ◽  
John S. Torday
Keyword(s):  
Lung Injury ◽  
Neonatal Rat ◽  
Peroxisome Proliferator ◽  
Rat Lung ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Proteomic Analysis of Radiation-Induced Changes in Rat Lung: Modulation by the Superoxide Dismutase Mimetic MnTE-2-PyP5+

2010 ◽  
Vol 78 (2) ◽  
pp. 547-554 ◽  
Author(s):  
Vasily A. Yakovlev ◽  
Christopher S. Rabender ◽  
Heidi Sankala ◽  
Ben Gauter-Fleckenstein ◽  
Katharina Fleckenstein ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Proteomic Analysis ◽  
Rat Lung ◽  
Radiation Induced ◽  
Induced Changes

Serine proteinase inhibitors influence the stability of tropoelastin mRNA in neonatal rat lung fibroblast cultures

1996 ◽  
Vol 270 (3) ◽  
pp. L376-L385
Author(s):  
S. E. McGowan ◽  
R. Liu ◽  
C. S. Harvey ◽  
E. C. Jaeckel
Keyword(s):  
Steady State ◽  
Culture Medium ◽  
Serine Proteinase ◽  
State Level ◽  
Lung Fibroblast ◽  
Neonatal Rat ◽  
Lung Fibroblasts ◽  
Steady State Level ◽  
Rat Lung ◽  
Fibroblast Cultures

Elastin, an elastic extracellular structural protein, is a polymer comprised of soluble tropoelastin (TE) monomers that are joined by covalent cross-links and become insoluble. In cultured vascular smooth muscle cells, the steady-state level of TE mRNA is influenced by soluble elastin moieties in the culture medium, either TE or its fragmentation products. We have hypothesized that an enzyme-mediated proteolytic event may modulate the quantities of TE and its fragmentation products in the culture medium of mesenchymal cells, and thereby indirectly regulate the steady-state level of TE mRNA. Neonatal rat lung fibroblasts were cultured in the presence or absence of the serine proteinase inhibitor, aprotinin, and the quantities of soluble elastin and TE mRNA were analyzed. Exposures to aprotinin lasting up to 12 h increased the soluble elastin content of the culture medium. The increase in the soluble elastin content did not reflect an increase in TE mRNA, which diminished after exposures for 12 h or longer. The decrease in TE mRNA resulted from a decrease in its half-life, rather than a decrease in the rate of TE gene transcription. Aprotinin did not reduce TE mRNA in plasminogen-depleted cultures, but the effect of aprotinin was evident when purified plasminogen was added back to the cultures. Therefore, a serine proteinase, possibly plasmin, may participate in a feedback mechanism and modulate the quantity of TE in lung fibroblast cultures. This mechanism may help ensure that intracellular TE synthesis occurs in tandem with extracellular elastin deposition and cross-linking.

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