Abstract

Our studies on oxygen toxicity in the red cell rely on the use of drugs as biochemical probes. In our initial approach we studied the interaction of cell components with drugs. In this application we concentrate our efforts on cellular studies to gain an understanding of the influence of drugs on cellular metabolism and changes in the intracellular environment. Our protocols approach questions concerning the interrelationships that exist in the red cell among oxygen metabolism, hemoglobin function and glycolysis. We also present experiments that focus on the role of ascorbate and metal catalysis in cellular toxicity. We measure flux of glucose metabolism, intracellular nucleotide concentration, glutathione turnover, intracellular pH, oxygen consumption, hydrogen peroxide concentration and activities of enzymes that catalyze the removal of the reduced products of oxygen metabolism, such as superoxide and hydrogen peroxide. There studies should yield insight into the biochemical mechanisms evolved for handling oxygen and should enhance our knowledge of the biochemical function of the red cell.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Research Project (R01)
Project #
5R01ES003425-09
Application #
3250695
Study Section
Physical Biochemistry Study Section (PB)
Project Start
1984-01-01
Project End
1986-12-31
Budget Start
1986-01-01
Budget End
1986-12-31
Support Year
9
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
New York University
Department
Type
Schools of Medicine
DUNS #
004514360
City
New York
State
NY
Country
United States
Zip Code
10012

  Publications

Oliveira, Carlos J R; Schindler, Fernanda; Ventura, Armando M et al. (2003) Nitric oxide and cGMP activate the Ras-MAP kinase pathway-stimulating protein tyrosine phosphorylation in rabbit aortic endothelial cells. Free Radic Biol Med 35:381-96
Barbosa de Oliveira, L C; Rocha Oliveira, C J; Fries, D M et al. (2002) Effects of lipopolysaccharide on low- and high-density cultured rabbit vascular smooth muscle cells: differential modulation of nitric oxide release, ERK1/ERK2 MAP kinase activity, protein tyrosine phosphatase activity, and DNA synthesis. Braz J Med Biol Res 35:181-90
Liu, T Z; Lee, K T; Chern, C L et al. (2001) Free radical-triggered hepatic injury of experimental obstructive jaundice of rats involves overproduction of proinflammatory cytokines and enhanced activation of nuclear factor kappaB. Ann Clin Lab Sci 31:383-90
Monteiro, H P; Gruia-Gray, J; Peranovich, T M et al. (2000) Nitric oxide stimulates tyrosine phosphorylation of focal adhesion kinase, Src kinase, and mitogen-activated protein kinases in murine fibroblasts. Free Radic Biol Med 28:174-82
Cheng, J; Luo, J; Zhang, X et al. (2000) Inhibition of cell proliferation in HCC-9204 hepatoma cells by a c-myc specific ribozyme. Cancer Gene Ther 7:407-12
Das, D; Pintucci, G; Stern, A (2000) MAPK-dependent expression of p21(WAF) and p27(kip1) in PMA-induced differentiation of HL60 cells. FEBS Lett 472:50-2
Ho, H Y; Cheng, M L; Lu, F J et al. (2000) Enhanced oxidative stress and accelerated cellular senescence in glucose-6-phosphate dehydrogenase (G6PD)-deficient human fibroblasts. Free Radic Biol Med 29:156-69
Liu, T Z; Stern, A; Emerit, I (1999) Clastogenic factors: biomarkers of oxidative stress of potential utility in the clinical chemistry laboratory. Ann Clin Lab Sci 29:134-9
Tsai, K J; Hung, I J; Chow, C K et al. (1998) Impaired production of nitric oxide, superoxide, and hydrogen peroxide in glucose 6-phosphate-dehydrogenase-deficient granulocytes. FEBS Lett 436:411-4
Chiu, D T; Huang, T Y; Hung, I J et al. (1997) Hemin-induced membrane sulfhydryl oxidation: possible involvement of thiyl radicals. Free Radic Res 27:55-62

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