Paraquat-induced phosphatidylserine oxidation and apoptosis are independent of activation of PLA2

American Journal of Physiology - Lung Cellular and Molecular Physiology

Volumn 274, Issue 5 18-5, 1998, Pages

  Fabisiak, James P ^a   Kagan, Valerian E ^a   Tyurina, Yulia Y ^a,b   Tyurin, Vladimir A ^a,b   Lazo, John S ^a  

^a UNIVERSITY OF PITTSBURGH SCHOOL OF MEDICINE   (United States)

^b SECHENOV INSTITUTE OF EVOLUTIONARY PHYSIOLOGY AND BIOCHEMISTRY   (Russian Federation)

Author keywords

Arachidonic acid; Lipid peroxidation; Oxidative stress; Phospholipase A2; Quinacrine

Indexed keywords

ARISTOLOCHIC ACID; KETONE; MEPACRINE; PARAQUAT; PHOSPHATIDYLSERINE; PHOSPHOLIPASE A2;

ANIMAL CELL; APOPTOSIS; ARACHIDONIC ACID METABOLISM; ARTICLE; ENZYME ACTIVATION; LIPID PEROXIDATION; LUNG INJURY; NONHUMAN; OXIDATION; OXIDATIVE STRESS; PRIORITY JOURNAL;

EID: 0031808532     PISSN: 10400605     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajplung.1998.274.5.l793     Document Type: Article

References (43)

1. Arduni, A., V. Tyurin, Y. Tyurina, E. Arrigoni-Martelli, F. Molajoni, S. Dottori, and G. Federici. Acyl-trafficking in membrane phospholipid fatty acid turnover: the transfer of fatty acid from the acyl-L-carnitine pool to membrane phospholipids in intact erythrocytes. Biochem. Biophys. Res. Commun. 187: 353-358, 1992.
2. Armstrong, S. C., and C. E. Ganote. Effects of the phospholipase inhibitor mepacrine on injury in ischemic and metabolically-inhibited adult isolated myocytes. Am. J. Pathol. 138: 545-555, 1991.
3. 2 by exogenous hydrogen peroxide. Biochem. Pharmacol. 50: 753-761, 1995.
4. Buttke, T. M., and P. A. Sandstrom. Oxidative stress as a mediator of apoptosis. Immunol. Today 15: 7-10, 1994.
5. Chalvardjian, A., and E. Rubnicki. Determination of lipid phosphorous in nanomolar range. Anal. Biochem. 36: 225-226, 1970.
6. 2: function and pharmacological regulation. Biochem. Pharmacol. 36: 2429-2436, 1987.
7. 2. J. Biol. Chem. 269: 13057-13060, 1994.
8. Fabisiak, J. P., V. E. Kagan, V. B. Ritov, D. E. Johnson, and J. S. Lazo. Bcl-2 inhibits selective oxidation and externalization of phosphatidylserine during paraquat-induced apoptosis. Am. J. Physiol. 272 (Cell Physiol. 41): C675-C684, 1997.
9. Fadok, J., M. Lees, and G. H. Sloane-Stanley. Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages. J. Immunol. 148: 2201-2216, 1992.
10. Farrington, J. A., M. Ebert, E. J. Land, and K. Fletcher. Bipyridylium quarternary salts and related compounds. V. Pulse radiolysis studies on the reaction of paraquat radical with oxygen. Implications for the mode of action of bipyridyl herbicides. Biochim. Biophys. Acta 314: 372-381, 1973.
11. 2. Free Radic. Biol. Med. 18: 203-213, 1995.
12. Gunasekar, P. G., A. G. Kanthasamy, J. L. Borowitz, and G. E. Isom. NMDA receptor activation produces concurrent generation of nitric oxide and reactive oxygen species: implication for cell death. J. Neurochem. 65: 2016-2021, 1995.
13. 2 is crucial in the cytotoxic action of tumor necrosis factor. J. Biol. Chem. 268: 11290-11295, 1993.
14. Hockenberry, D. M., Z. N. Oltavi, X.-M. Yin, C. L. Milliman, and S. J. Korsmeyer. Bcl-2 functions in an antioxidant pathway to prevent apoptosis. Cell 75: 241-251, 1995.
15. 2. J. Immunol. 8: 4286-4294, 1993.
16. 2 on bilayers containing lysophosphatidylcholine analogs and the effect of inhibitors. Biochem. Pharmacol. 33: 2541-2551, 1984.
17. Johnson, D. A., and S. Ayres. Quinacrine noncompetitive inhibitor binding site localized on the torpedo acetylcholine receptor in the open state. Biochemistry 35: 6330-6336, 1996.
18. Kagan, V. E. Lipid Peroxidation. Boca Raton, FL: CRC, 1988.
19. Khader, A. A., A. Sulaiman, P. N. Kishore, C. Morais, and M. Tariq. Quinacrine attenuates cyclosporine-induced nephrotoxicity in rats. Transplantation 62: 427-435, 1996.
20. Kluck, R. M., E. Bossy-Wetzel, D. R. Green, and D. D. Newmeyer. The release of cytochrome c from mitochondria: a primary site for the Bcl-2 regulation of apoptosis. Science 275: 1132-1136, 1997.
21. Knauer, M. F., K. J. Longmuir, R. S. Yamamoto, T. P. Fitzgerald, and G. A. Granger. Mechanism of human lymphotoxin- and tumor necrosis factor-induced destruction of cells in vitro: phospholipase activation and deacylation of specific-membrane phospholipids. J. Cell. Physiol. 142: 469-479, 1990.
22. Laster, S. M., J. G. Wood, and L. R. Gooding. Tumor necrosis factor can induce both apoptotic and necrotic forms of cell lysis. J. Immunol. 141: 2629-2634, 1988.
23. Lie, S. O., and B. Schofield. Inactivation of lysosomal function in normal cultured human fibroblasts by chloroquine. Biochem. Pharmacol. 22: 3109-3114, 1973.
24. Loffler, B.-M., E. Bohn, B. Hessem, and H. Kunze. Effects of antimalarial drugs on phospholipase A and lysophospholipase activities in plasma membrane, mitochondrial, microsomal, and cytosolic subcellular fractions of rat liver. Biochim. Biophys. Acta 835: 448-455, 1985.
25. 2 in mitochondria enriched with n-3 fatty acids. Proc. Natl. Acad. Sci. USA 87: 8845-8849, 1990.
26. Mayer, A. M. S., K. B. Glaser, and R. S. Jacobs. Regulation of eicosanoid biosynthesis in vitro and in vivo by the natural product manoalide: a potent inactivator of venom phospholipases. J. Pharmacol. Exp. Ther. 244: 871-878, 1988.
27. Miyachi, Y., A. Yoshioka, S. Imamura, and Y. Niwa. Antioxidant action of antimalarials. Ann. Rheum. Dis. 45: 244-248, 1986.
28. 2+ current by quinacrine in smooth muscle cells of the guinea pig. Jpn. J. Pharmacol. 71: 51-60, 1996.
29. Nunez, G., D. London, D. Hockenberry, M. Alexander, J. P. McKern, and S. J. Korsmeyer. Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived cell lines. J. Immunol. 144: 3602-3610, 1990.
30. Pacifici, E. H. K., L. L. McLeod, and A. Sevanian. Lipid hydroperoxide-induced peroxidation and turnover of endothelial cell phospholipids. Free Radic. Biol. Med. 17: 297-309, 1994.
31. Patel, T., G. J. Gores, and S. H. Kaufmann. The role of proteases during apoptosis. FASEB J. 10: 587-597, 1996.
32. Phillis, J. W. Cerebroprotective action of the phospholipase inhibitor quinacrine in the ischemia/reperfused gerbil hippocampus. Life Sci. 58: PL97-PL101, 1996.
33. 2, blocks production of arachidonate and 12-hydroxyeicosatetraenoic acid by calcium ionophore-challenged platelets. J. Biol. Chem. 269: 15619-15624, 1994.
34. +-channels in follicle-enclosed Xenopus oocytes. Eur. J. Pharmacol. 252: 117-121, 1994.
35. 2 hydrolytic susceptibility of liposomes consisting of mixed species of phosphatidylcholine and phosphatidylethanolamine. Biochim. Biophys. Acta 1127: 131-140, 1992.
36. 2, potentiates hydrogen peroxide cytotoxicity in kidney epithelial cells. J. Biol. Chem. 271: 21505-21513, 1996.
37. Schulze-Osthoff, K., A. C. Bakker, B. Vanhaesebroeck, R. Beyaert, W. A. Jacob, and W. Fiers. Cytoxic activity of tumor necrosis factor is mediated by early damage to mitochondrial functions. Evidence for the involvement of mitochondrial radical generation. J. Biol. Chem. 267: 5317-5323, 1992.
38. Smith, P., and D. Heath. Paraquat. CRC Crit. Rev. Toxicol. 14: 411-445, 1976.
39. Struhar, D., S. Kitvity, and M. Topisly. Quinacrine inhibits oxygen radical release from human alveolar macrophages. Int. J. Immunopharmacol. 14: 275-277, 1992.
40. 2 is required for the lysis of adenovirus-infected cells by tumor necrosis factor. J. Virol. 70: 8502-8507, 1996.
41. 2 is involved in the mechanism of activation of neutrophils by polychlorinated biphenyls. Environ. Health Perspect. 104: 52-58, 1996.
42. 2 in human melanoma cells. J. Immunol. 156: 201-207, 1996.
43. 2, and CoA-independent transacylase. J. Lipid Mediat. Cell Signal. 10: 315-330, 1994.