The DOI matches its Crossref record; 117 of the 117 references it cites were found in a registry or an index.
Reactive Species in Sickle Cell Disease
Abstract
A bstract: The red cell is a relatively abundant locus of both free radical generation and reaction. Erythrocytes have a high content of unsaturated membrane lipids, a rich oxygen supply and are densely packed with redox‐active hemoglobin residues. In response, red cells have a highly evolved and well‐integrated network of oxidant defense mechanisms that lend an ability to withstand oxidative stress. In the case of congenital hemoglobin mutations that underlie sickle cell disease, they become very susceptible to free radical‐mediated injury by virtue of enhanced endogenous rates of production of reactive species and impairment of tissue free radical defense mechanisms. In sickle cell disease, a combination of these susceptibility factors are hypothesized to lead to an overall impairment of vascular function, in large part due to loss of “bioactive” nitric oxide via the free radical‐mediated consumption of this vasoactive molecule.
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“It has been reported that sickle cells produce greater amounts of O2•−, H2O2, and hydroxyl radical •OH compared with healthy RBCs (8, 80, 100).”
From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [8]
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Cites
Beckman, J. S., Beckman, T. W., Chen, J., Marshall, P. A., & Freeman, B. A. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.4.1620 · Cited by 7,029
Self-citationThe L-Arginine-Nitric Oxide Pathway
Epstein, F. H., Moncada, S., & Higgs, A. (1993) · New England Journal of Medicine · doi:10.1056/nejm199312303292706 · Cited by 6,678
Biology of disease: free radicals and tissue injury.
Freeman, B. Α., & Jd, C. (1982) · PubMed · Cited by 3,038
Self-citationWendel, A. (1981) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/s0076-6879(81)77046-0 · Cited by 3,032
Biochemistry of nitric oxide and its redox-activated forms
Stamler, J. S., Singel, D. J., & Loscalzo, J. (1992) · Science · doi:10.1126/science.1281928 · Cited by 2,744
The Pecking Order of Free Radicals and Antioxidants: Lipid Peroxidation, α-Tocopherol, and Ascorbate
Buettner, G. R. (1993) · Archives of Biochemistry and Biophysics · doi:10.1006/abbi.1993.1074 · Cited by 2,417
Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factor
Gryglewski, R. J., Palmer, R. M. J., & Moncada, S. (1986) · Nature · doi:10.1038/320454a0 · Cited by 2,400
Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia
Charache, S., Terrin, M. L., Moore, R. D., Dover, G. J., Barton, F. B., Eckert, S. V., McMahon, R. P., & Bonds, D. R. (1995) · New England Journal of Medicine · doi:10.1056/nejm199505183322001 · Cited by 2,340
Radí, R., Beckman, J. S., Bush, K. M., & Freeman, B. Α. (1991) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(91)90224-7 · Cited by 2,201
Self-citationHyperhomocysteinemia: An Independent Risk Factor for Vascular Disease
Clarke, R., Daly, L., Robinson, K., Naughten, E. R., Cahalane, S. F., Fowler, B., & Graham, I. M. (1991) · New England Journal of Medicine · doi:10.1056/nejm199104253241701 · Cited by 2,160
Research works printed but not linked: 11
- Embury S.H. R.P. Hebbel N. Mohandas & M.H. Steinberg. 1996.InSickle Cell Disease. Philadelphia New York. Lippincott‐Raven.
- Sadrzadeh S.M.H., 1984, Hemoglobin, J. Biol. Chem., 259, 14354
- Chui D., 1979, Abnormal vitamin E and Glutathione peroxidase levels in sickle cell anemia, J. Clin. Med., 94, 542
- Enwonwu C.O., 1989, Increased metabolic demand for arginine in sickle cell anaemia, Med. Sci. Res., 17, 997
- 10.1097/00000441-199012000-00005 · DOI
- 10.1016/S0002-9343(97)00129-0 · DOI
- 10.1056/NEJM196310242691701 · DOI
- 10.1016/S0002-9343(97)00129-0 · DOI
- 10.1111/j.1365-2796.1995.tb00884.x · DOI
- 10.1093/ajcn/40.2.235 · DOI
- 10.3109/10715769609149918 · DOI
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Intravascular hemolysis and the pathophysiology of sickle cell disease
Kato, G. J., Steinberg, M. H., & Gladwin, M. T. (2017) · Journal of Clinical Investigation · doi:10.1172/jci89741 · Cited by 748
Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia
Kuhn, V., Diederich, L., Keller, T. C. S., Kramer, C. M., Lückstädt, W., Panknin, C., Suvorava, T., Isakson, B. E., Kelm, M., & Cortese-Krott, M. M. (2017) · Antioxidants & Redox Signaling · doi:10.1089/ars.2016.6954 · Cited by 469
Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease
Aslan, M., Ryan, T. M., Adler, B., Townes, T. M., Parks, D. A., Thompson, J. A., Tousson, A., Gladwin, M. T., Patel, R. P., Tarpey, M. M., et al. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.221292098 · Cited by 391
Self-citationRedox and antioxidant systems of the malaria parasite Plasmodium falciparum
Müller, S. (2004) · Molecular Microbiology · doi:10.1111/j.1365-2958.2004.04257.x · Cited by 307
Walter, P. B., Fung, E. B., Killilea, D. W., Jiang, Q., Hudes, M. L., Madden, J., Porter, J. B., Evans, P., Vichinsky, E. P., & Harmatz, P. (2006) · British Journal of Haematology · doi:10.1111/j.1365-2141.2006.06277.x · Cited by 291
Metadata
- Authors
- ASLAN, M., THORNLEY‐BROWN, D., & FREEMAN, B. A.
- Affiliations
- University of Alabama at Birmingham (US)
- ORCID
- ASLAN, MUTAY
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2000-01
- Volume
- 899
- Issue
- 1
- Pages
- 375-391
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2010943728
- Cited by
- 136
- References
- 116
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 3 · 2021: 6 · 2020: 6 · 2019: 9 · 2018: 7 · 2017: 8 · 2016: 7 · 2015: 9 · 2014: 8 · 2013: 5 · 2012: 7
- FWCI
- 0.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Genetics (clinical) › Hemoglobinopathies and Related Disorders
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Hemoglobin structure and function
- Keywords
- sickle cell disease, reactive oxygen species, free radicals, erythrocytes, oxidative stress, hemoglobin, nitric oxide, vascular function
- MeSH terms
- Anemia, Sickle Cell, Humans, Reactive Oxygen Species
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