Free radicals, oxidative stress, and antioxidants in human health and disease
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Free radicals and other reactive oxygen species (ROS) are constantly formed in the human body. Free‐radical mechanisms have been implicated in the pathology of several human diseases, including cancer, atherosclerosis, malaria, and rheumatoid arthritis and neurodegenerative diseases. For example, the superoxide radical (O 2 ·− ) and hydrogen peroxide (H 2 O 2 ) are known to be generated in the brain and nervous system in vivo , and several areas of the human brain are rich in iron, which appears to be easily mobilizable in a form that can stimulate free‐radical reactions. Antioxidant defenses to remove O 2 ·− and H 2 O 2 exist. Superoxide dismutases (SOD) remove O 2 ·− by greatly accelerating its conversion to H 2 O 2 . Catalases in peroxisomes convert H 2 O 2 into water and O 2 and help to dispose of H 2 O 2 generated by the action of the oxidase enzymes that are located in these organelles. Other important H 2 O 2 ‐removing enzymes in human cells are the glutathione peroxidases. When produced in excess, ROS can cause tissue injury. However, tissue injury can itself cause ROS generation (e.g., by causing activation of phagocytes or releasing transition metal ions from damaged cells), which may (or may not, depending on the situation) contribute to a worsening of the injury. Assessment of oxidative damage to biomolecules by means of emerging technologies based on products of oxidative damage to DNA (e.g., 8‐hydroxydeoxyguanosine), lipids (e.g., isoprostanes), and proteins (altered amino acids) would not only advance our understanding of the underlying mechanisms but also facilitate supplementation and intervention studies designed and conducted to test antioxidant efficacy in human health and disease.
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“Increasing evidence has suggested that these diseases may result from cellular damage caused by free radicals [16,17].”
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Not aging but calorie restriction strongly affects protein oxidation in heart and brain mitochondria
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- Authors
- Aruoma, O. I.
- Affiliations
- King's College London (GB)
- Corresponding author
- Aruoma, Okezie I.
- ORCID
- Aruoma, Okezie I.
- Venue
- Journal of the American Oil Chemists' Society
- Publisher
- Wiley
- Published
- 1998-02
- Volume
- 75
- Issue
- 2
- Pages
- 199-212
- ISSN
- 0003-021X (ISSN-L)
- 1558-9331
- PMC
- PMC7101596
- OpenAlex
- W2078601501
- Cited by
- 1,682
- References
- 165
- Citations by year
- 2026: 24 · 2025: 46 · 2024: 64 · 2023: 55 · 2022: 97 · 2021: 88 · 2020: 85 · 2019: 108 · 2018: 81 · 2017: 97 · 2016: 84 · 2015: 94 · 2014: 115 · 2013: 101 · 2012: 96
- FWCI
- 6.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of the American Oil Chemists Society (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Nestec
- World Cancer Research Fund
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- free radicals, reactive oxygen species, oxidative stress, antioxidants, superoxide, hydrogen peroxide, superoxide dismutase, catalase, glutathione peroxidase, peroxisomes, oxidative DNA damage, 8-hydroxy-2'-deoxyguanosine, isoprostanes, oxidative protein damage, antioxidant supplementation, iron, phagocytes, transition metal ions, cancer, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, malaria
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