The Oxidative Stress of Zinc Deficiency
Abstract
Zinc is an essential catalytic and structural cofactor for many enzymes and other proteins. While Zn2+ is not redox active under physiological conditions, it has been known for many years that zinc deficiency causes increased oxidative stress and, consequently, increased oxidative damage to DNA, proteins, and lipids. These results have indicated that zinc plays an indirect antioxidant role and that dietary inadequacy may contribute to human diseases such as cancer. Recent studies are helping to identify the primary sources of oxidative stress in low zinc. In addition, through studies of the model eukaryotic cell, Saccharomyces cerevisiae, we are now beginning to understand the strategies cells use to limit this stress and reduce its damage.
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In vitro, zinc deficiency is associated with increased ROS production, oxidative damage to DNA, proteins, and lipids, membrane destabilization, and dysregulation of metallothionein.
“In vitro studies have shown that Zn deficiency is associated with an increased production of ROS, oxidative damage to DNA, proteins and lipids, destabilization of membrane structure, dysregulation of Zn-binding protein metallothionein [426,429].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [429]
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- Authors
- Eide, D. J.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Eide, David J.
- ORCID
- Eide, David J.
- Venue
- Metallomics
- Publisher
- Oxford University Press (OUP)
- Published
- 2011
- Volume
- 3
- Issue
- 11
- Pages
- 1124
- ISSN
- 1756-5901 (ISSN-L)
- 1756-591X
- OpenAlex
- W2041573771
- Cited by
- 214
- References
- 62
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 21 · 2023: 13 · 2022: 15 · 2021: 23 · 2020: 17 · 2019: 16 · 2018: 7 · 2017: 13 · 2016: 6 · 2015: 18 · 2014: 23 · 2013: 13 · 2012: 7
- FWCI
- 1.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Metallomics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Missouri
- University of Minnesota
- University of Utah
- National Institutes of Health
- National Institute of General Medical Sciences (GM093303, R01GM056285, R01GM093303, GM056285)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- zinc deficiency, oxidative stress, DNA oxidation, protein oxidation, lipid peroxidation, zinc cofactor, Saccharomyces cerevisiae, cellular stress response, dietary zinc, cancer
- MeSH terms
- Animals, Antioxidants, Humans, Oxidation-Reduction, Saccharomyces cerevisiae, Zinc, Reactive Oxygen Species, Oxidative Stress
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