Antioxidant N-acetyl-L-cysteine ameliorates symptoms of premature aging associated with the deficiency of the circadian protein BMAL1
Open accessAbstract
Deficiency of the circadian clock protein BMAL1 leads to premature aging and increased levels of reactivate oxygen species in several tissues of mice. In order to investigate the role of oxidative stress in accelerated aging and development of age-related pathologies, we continuously administered the antioxidant N-acetyl-L-cysteine toBmal1-deficient mice through their entire lifespan by supplementing drinking water. We found that the life long treatment with antioxidant significantly increased average and maximal lifespan and reduced the rate of age-dependent weight loss and development of cataracts. At the same time, it had no effect on time of onset and severity of other age-related pathologies characteristic of Bmal1-/- mice, such as joint ossification, reduced hair regrowth and sarcopenia. We conclude that chronic oxidative stress affects longevity and contributes to the development of at least some age-associated pathology, although ROS-independent mechanisms may also play a role. Our bioinformatics analysis identified the presence of a conservative E box element in the promoter regions of several genes encoding major antioxidant enzymes. We speculate that BMAL1 controls antioxidant defense by regulating the expression of major antioxidant enzymes.
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Treating Bmal1−/− mice with the antioxidant N-acetyl-l-cysteine partially rescues their lifespan and prevents age-dependent pathology.
“Treating Bmal1−/− mice with the antioxidant N-acetyl-l-cysteine partially rescues their lifespan and prevents age-dependent pathology292.”
From Rhythms of life: circadian disruption and brain disorders across the lifespan (2019) · cites this paper as [292]
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- Authors
- Kondratov, R. V., Vykhovanets, O., Kondratova, A. A., & Antoch, M. P.
- Affiliations
- Cleveland State University (US)
- Cleveland Clinic (US)
- Roswell Park Comprehensive Cancer Center (US)
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2009-12-30
- Volume
- 1
- Issue
- 12
- Pages
- 979-987
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC2815755
- OpenAlex
- W2107213125
- Cited by
- 159
- References
- 29
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 4 · 2023: 11 · 2022: 14 · 2021: 11 · 2020: 13 · 2019: 8 · 2018: 16 · 2017: 12 · 2016: 9 · 2015: 8 · 2014: 13 · 2013: 10 · 2012: 7
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- National Cancer Institute (R01CA102522, CA102522)
- National Institute of General Medical Sciences (GM 075226, R01GM075226)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- N-acetylcysteine, Bmal1, circadian clock, premature aging, oxidative stress, reactive oxygen species, lifespan, antioxidant enzymes, E-box promoter elements, cataract, age-related diseases
- MeSH terms
- Acetylcysteine, Animals, Antioxidants, Arthritis, Body Weight, Catalase, Cataract, Pan troglodytes, Glutathione Peroxidase, Humans, Longevity, Macaca mulatta, Male, Ossification, Heterotopic, Superoxide Dismutase, Reactive Oxygen Species, Oxidative Stress, Aging, Premature, E-Box Elements, Mice, Rats, Peroxiredoxins, ARNTL Transcription Factors
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