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Updated: Apr 25, 2026
07:35
Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
Published on: June 1, 2022
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Nutritional programming of coenzyme Q: potential for prevention and intervention?
Jane L Tarry-Adkins1, Denise S Fernandez-Twinn2, Jian-Hua Chen2
1Metabolic Research Laboratories, Institute of Metabolic Science, University of Cambridge, Cambridge, UK; and janeadkins@googlemail.com.
Summary
Early life nutrition impacts cardiovascular health. Supplementing with coenzyme Q (CoQ) in at-risk individuals may prevent programmed aging and reduce cardiovascular disease risk.
Area of Science:
- Biomedical Science
- Nutritional Science
- Cardiovascular Research
Background:
- Low birth weight and rapid postnatal growth are linked to increased cardiovascular disease (CVD) risk.
- Underlying mechanisms remain unclear, but programmed deficits in cardiac coenzyme Q (CoQ) and accelerated aging were previously observed in rats.
- It is unknown if this CoQ deficit extends to clinically accessible tissues.
Purpose of the Study:
- To investigate if suboptimal early nutrition programs CoQ deficits in the aorta and white blood cells (WBCs) in rats.
- To determine if postweaning dietary CoQ supplementation can prevent programmed accelerated aging.
- To explore the potential of WBC CoQ levels as a diagnostic marker for vascular aging.
Main Methods:
- Rats were exposed to a low-protein diet in utero and underwent postnatal catch-up growth (recuperated).
- Aortic and WBC CoQ levels, aortic telomere length, DNA damage, oxidative stress markers, and mitochondrial activity were assessed.
- Some recuperated rats received postweaning dietary CoQ supplementation.
Main Results:
- Recuperated rats showed significantly reduced aortic CoQ levels at both 22 days and 12 months.
- Accelerated aortic telomere shortening, increased DNA damage, oxidative stress, and decreased mitochondrial complex II-III activity were observed in recuperated rats.
- Postweaning CoQ supplementation prevented these detrimental programming effects.
- Recuperated WBCs also exhibited reduced CoQ, and WBC CoQ levels strongly correlated with aortic telomere length.
Conclusions:
- Suboptimal early nutrition programs CoQ deficits in the aorta and WBCs, contributing to accelerated vascular aging.
- Early intervention with CoQ supplementation can prevent these programmed effects.
- WBC CoQ levels may serve as a valuable, non-invasive diagnostic marker for vascular aging in at-risk individuals.
- CoQ supplementation represents a potential cost-effective strategy to mitigate the global burden of CVDs.
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