Oxidative stress and ageing
Open accessAbstract
Oxidative stress is the resultant damage due to redox imbalances (increase in destructive free radicals [reactive oxygen species (ROS)] and reduction in antioxidant protection/pathways) and is linked to ageing in many tissues including skin. In ageing skin there are bioenergetic differences between keratinocytes and fibroblasts which provide a potential ageing biomarker. The differences in skin bioenergy are part of the mitochondrial theory of ageing which remains one of the most widely accepted ageing theories describing subsequent increasing free radical generation. Mitochondria are the major source of cellular oxidative stress and form part of the vicious cycle theory of ageing. External and internal sources of oxidative stress include UVR/IR, pollution (environment), lifestyle (exercise and diet), alcohol and smoking all of which may potentially impact on skin although many exogenous actives and endogenous antioxidant defence systems have been described to help abrogate the increased stress. This also links to differences in skin cell types in terms of the UVR action spectrum for nuclear and mitochondrial DNA damage (the latter a previously described UVR biomarker in skin). Recent work associates bioenergy production and oxidative stress with pigment production thereby providing another additional potential avenue for targeted anti-ageing intervention in skin. This new data supporting the detrimental effects of the numerous wavelengths of UVR may aid in the development of cosmetic/sunscreen design to reduce the effects of photoageing. Recently, complex II of the mitochondrial electron transport chain appears to be more important than previously thought in the generation of free radicals (suggested predominantly by non-human studies). We investigated the relationship between complex II and ageing using human skin as a model tissue. The rate of complex II activity per unit of mitochondria was determined in fibroblasts and keratinocytes cultured from skin covering a wide age range. Complex II activity significantly decreased with age in fibroblasts (P = 0·015), but not in keratinocytes. This was associated with a significant decline in transcript expression (P = 0·008 and P = 0·001) and protein levels (P = 0·0006 and P = 0·005) of the SDHA and SDHB catalytic subunits of complex II respectively. In addition there was a significant decrease in complex II activity with age (P = 0·029) that was specific to senescent skin cells, our study being the first to investigate these differences with senescence and skin age. There was no decrease in complex IV activity with increasing age, suggesting possible locality to complex II. Our study provides a future potential biomarker for monitoring the progression of skin ageing.
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Written from the paper’s full text.
TL;DR
This review links oxidative stress and mitochondrial dysfunction, particularly complex II, to skin ageing, with bioenergetic differences between keratinocytes and fibroblasts as potential ageing biomarkers. It reports that complex II activity, SDHA/SDHB transcript and protein levels decline with age in fibroblasts and in senescent skin cells, while complex IV activity does not.
Key findings
- In human skin cells, complex II activity per unit mitochondria significantly decreased with age in fibroblasts (P=0.015), but not in keratinocytes; this was associated with significant declines in SDHA and SDHB transcript expression (P=0.008 and P=0.001) and protein levels (P=0.0006 and P=0.005), respectively.
- Complex II activity also significantly decreased with age specifically in senescent skin cells (P=0.029); no decrease in complex IV activity with increasing age was observed, suggesting possible locality to complex II.
- Mitochondria produce approximately 90% of cellular energy via oxidative phosphorylation and the electron transport chain, and are a major source of cellular ROS; mtDNA is vulnerable due to proximity to the ETC and limited repair mechanisms.
- Solar radiation is approximately 6% UVR, 40% visible light, and 54% infrared; UVR is described as the main extrinsic influence on skin ageing, and external/internal ROS sources include UVR/IR, pollution (ultrafine particles <0.1 μm), lifestyle, alcohol, and smoking.
Methods
- Narrative review of the mitochondrial free radical theory of ageing and oxidative stress in skin, incorporating the authors’ human skin cell investigation.
- The investigation used fibroblasts and keratinocytes cultured from skin covering a wide age range; complex II activity per unit mitochondria was determined, along with transcript and protein levels of the SDHA and SDHB catalytic subunits, and comparisons with senescence and complex IV.
- Main analysis reported P-values for age-related changes; no systematic review methods or detailed experimental protocol are provided in this text.
Limitations
- Stated: the exact causes of ageing remain unknown; further work is required to support the relationship between pollution and premature ageing via mitochondria-mediated mechanisms; complex II’s importance in free radical generation is suggested predominantly by non-human studies.
- Evident: as a narrative review, it lacks systematic search/inclusion criteria and does not report sample size, age range, culture conditions, or full statistical models for the original skin cell data.
- Evident: many mechanistic claims rely on cited studies rather than new data, and the review notes ROS can have beneficial signalling roles, complicating antioxidant targeting.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
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- Findingown data§ Summary
The age-related decrease in complex II activity in fibroblasts was associated with a significant decline in transcript expression of the SDHA and SDHB catalytic subunits of complex II.
“This was associated with a significant decline in transcript expression ( P =0.008 and P =0.001) and protein levels ( P =0.0006 and P =0.005) of the SDHA and SDHB catalytic subunits of complex II respectively.”
Quote in the paperSubstantial claim - Findingown data§ Summary
There was no decrease in complex IV activity with increasing age.
“There was no decrease in complex IV activity with increasing age, suggesting possible locality to complex II.”
Quote in the paperSubstantial claim - Findingown data§ Summary
There was a significant decrease in complex II activity with age that was specific to senescent skin cells.
“In addition there was a significant decrease in complex II activity with age ( P =0.029) that was specific to senescent skin cells, our study being the first to investigate these differences with senescence and skin age.”
Quote in the paperSubstantial claim - Findingown data§ Summary
The age-related decrease in complex II activity in fibroblasts was associated with a significant decline in protein levels of the SDHA and SDHB catalytic subunits of complex II.
“This was associated with a significant decline in transcript expression ( P =0.008 and P =0.001) and protein levels ( P =0.0006 and P =0.005) of the SDHA and SDHB catalytic subunits of complex II respectively.”
Quote in the paperSubstantial claim - Premisecitation§ Sources of ROS
Pollution is another major environmental cause of ROS production.
“Pollution is another major environmental cause of ROS production [Koohgoli et al., 2016].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Koohgoli et al., 2016
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- Interpretationown data§ Summary
In ageing skin there are bioenergetic differences between keratinocytes and fibroblasts which provide a potential ageing biomarker.
“In ageing skin there are bioenergetic differences between keratinocytes and fibroblasts which provide a potential ageing biomarker.”
Quote in the paperSubstantial claim- Rests on an assumption: Cultured fibroblasts and keratinocytes from skin covering a wide age range are representative of in vivo skin ageing.
- Rests on an assumption: The senescent skin cell model reflects the senescent state of cells in aged skin in vivo.
- Rests on an assumption: Complex II activity per unit mitochondria measured in vitro reflects mitochondrial function in vivo.
- Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and Senescence
More recently complex II has been shown to be implicated in human dermal fibroblast senescence and ageing.
“More recently complex II has been shown to be implicated in human dermal fibroblast senescence and ageing [Anderson et al., 2014; Bowman and Birch-Machin, 2016; Boulton and Birch-Machin 2015].”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites Anderson et al., 2014 source
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- cites Bowman and Birch-Machin, 2016
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- cites Boulton and Birch-Machin 2015
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- Interpretationown data§ Summary
The study provides a future potential biomarker for monitoring the progression of skin ageing.
“Our study provides a future potential biomarker for monitoring the progression of skin ageing.”
Quote in the paperSubstantial claim- Rests on an assumption: Cultured fibroblasts and keratinocytes from skin covering a wide age range are representative of in vivo skin ageing.
- Rests on an assumption: The senescent skin cell model reflects the senescent state of cells in aged skin in vivo.
- Rests on an assumption: Complex II activity per unit mitochondria measured in vitro reflects mitochondrial function in vivo.
- Interpretationown data§ Summary
The lack of decrease in complex IV activity with increasing age suggests possible locality to complex II.
“There was no decrease in complex IV activity with increasing age, suggesting possible locality to complex II.”
Quote in the paperSubstantial claim - Premisecitation§ Sources of ROS
Tomato paste can protect human skin against UVR-induced effects partially mediated by oxidative stress such as erythema and extracellular changes such as mtDNA damage.
“In addition, a study showed that tomato paste can protect human skin against UVR-induced effects partially mediated by oxidative stress such as erythema (skin redness) and extracellular changes such as mtDNA damage [Rizwan et al., 2011].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Rizwan et al., 2011 source
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- Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and Senescence
Mitochondrial dysfunction is thought to play a role in the increased levels of senescent cells observed with age.
“Mitochondrial dysfunction is thought to play a role in the increased levels of senescent cells observed with age [Passos et al., 2007; Birket et al., 2009; Passos et al., 2010] .”
Quote in the paperNot a substantial claim0 of 3 sources checked - Premisecitation§ Sources of ROS
mtDNA is an established biomarker of UVR-induced damage.
“This has led to the development of mtDNA as an established biomarker of UVR-induced damage [Birch-Machin et al., 2013].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Birch-Machin et al., 2013 source
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- Premisecitation§ Sources of ROS
Inducers of ROS, for example smoking and UVR exposure, can reduce levels of carotenoid antioxidants and thereby further potentiate levels of oxidative stress.
“Inducers of ROS, for example smoking and UVR exposure, can reduce levels of carotenoid antioxidants and thereby further potentiate levels of oxidative stress [Darvin et al., 2008].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Darvin et al., 2008 source
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- Premisecitation§ Sources of ROS
Mitochondria are responsible for the production of the majority of ROS within a cell.
“Mitochondria are responsible for the production of the majority of ROS within a cell, and these potentially harmful radicals are modulated by the expression of endogenous antioxidants involving the nuclear factor erythroid 2-related factor 2 (Nrf2)- kelch-like ECH-associated protein 1 (Keap1) pathway [Magesh et al., 2012] or via external anti-oxidants in the diet [Birch-Machin and Oyewole 2015;”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Magesh et al., 2012 source
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- Classified as probably not a substantial claim. 8
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Findingown data§ SummaryComplex II activity significantly decreased with age in fibroblasts, but not in keratinocytes.
“Complex II activity significantly decreased with age in fibroblasts ( P =0.015), but not in keratinocytes.”
Quote in the paperSubstantial claimMay combine two claims.
Premisecitation§ Sources of ROSUVR is the main extrinsic influence of skin ageing; either by the production of ROS or via direct DNA damage.
“UVR is the main extrinsic influence of skin ageing [Kandola et al., 2015; Oyewole et al., 2013]; either by the production of ROS or via direct DNA damage.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Kandola et al., 2015 source
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- cites Oyewole et al., 2013
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Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).
Interpretationcitation§ Sources of ROSSince ROS are important signalling molecules, the dose and target of the administered antioxidant would have to be considered to prevent the alteration of cellular homeostasis.
“Since ROS are important signalling molecules [Desler et al., 2011; Fischer et al., 2012], the dose and target of the administered antioxidant would have to be considered to prevent the alteration of cellular homeostasis.”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
Interpretationcitation§ Sources of ROSUVR may increase ROS levels, or cause mtDNA damage directly, which could result in an increase in mitochondrial dysfunction and a further production of ROS in a continuing vicious cycle and a putative increase in photoageing.
“UVR may increase ROS levels, or cause mtDNA damage directly, which could result in an increase in mitochondrial dysfunction and a further production of ROS in a continuing vicious cycle and a putative increase in photoageing, as mitochondria are thought to play a prominent role in this process [Kandola et al., 2015].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Kandola et al., 2015 source
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Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and SenescenceMore recently the process of mitohormesis has been proposed based on observations that low concentrations of ROS can induce a positive response whilst higher concentrations of ROS promotes damage; different levels of oxidative stress may have opposite biological outcomes.
“More recently the process of mitohormesis has been proposed based on observations that low concentrations of ROS can induce a positive response whilst higher concentrations of ROS promotes damage; an interesting concept that different levels of oxidative stress may have opposite biological outcomes [Hudson et al., 2016].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Hudson et al., 2016 source
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Premisecitation§ Sources of ROSThe skin can undergo two distinct types of ageing; intrinsic (chronological) and extrinsic ageing (photoageing) via environmental insults, such as ultra violet radiation (UVR).
“The skin can undergo two distinct types of ageing; intrinsic (chronological) and extrinsic ageing (photoageing) via environmental insults, such as ultra violet radiation (UVR) [Birket and BirchMachin 2007; Krutman and Schroeder 2009].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Birket and BirchMachin 2007
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- cites Krutman and Schroeder 2009
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Interpretationnone given§ Sources of ROSContinuing evidence supports the proposal that mitochondria are heavily implicated in the ageing process.
“Continuing evidence supports the proposal that mitochondria are heavily implicated in the ageing process and warrants further work in this intriguing area.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and SenescenceWithin this theory the Vicious Cycle Theory of Ageing was included which proposes that ROS production from the mitochondrial ETC is able to cause damage to the mtDNA found in close proximity.
“Within this theory the Vicious Cycle Theory of Ageing was included which proposes that ROS production from the mitochondrial ETC is able to cause damage to the mtDNA found in close proximity.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Bandy and Davison 1990
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- cites Kandola et al., 2015 source
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Premisereasoning§ The Mitochondrial Free Radical Theory of Ageing and SenescenceMtDNA encodes the majority of mitochondrial proteins, so errors in gene expression of mtDNA may result in dysfunctional mitochondrial subunits.
“MtDNA encodes the majority of mitochondrial proteins, so errors in gene expression of mtDNA may result in dysfunctional mitochondrial subunits.”
Quote in the paperNot a substantial claimMay combine two claims.
Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and SenescenceUnlike nuclear DNA (nDNA), multiple copies of mitochondrial DNA (mtDNA) exist within each cell and are found in close proximity to the electron transport chain (ETC) making them extremely vulnerable to the effects of oxidative stress, exacerbated further by the fact that mtDNA has limited repair mechanisms.
“Unlike nuclear DNA (nDNA), multiple copies of mitochondrial DNA (mtDNA) exist within each cell and are found in close proximity to the electron transport chain (ETC) making them extremely vulnerable to the effects of oxidative stress, exacerbated further by the fact that mtDNA has limited repair mechanisms [Anderson et al., 2014].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Anderson et al., 2014 source
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Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and SenescenceDysfunctional mitochondria are then thought to contribute to further ROS leakage due to their inefficiency, which could then exacerbate mtDNA damage in a continuing vicious cycle.
“Dysfunctional mitochondria are then thought to contribute to further ROS leakage due to their inefficiency, which could then exacerbate mtDNA damage in a continuing vicious cycle [Bandy and Davison 1990, Kandola et al., 2015].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Bandy and Davison 1990
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- cites Kandola et al., 2015 source
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Interpretationnone given§ Sources of ROSThe Mitochondrial Free Radical Theory of Ageing is one of the most accepted theories as to why we age.
“In conclusion, the Mitochondrial Free Radical Theory of Ageing is one of the most accepted theories as to why we age”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and SenescenceHarman proposed the 'free radical theory of ageing', which suggested that free radicals can affect and are possibly the cause of the ageing process of animals.
“Harman proposed the 'free radical theory of ageing', which suggested that free radicals can affect and are possibly the cause of the ageing process of animals. [Barja 2013].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Barja 2013 source
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Premisecitation§ The Mitochondrial Free Radical Theory of Ageing and SenescenceMitochondria are dynamic organelles found within the cytoplasm of eukaryotic cells, and are responsible for the production of the majority (approximately 90%) of cellular energy via oxidative phosphorylation and the electron transport chain (ETC), in the form of adenosine triphosphate (ATP).
“There are a large number of studies into how and why we age that involve the mitochondria which are dynamic organelles found within the cytoplasm of eukaryotic cells, and are responsible for the production of the majority (approximately 90%) of cellular energy via oxidative phosphorylation and the electron transport chain (ETC), in the form of adenosine triphosphate (ATP) [Birch-Machin 2006].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Birch-Machin 2006 source
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Premisereasoning§ The Mitochondrial Free Radical Theory of Ageing and SenescenceAs mtDNA encodes subunits of the ETC, ROS-induced damage has the potential to alter ETC function and decrease the efficiency of ATP production.
“As mtDNA encodes subunits of the ETC, ROS-induced damage has the potential to alter ETC function and decrease the efficiency of ATP production.”
Quote in the paperSubstantial claim
The paper relies on this without support.
Cultured fibroblasts and keratinocytes from skin covering a wide age range are representative of in vivo skin ageing.
“The rate of complex II activity per unit of mitochondria was determined in fibroblasts and keratinocytes cultured from skin covering a wide age range.”
The paper relies on this without support.
The senescent skin cell model reflects the senescent state of cells in aged skin in vivo.
“In addition there was a significant decrease in complex II activity with age ( P =0.029) that was specific to senescent skin cells, our study being the first to investigate these differences with senescence and skin age.”
The paper relies on this without support.
Complex II activity per unit mitochondria measured in vitro reflects mitochondrial function in vivo.
“The rate of complex II activity per unit of mitochondria was determined in fibroblasts and keratinocytes cultured from skin covering a wide age range.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Oxidation of lipids by ROS can damage cellular structures and result in premature cell death.
“Oxidation of lipids by ROS can damage cellular structures and result in premature cell death [13].”
From Oxidative Stress and Ageing: The Influence of Environmental Pollution, Sunlight and Diet on Skin (2017) · cites this paper as [13]
Interaction of ROS with nuclear and mitochondrial nucleic acids results in mutations that predispose them to strand breaks.
“In addition, interaction with nuclear and mitochondrial nucleic acids results in mutations that predispose them to strand breaks [13].”
From Oxidative Stress and Ageing: The Influence of Environmental Pollution, Sunlight and Diet on Skin (2017) · cites this paper as [13]
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- Authors
- Birch-Machin, M. A., & Bowman, A.
- Affiliations
- Dermatological Sciences; Institute of Cellular Medicine; Newcastle University (medical school); Newcastle upon Tyne NE24HH U.K
- Newcastle University (GB)
- ORCID
- Bowman, A.
- Venue
- British Journal of Dermatology
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-09-26
- Volume
- 175
- Pages
- 26-29
- ISSN
- 0007-0963 (ISSN-L)
- OpenAlex
- W2524832026
- Cited by
- 225
- References
- 33
- Citations by year
- 2026: 19 · 2025: 19 · 2024: 20 · 2023: 35 · 2022: 23 · 2021: 27 · 2020: 21 · 2019: 19 · 2018: 14 · 2017: 12 · 2016: 4 · 2015: 2 · 2014: 2 · 2013: 1
- FWCI
- 2.34
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- British Journal of Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- oxidative stress, skin aging, photoaging, succinate dehydrogenase, SDHA, SDHB, keratinocytes, fibroblasts, cellular senescence, reactive oxygen species, antioxidant defense, mitochondrial electron transport chain, ultraviolet radiation, mitochondrial DNA damage, cytochrome c oxidase, pigment production
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-10.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-10.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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