Oxidative Stress, ROS and Light
Oxidative stress does not appear suddenly, nor is it caused by a single factor. It is a process linked to the everyday functioning of cells, the activity of mitochondria, and the balance between physiological load and regeneration.
By looking at how the body responds to energy, light, and environmental conditions, it becomes easier to see why context matters more than any one factor on its own.
How Mitochondria, Redox Balance, and the Light Spectrum Shape Cellular Function
Introduction
Oxidative stress is one of the most frequently used terms in modern biology and medicine. It is often associated solely with “free radicals” and the ageing process, yet in reality it describes a phenomenon that is far more complex and dynamic. It is closely linked to cellular metabolism, mitochondrial function, and environmental influences, including light.
In this article, we clarify the key concepts and explore where reactive oxygen species (ROS) come from, what redox balance means, and how different ranges of the light spectrum may influence the body’s oxidative–reductive state.
What Is Oxidative Stress?
Oxidative stress is a state in which redox balance becomes disrupted, meaning that oxidative processes outweigh the body’s ability to regulate and neutralise them. It does not simply refer to the presence of ROS.
Reactive oxygen species are constantly produced in the body and are essential for life. They play signalling roles, participate in immune responses, and regulate many metabolic processes.
Problems arise when:
- The amount of ROS exceeds the cell’s regulatory capacity,
- Or antioxidant systems are unable to maintain redox balance.
Under these conditions, ROS lose their physiological role and begin to exert destabilising effects on cellular structures.
Where Do ROS Come From?
The vast majority of reactive oxygen species are generated inside cells, rather than as a result of external factors.
It is estimated that around 90–95% of ROS originate in the mitochondria, the structures responsible for energy production through cellular respiration.
During the production of energy in the form of ATP (adenosine triphosphate), the body’s main and universal energy carrier, oxygen participates in redox reactions, and a small fraction of it is converted into reactive oxygen species.
This is a natural part of metabolism and does not pose a threat on its own. Oxidative stress arises only when mitochondria operate under prolonged overload or when the cell’s ability to maintain redox balance becomes impaired.
Redox Balance as a Dynamic Process
The redox system is not a simple “on–off” state. It is a process of continuous regulation in which oxidation and reduction reactions occur simultaneously and balance one another.
Cells are adapted to function in an environment where ROS are constantly being produced. What matters most is not their temporary presence, but the duration and scale of any imbalance. Oxidative stress develops gradually, over weeks, months, or even years, rather than as a result of a single trigger.
Factors That Contribute to the Build-Up of Oxidative Stress
1 – Prolonged Metabolic Load
Oxidative stress is more likely to occur under conditions of chronically increased energy demand. This applies to situations in which cells operate for extended periods in a state of elevated metabolic activity, and mitochondria work more intensively than they do under balanced conditions.
One example of such a load can be excessive physical exertion, particularly when intense training is repeated frequently without sufficient recovery. Under these conditions, increased energy production is accompanied by a proportional rise in redox reactions, and consequently, greater ROS production.
2 – Chronic Inflammatory Processes
During inflammation, immune system cells intentionally produce ROS as part of their defence mechanisms. When inflammation is short-lived, these reactions remain tightly regulated.
However, when inflammation becomes chronic, ROS begin to exert broader effects, extending to tissues not directly involved in the immune response. In such cases, oxidative stress ceases to be a localised phenomenon and may begin to affect the functioning of the entire organism.
3 – Sleep Disruption, Recovery, and Circadian Rhythm
Sleep is a key period for regulating metabolism and maintaining redox balance. During sleep, the body slows down energy-demanding processes and activates cellular repair mechanisms. What matters is not only the duration of sleep, but also its quality and alignment with the natural circadian rhythm.
The circadian rhythm is the body’s internal biological clock that synchronises physiological functions with the day-night cycle. It influences, among other things, hormone secretion, mitochondrial activity, and the pace of metabolic processes. When this rhythm is disrupted, for example, by irregular sleep schedules or exposure to light at night, the body may remain in a state of heightened activity for longer periods.
Under such conditions, mitochondria work more intensively, and the natural slowing of energy-related processes becomes limited. If this state persists over time, it may contribute to the gradual build-up of oxidative stress, especially when regenerative processes do not have sufficient opportunity to restore redox balance.
4 – Chronic Physiological and Psychological Stress
Long-term stress, regardless of its nature, is associated with sustained activation of the body. This state affects cellular energy management by increasing energy demand and intensifying mitochondrial activity.
When stress persists over extended periods, it may become one of the factors that contribute to disruptions in redox balance, particularly when recovery is limited.
Light and Radiation in the Context of Oxidative Stress
Electromagnetic radiation spans the full spectrum of light – see here – from ultraviolet, through visible light, to red light and infrared. Each of these ranges carries energy that interacts with tissues and can influence biological processes at the cellular level.
In the context of oxidative stress, however, what matters most is not the wavelength itself, but the dose and duration of exposure. Excessive radiation exposure, regardless of the part of the spectrum, may increase the metabolic load on cells and promote increased production of reactive oxygen species (ROS). This becomes particularly relevant when mitochondria are already operating under conditions of energetic overload or limited recovery.
It is also important to emphasise that the biological effect of light depends on the context in which it acts. The same type of radiation can play different roles under different conditions, ranging from regulatory to burdensome. For this reason, light and radiation are best understood as part of a broader environmental background that modulates oxidative-reductive processes, rather than serving as their primary source.
Vitamin D and Oxidative Stress
In the context of oxidative stress, increasing attention is being paid to the role of vitamin D as a regulator of cellular processes, rather than solely as a component of calcium-phosphate metabolism. The active form of vitamin D influences the expression of genes involved in cellular function, including those related to the regulation of reactive oxygen species.
Studies observe associations between vitamin D levels and the activity of enzymes involved in maintaining redox balance.
Vitamin D is also linked to mitochondrial function. Through its role in cellular energy metabolism, it may be associated with the stability of redox processes, particularly under conditions of increased metabolic load or stress.
Vitamin D deficiency is not a direct cause of oxidative stress, but it may be associated with its persistence over time, especially when it is prolonged.
Final Thoughts
Oxidative stress develops over time and reflects how the body balances energy, exposure, and recovery. Seen this way, light, including sunlight, can be understood as part of a wider context.
Sources & Further Reading:
- ALAB Laboratoria – Educational lecture (video): dr n. med. Mirosław Mastej, pt:. “Stres Oksydacyjny Choroba Cywilizacyjna XXI wieku część I” na YouTube, 2020
- Murphy MP. How mitochondria produce reactive oxygen species. Biochem J. 2009 Jan 1;417(1):1-13. doi: 10.1042/BJ20081386. PMID: 19061483; PMCID: PMC2605959.
- Pizzino G, Irrera N, Cucinotta M, Pallio G, Mannino F, Arcoraci V, Squadrito F, Altavilla D, Bitto A. Oxidative Stress: Harms and Benefits for Human Health. Oxid Med Cell Longev. 2017;2017:8416763. doi: 10.1155/2017/8416763. Epub 2017 Jul 27. PMID: 28819546; PMCID: PMC5551541.
- Michael P. Murphy; How mitochondria produce reactive oxygen species, Biochem J 1 January 2009; 417 (1): 1–13.
- Brar G, Dhaliwal A, Brar A S, et al. (March 24, 2025) A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin. Cureus 17(3): e81109. doi:10.7759/cureus.81109
- Vázquez-Lorente H, Herrera-Quintana L, Jiménez-Sánchez L, Fernández-Perea B, Plaza-Diaz J. Antioxidant Functions of Vitamin D and CYP11A1-Derived Vitamin D, Tachysterol, and Lumisterol Metabolites: Mechanisms, Clinical Implications, and Future Directions. Antioxidants (Basel). 2024 Aug 17;13(8):996. doi: 10.3390/antiox13080996. PMID: 39199241; PMCID: PMC11351441.