The last two posts I wrote had a unifying theme: oxidative damage. The first post explored tissue-specific oxidative damage experienced by hibernating mammals. The second detailed how scientists are using mitochondria-specific antioxidants to limit oxidative damage in muscles while maintaining proper muscle cell signaling and function. While I think these specific occurrences of oxidative damage are fascinating, I think it’s important to take a step back and talk about oxidative damage and stress in a more general way.
What is oxidative damage?
Before answering this question, I’ll take one more step back and explain what oxidation and reduction are.
When a compound loses electrons, it is oxidized. When a compound gains electrons (and this is where it gets a little confusing to me), it is reduced. A common example of oxidation is found in the rusting process. When iron gives electrons to oxygen, iron is oxidized and oxygen is reduced to produce rust.
Perhaps a bit more interesting than the oxidation of iron is the oxidation that is constantly occurring in every one of your cells: the oxidation of nicotinamide adenine dinucleotide, or NADH. NADH is an important part of the electron transport chain, which is the series of proteins located in the mitochondria (the “powerhouses” of your cells) that transfer electrons from electron donors (like NADH) to electron acceptors (like oxygen). This transfer drives proton transport, which ultimately produces adenosine triphosphate (ATP), our essential cellular energy currency.
The electron transport chain in the cell is the site of oxidative phosphorylation. The NADH and succinate generated in the citric acid cycle are oxidized, releasing energy to power the ATP synthase. Via Wikimedia.
Oxygen molecules that have grabbed electrons from NADH are highly unstable and are quick to react with macromolecules in the cell, including DNA, lipids (fats) and amino acids (the building blocks of proteins). The interaction of these so-called reactive oxygen species (ROS) can interfere with macromolecular structure and function. Essentially, this is the process of oxidative damage.
Importantly, ROS can also be taken into the body through ingestion or inhalation of environmental pollutants. These include cigarette smoke, pesticides, some household cleaners and ozone.
(For more on the basics of oxidation/reduction and ROS, consult this thorough review.)
What is the difference between oxidative damage and oxidative stress?
This question is simpler to answer. I’ve already described the process of oxidative damage: ROS interference with macromolecular structure and function. But how does this process relate to oxidative stress? Basically, oxidative stress is a state of overwhelming oxidative damage. Oxidative damage can be counteracted by compounds we’ve all heard of: antioxidants. Antioxidants produced by our bodies or ingested through the food we eat essentially neutralize ROS, preventing these wild molecules from damaging our macromolecules.
Even if you are a non-smoker living in a pristine, unpolluted environment, your mitochondria are constantly pumping out reactive oxygen species. Fortunately, your body is also continually producing antioxidants. When ROS and antioxidants are present in similar quantities, these two types of compounds balance each other out and little to no oxidative stress is present. It is when ROS outnumber available antioxidants that oxidative damage can spin out of control and become oxidative stress.
Editor’s note: It’s important to point out that ROS are not inherently “bad” – in fact, ROS are very important signaling molecules in the body. ROS are formed in response to metabolism and activities such as exercise, and actually activate adaptive stress responses such as production of natural antioxidants in the body. It is for this reason that taking strong antioxidant supplements, beyond consumption of naturally antioxidant-rich foods, can in cases be detrimental, for example by blocking adaptive stress responses when taken before exercise. However, here we are mostly considering the impacts of an overabundance of ROS.
What are the health implications of oxidative damage/stress?
As ROS can damage the very building blocks of life, it is intuitive that long-term, unchecked oxidative stress can have deleterious effects on the body. Oxidative damage and stress are associated with many diseases, including cancer, atherosclerosis (hardening of the arteries), diabetes and neurogenerative diseases (illnesses that impair brain and nervous system function). Oxidative stress is also thought to accelerate aging, although this theory remains controversial.
Even though ROS are continuously being internally produced and externally introduced, there are many ways in which we can work to limit the amount of damage that these molecules can cause. Minimizing and coping with stress is an essential strategy in supporting health. Physiological stress, such as that experienced through school, work and childrearing, increases markers of oxidative stress and can shorten telomeres, the protective sequences at the ends of our chromosomes. To support ourselves in times of stress, we need to prioritize sleep, improve our diet by selecting a variety of antioxidant-rich foods, and incorporate regular exercise. Seeking to reduce stress (especially chronic stress) might be the most important thing we can do for our health and longevity, as a calm mind and body naturally lead to healthier and more self-positive choices.
Editor’s note: Learn more about harnessing health behaviors that can reduce oxidative stress, including mindfulness training, plant-based nutrition, exercise, intermittent fasting and adequate sleep, with LifeOmic’s LIFE Extend app.
