Oxidative Stress: What is it?

Oxidative Stress Simplified

Oxidative stress is an imbalanced state in the body that represents an elevated level of free radical production coupled with a low level of antioxidant compounds to counteract the damaging cellular affects.  Thus, the result may lead to oxidative modifications of proteins, lipids, DNA, and other cellular structures vital to optimal health and body function.

Free radicals refer to unstable and highly reactive molecules capable of attacking other important macromolecules in the body (such as protein).

Antioxidant compounds scavenge, neutralise, and prevent free radical damage to help restore homeostasis, or balance, to the body.

Examples of antioxidants include lycopene in tomatoes, vitamin C, E, A, the minerals selenium and zinc, and other phytonutrients, including anthocyanins in cranberries and sulforaphane from brassica vegetables.

How does free radical damage contribute to chronic disease?

Free radical damage can create a state of chronic inflammation and a breakdown of important cellular defence molecules in the body.  Overtime, this leads to degeneration and loss of function of these affected structures.

Free radical damage is implicated in cardiovascular disease, neurogenerative diseases, carcinogenesis, cancer, autoimmune conditions, accelerated aging, and oxidative damage to DNA.

How does the body defend itself against free radical damage?

The first line of defence includes internally produced enzymes, which help to suppress the formation of free radicals.  Such compounds include glutathione perioxidase, glutathione-s-transferase, and phospholipid hydroperoxide glutathione perioxidase.  These are deemed antioxidant enzymes.

The second set of troupes called in are external sources of compounds, obtained from foods, including the pre-formed compounds from foods that are activated by internally produced enzymes.  These compounds include vitamin C, vitamin E, and ubinquinol (Co Enzyme Q10).

Lastly, proteolytic enzymes, such as proteinases, proteases, and peptidases present in the fluid of the mitochondria of our body cells (the ‘powerhouse’ of the cell) recognise, degrade, and remove damaged proteins to prevent further accumulation.

How can I protect myself against free radical damage?

Arguably, diet and lifestyle factors are the two most important modifications you can make to protect yourself against chronic disease.

The field of epigenetics refers to the effect diet and lifestyle factors has on the expression of our genes, switching ‘on’ or ‘off’ particular pathways that may exacerbate or decrease our body’s protective mechanisms.

It is important to note that even ‘healthy’ activities will produce free radicals—our bodies produce them as natural byproducts of detoxification!

Many people are surprised to know exercise and physical activity produces free radicals.  This doesn’t mean you need to put an end to your weekly workouts.  It’s all about balance.  In order to achieve healthy and longevity, you must counteract the ‘bad’ with the ‘good’.

Particular foods that are high in antioxidants include:

  • Broccoli and broccoli sprouts
  • Leeks, onions, garlic
  • Berries (blueberries, cherries, raspberries, blackberries)
  • Artichokes
  • Spinach (including other leafy greens)
  • Asparagus
  • Pecans, walnuts, pumpkin seeds, flax seeds, hemp seeds
  • Alfalfa sprouts, radish sprouts
  • Watercress
  • Tomatoes (antioxidant value increases when cooked)

Lifestyle factors include:

  • Stress management
  • Exercise (including both cardio and most importantly, weight training)
  • Relaxation
  • Work/life balance
  • Stretching
  • Good oral hygiene
  • Low screen time
  • 7-8 hour of sleep per night

Amanda Harasym

Naturopath, Nutritionist, Herbalist



Lobo V, Patil A, Phatak A, Chandra N. Free radicals, antioxidants, and functional foods: impact on human health. Pharmacogn Rev. 2010 July-Dec; 4(8): 118-126. Doi: 10.4103/0973-7847.70902.

Zhao H, Han Z, Ji X, Luo Y. Epigenetic regulation of oxidative stress in ischemic stroke. Aging Dis. 2016 May; 7(3): 295-306.  Doi: 10.14336/AD.2015.1009.


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