Introduction to free radicals and ageing


What are free radicals?

You have probably heard about these factors before, but what do they do and why are they important in ageing? Free radicals are produced in our cells and tissues every day, as part of their normal functioning, but they quietly go about damaging our tissues and organs without us realizing it.

As we age, our bodies naturally produce more free radicals. As yet, we don’t know whether the damage of free radicals causes aging, or vice versa. We just know that happen at the same time.

What are the different types of free radicals?

One of the major types of free radicals are called reactive oxygen species (ROS). These are produced when food macronutrients are broken down in our bodies, along with the oxygen we breathe in, to produce energy in a microscopic part of the cell called mitochondria [1]. Mitochondria are known to become faulty as we age, resulting in more ROS production [2].

ROS are short lived but can cause damage to DNA, lipids and other parts of cells all over the body. Under normal circumstance, this small amount of ROS is actually beneficial for the cell in supporting physiological function [3]. But they are increased when we have an infection or injury, and are associated with different health problems such as diabetes[3, 4]. They can also start a chain reaction that leads to other kinds of toxic products being produced in a process called oxidative stress.

Another type of free radical is reactive nitrogen species (RNS). These come from within blood vessels from the production of nitric oxide, a compound that is used to promote healthy circulation. Overproduction of RNS leads to a similar process called nitrosative stress [5].

Antioxidants – protection against oxidative stress

As a protective mechanism, the body naturally produces antioxidants to re-balance ROS and oxidative stress. But the body’s ability to make antioxidants like SOD, CAT and GPX also decreases with age.

Therefore, dietary sources of antioxidants are advocated for those of advancing age, and why antioxidants are said to have “anti-aging” effects, putting the brakes on oxidative stress and the problems that follow from it.

External factors that can elevate ROS include poor diet, alcoholism, smoking and some prescription medication [3]. Importantly, if more than one of these factors are present (e.g. older in age, obese and poor diet) it accelerates the development of oxidative stress [3]. Some more bad news is, once oxidative stress is established, excess ROS further drives the progression of chronic disease or in this case, the effects of ageing [3]. This creases a “vicious cycle” that continuously degrades cellular and ultimately, tissue/organ function over time [1].

How can we control free radicals as we age?

Being mindful of how our lifestyle choices can impact upon our overall long-term health is an important consideration, especially for those approaching middle-age. Excessive ROS and oxidative stress can affect every cell in your body from head-to-toe, inside-to-outside. Therefore, the consumption of antioxidants can help reduce the burden induced by excessive ROS and alleviate oxidative stress, in combination with a healthy diet, adequate physical activity, decreased stress, and cutting out some of those poor lifestyle choices.


  1. Hajam, Y.A., et al., Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives. Cells, 2022. 11(3): p. 552.
  2. Bratic, A. and N.G. Larsson, The role of mitochondria in aging. J Clin Invest., 2013. 123(3): p. 951-7. doi: 10.1172/JCI64125. Epub 2013 Mar 1.
  3. Pizzino, G., et al., Oxidative Stress: Harms and Benefits for Human Health. Oxidative medicine and cellular longevity, 2017. 2017: p. 8416763-8416763.
  4. Liguori, I., et al., Oxidative stress, aging, and diseases. Clin Interv Aging, 2018. 13: p. 757-772.
  5. Pacher, P., et al., Role of nitrosative stress and peroxynitrite in the pathogenesis of diabetic complications. Emerging new therapeutical strategies. Curr Med Chem, 2005. 12(3): p. 267-75. doi: 10.2174/0929867053363207.

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