Antioxidants – Double Agents?

Did you know we offer a Winter School course in Communicating Science? If you’re interested in science writing for both specialist and non-specialist audiences, presenting to communicate science and the use of emerging online social media in science communication, this is a great course for you. If you’re interested, check out “Communicating Science” in course outlines for more details.

Over the coming weeks we’ll be showcasing blog posts written by Communicating Science students during their course last year. The next blog in the series is “Antioxidants – Double Agents?” by Alex Jackson.


In Western society, a commonly held belief is antioxidants (AOs) are “good”, and fight cancer. You can see this advertised everywhere – being high in AOs is a selling point of many foods, dietary supplements and cosmetics. Just looking through my cupboard at home, it wasn’t hard to find a product mentioning antioxidants.

Dilmah tea, which is “rich in antioxidants”. Credit: the mighty me.

Dilmah tea, which is “rich in antioxidants”.
Credit: the mighty me.

Here’s the basis of the “antioxidants fight cancer” claim. In our body, there are low levels of molecules called reactive oxygen species (ROS). Examples of ROS include hydrogen peroxide (H2O2), the hydroxyl radical (OH) and the superoxide ion (O2). As the name suggests, ROS are highly reactive, and can damage DNA and other biomolecules. DNA damage can be repaired, but our body’s repair mechanisms are not perfect, and genetic mutations can arise as a result of DNA damage. Mutations in our genetic code are the cause of cancer. What antioxidants do is neutralise the ROS by reacting with them, preventing damage to DNA and protecting us from cancer.

That actually sounds pretty good! But does it hold up under scientific scrutiny?

The answer is… sort of, but not necessarily. The effects of antioxidants aren’t so clear-cut as to be easily classified into categories of “good” or “bad”. There is evidence that AOs do have a preventative effect against the development of cancers. However, large randomised trials have been inconclusive.

The Normal Role of ROS

Reactive oxygen species are produced as part of normal cell function, albeit at very low levels. They are involved in cell signalling pathways that control cell proliferation and differentiation. Cancer cells often have higher levels of ROS than non-cancerous cells. This increases signalling which tells the cells to grow and divide, in addition to increasing oxidative damage to DNA which results in high mutation rates. However, high ROS levels can be toxic.  In particular, hydrogen peroxide can easily diffuse through the whole cell and cause damage, resulting in cell death.

Therefore, tumours need to manage their ROS levels and keep the levels below a certain threshold. Cancers often contain stores of natural AOs such as glutathione and thioredoxin. This allows tumours to increase ROS levels, increasing signalling, but oxidative stress is prevented by the natural AOs. Dietary AOs contribute to this pool of AOs. While they neutralise ROS which cause oxidative damage, they can’t readily access parts of the cell which have the “signalling ROS”. So the cancer cell keeps on proliferating, but isn’t overly damaged by the ROS.

Antioxidants accelerate tumour growth in mice

There is now growing evidence that in some cases, AOs help cancer cells proliferate. In their recent article, Sayin et al. showed that N-acetyl cysteine (NAC) and Vitamin E (VE) both increased lung tumour proliferation and reduced survival time in mice. NAC and VE are both antioxidants, but their structures are completely different. Given the results from NAC and VE were very similar, the team proposed that it was the two molecules’ antioxidant properties caused this result.
Their findings included:

  • NAC and VE decreased ROS damage in tumours.
  • NAC and VE also suppressed a gene called Trp53. This gene encodes the “tumour suppressor protein” called p53. Suppression of this gene means that tumours cannot be regulated effectively, and cancer growth is increased.
  • 2.8 times greater tumour burden in mice treated with NAC and VE compared with untreated mice.
N-acetyl-L-cysteine. ? Credit: Calvero

N-acetyl-L-cysteine. ?
Credit: Calvero

α-tocopherol, a.k.a. Vitamin E. Credit: Calvero

α-tocopherol, a.k.a. Vitamin E.
Credit: Calvero

The study was only on the effect of AOs on tumour progression, and didn’t touch upon tumour prevention. However, the authors suggest AOs should not be used for lung cancer patients, as this may promote their cancer.

It seems antioxidants are a more complex topic than many of us may have imagined. Hopefully, further research will better characterise the role of antioxidants in our body.

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