Dietary supplements that contain antioxidants such as vitamin C can facilitate the growth of cancer and its spread to other areas of the body –metastasis–, according to new research from the Karolinska Institute (Sweden) that has found that these products stimulate the formation of new vessels blood vessels in lung cancer tumors.
“We found that antioxidants activate a mechanism that causes cancerous tumors to form new blood vessels, which is surprising because antioxidants were previously thought to have a protective effect. The blood vessels supply nutrients that help the tumor to grow and spread throughout the body,” explained Martin Bergö, professor at the department of life sciences and nutrition and vice-rector of the Karolinska Institutet, who led the study.
The ‘dark side’ of antioxidants
Antioxidants have beneficial properties for health because they are in charge of counteracting free oxygen radicals that can have harmful effects on the body, and for this reason they are usually incorporated into different food supplements; however, their consumption in excessively high doses can result in harmful.
“We have discovered that antioxidants activate a mechanism that causes cancerous tumors to form new blood vessels”
“Antioxidants in the regular diet are not to be feared, but most people don’t need an extra antioxidant supplement. It can even be harmful for cancer patients and people at increased risk of cancer,” Martin Bergö said. The results of the work have been published in the Journal of Clinical Investigation.
Martin Bergö’s research group had already shown that antioxidants such as vitamin C and E accelerate the growth and spread of lung cancer by stabilizing a protein called BACH1, which is activated when the level of oxygen free radicals decreases, something that it occurs when additional antioxidants are supplied through the diet, or when spontaneous mutations in tumor cells activate the body’s own antioxidants. These scientists have now been able to show that activation of BACH1 leads to increased formation of new blood vessels, known as angiogenesis.
“Several trials are underway with drugs that inhibit the formation of new blood vessels, so-called angiogenesis inhibitors, but the results have not been as successful as expected. Our study opens up more effective ways to prevent angiogenesis in tumors; for example, patients whose tumors have elevated BACH1 levels might respond better to angiogenesis inhibitor treatment than patients with low BACH1 levels,” says Ting Wang, PhD student in Martin Bergö’s research group at the Institute Karolinska.
The researchers used different cell biology methods and studied mainly lung cancer tumors using organoids (cultured microtumors from patients), but also mice and human breast and kidney cancer tumor samples. They found that tumors in which BACH1 was activated by antioxidant supplementation, or by overproduction of the BACH1 protein, produced more new blood vessels and were more sensitive to angiogenesis inhibitors.
“The next step is to investigate in detail how oxygen and free radical levels can regulate the BACH1 protein, and we will continue to study the clinical significance of our results. We will also continue similar studies in other forms of cancer, such as breast, kidney, and skin cancer,” concludes Ting Wang.
