According to research published in The Journal of Clinical Investigation, vitamin C and additional antioxidants can encourage the growth of new blood vessels in lung cancer tumors. The research was conducted by a team from the Karolinska Institute in Sweden. This lends support to the idea that taking too many dietary supplements containing antioxidants may hasten the growth and metastasis of tumors.

Study leader Martin Bergo, Professor at the Department of Biosciences and Nutrition at Karolinska Institute in Sweden said, “We’ve found that antioxidants activate a mechanism that causes cancer tumors to form new blood vessels, which is surprising, since it was previously thought that antioxidants have a protective effect.” “The new blood vessels nourish the tumors and can help them grow and spread,” Bergo added.

Antioxidants neutralize free oxygen radicals, which can damage the body, and are therefore commonly found in dietary supplements. But overly high doses can be harmful. “There’s no need to fear antioxidants in normal food but most people don’t need additional amounts of them,” Bergo said.

“In fact, it can be harmful for cancer patients and people with an elevated cancer risk.” Prof. Bergo’s research group has previously shown that antioxidants like vitamin C and E accelerate the growth and spread of lung cancer by stabilizing a protein called BACH1.

When free oxygen radicals decrease, BACH1 becomes active, as when additional antioxidants are introduced through diet or when spontaneous mutations in tumor cells activate internal antioxidants. The researchers demonstrated that activating BACH1 causes the formation of new blood vessels, a process known as angiogenesis.

Researchers discovered that tumors can form blood vessels even when oxygen levels are normal, using a mechanism similar to the Nobel Prize-winning HIF-1alpha protein, indicating that HIF-1alpha and BACH1 collaborate within tumors.

Ting Wang, doctoral student in Professor Bergo’s group at Karolinska Institute said, “Many clinical trials have evaluated the efficacy of angiogenesis inhibitors, but the results have not been as successful as anticipated.”

“Our study opens the door to more effective ways of preventing angiogenesis in tumors, for example, patients whose tumors exhibit high levels of BACH1 might benefit more from anti-angiogenesis therapy than patients with low BACH1 levels.”

The researchers used a variety of cell-biological methods and focused on lung cancer tumors by studying organoids, which are small cultivated micro tumors from patients. They did, however, study mice as well as human breast and kidney tumor samples.

Tumors that were activated by BACH1, either through ingested antioxidants or by overexpression of the BACH1 gene, produced more new blood vessels and were more sensitive.

“The next step is in detail how levels of oxygen and free radicals can regulate the BACH1 protein, and we will continue to determine the clinical relevance of our results,” Wang said. “We’ll also be doing similar studies in other cancer forms such as breast, kidney and skin cancer.”