Vitamin C May Be the Answer in the Fight Against Tuberculosis
In a stunning and wholly unexpected discovery, researchers at Albert Einstein College of Medicine of Yeshiva University found that vitamin C kills drug-resistant tuberculosis (TB) bacteria in laboratory culture.
Knowing this, the scientists believe, could mean that adding the common vitamin to existing TB drugs could render them more potent, thus shortening the TB therapy overall.
The lead investigator and senior author of the study, William Jacobs Jr. is a professor of microbiology and immunology as well as genetics at Einstein as well as a recently-elected member of the National Academy of Sciences.
Of the discovery, Jacobs said in a press release, “We hypothesized that TB bacteria that can’t make mycothiol might contain more cysteine, an amino acid.”
For this reason, they predicted that if they added the drug, isoniazid, and cysteine to isoniazid-sensitive M. tuberculosis in culture, the bacteria would develop resistance.
“Instead, we ended up killing off the culture – something totally unexpected.”
Upon finding this, the team further hypothesized that cysteine was helping to kill TB bacteria in becoming a “reducing agent” by acting as a free radical, or something that triggers the production of reactive oxygen species that then damage the DNA.
So they repeated the experiment, this time using isoniazid and a different reacting agent – vitamin C. Sure enough, the two sterilized the culture.
Then came the final discovery in which the team was “amazed” to discover that only did vitamin C sterilize the drug-susceptible TB by itself, but the multi-drug-resistant and extensively drug-resistant strains as well.
Further research revealed the reason: vitamin C induced what is known as the Fenton reaction, causing iron to react with other molecules to create reactive oxygen species that decimated the TB bacteria.
Whether or not vitamin C, which is inexpensive and widely available, will prove as effective in humans is not clear, though Jacobs plans on finding out.
“At the very least,” he said, “this work shows us a new mechanism that we can exploit to attack TB.”
The study was supported by the National Institute of Allergy and Infections Diseases.