In an unexpected discovery, researchers at Albert Einstein College of Medicine of Yeshiva University have determined that vitamin C kills drug-resistant tuberculosis (TB) bacteria in laboratory culture. The finding suggests that vitamin C, added to existing TB drugs, could shorten TB therapy, and it highlights a new area for drug design. The study was recently published in the online journal Nature Communications.
The discovery arose during research into how TB bacteria become resistant to isoniazid, a potent first-line TB drug. The lead investigator and senior author of the study was William Jacobs, Jr., PhD, professor of microbiology & immunology and of genetics at Einstein.
Dr. Jacobs and colleagues observed that isoniazid-resistant TB bacteria were deficient in a molecule called mycothiol. “We hypothesized that TB bacteria that can't make mycothiol might contain more cysteine, an amino acid,” says Dr. Jacobs. “So, we predicted that if we added isoniazid and cysteine to isoniazid-sensitive M. tuberculosis in culture, the bacteria would develop resistance. Instead, we ended up killing off the culture!”
The researchers suspected that cysteine was helping to kill TB bacteria by acting as a “reducing agent” that triggers the production of reactive oxygen species (sometimes called free radicals), which can damage DNA. To test this hypothesis, they repeated the experiment using isoniazid and a different reducing agent—vitamin C. “We were then amazed to discover that vitamin C by itself not only sterilized the drug-susceptible TB, but also sterilized multi-drug-resistant TB (MDR-TB), and extensively drug-resistant TB (XDR-TB) strains. Read the study abstract.
