Mycobacterium tuberculosis, the cause, as the name implies, of tuberculosis, has become resistant to many antibiotics. But a recent report shows that it’s sensitive to vitamin C.
Drugs that kill tuberculosis more quickly could shorten chemotherapy significantly. In Escherichia coli, a common mechanism of cell death by bactericidal antibiotics involves the generation of highly reactive hydroxyl radicals via the Fenton reaction. Here we show that vitamin C, a compound known to drive the Fenton reaction, sterilizes cultures of drug-susceptible and drug-resistant Mycobacterium tuberculosis, the causative agent of tuberculosis. While M. tuberculosis is highly susceptible to killing by vitamin C, other Gram-positive and Gram-negative pathogens are not. The bactericidal activity of vitamin C against M. tuberculosis is dependent on high ferrous ion levels and reactive oxygen species production, and causes a pleiotropic effect affecting several biological processes. This study enlightens the possible benefits of adding vitamin C to an anti-tuberculosis regimen and suggests that the development of drugs that generate high oxidative burst could be of great use in tuberculosis treatment.
Of interest, vitamin C kills M. tuberculosis by increasing iron concentrations, specifically the concentration of free iron, which is the damaging kind. The combination of vitamin C and free iron produces a pro-oxidant reaction which kills the bacterium by producing DNA damage.
The investigators suggest that adding vitamin C to antibiotic regimens in tuberculosis needs further investigation, and could be a useful adjunct to treatment.
The fact that M. tuberculosis was highly sensitive to vitamin C, but other bacteria were not, points to its unique nature.
The pro-oxidant reaction produced by vitamin C, in combination with the iron already inside the bacterium, is shared by other antibiotics. Antibiotics alter cellular respiration and produce high levels of hydrogen peroxide, which kills the cell, the bacterium.
Would adding vitamin C to antibiotic regimens potentiate the effect of antibiotics?