Researchers have discovered that Vitamin B12 improves mitochondrial health during infection, thereby improving the chances of survival. Mitochondria are organelles within cells that convert oxygen and nutrients into adenosine triphosphate (ATP), which the chemical that cells use as energy to power cellular metabolic activity.
Danger of vitamin B12 deficiency
Using roundworms, one of Earth’s simplest animals, Rice University bioscientists have found the first direct link between a diet with too little vitamin B12 and an increased risk of infection by two potentially deadly pathogens.
Despite their simplicity, 1-millimeter-long nematodes called Caenorhabditis elegans (C. elegans) share an important limitation with humans: They cannot make B12 and must get all they need from their diet. In a study published today in PLOS Genetics, researchers from the lab of Rice biochemist and cancer researcher Natasha Kirienko describe how a B12-deficient diet harms C. elegans’ health at a cellular level, reducing the worms’ ability to metabolize branched-chain amino acids (BCAA). The research showed that the reduced ability to break down BCAAs led to a toxic buildup of partially metabolized BCAA byproducts that damaged mitochondrial health.
The lead scientist and co-author of the study, Kirienko said the B12 finding came as a surprise to her team, which first noticed the effect in experiments designed to investigate the mechanisms of pathogenesis of Pseudomonas aeruginosa (P. aeruginosa), a potentially deadly disease in both worms and humans that infects some 51,000 U.S. hospital patients each year, according to the Centers for Disease Control.
The researchers used numerous tests to confirm their results and rule out other possible mechanisms for the effect. They also found that C. elegans on an HT115 diet had the ability to resist infection by another deadly human pathogen, Enterococcus faecalis.