Using cockroaches, one of the simplest animals on the planet, Rice University's bioscientists found the first direct link between a diet with too little vitamin B12 and an increased risk of two potentially fatal pathogens. .
Although they are simple, the 1 mm long nematode is called C. elegans (19459006) ( C. elegans ) has important limitations with humans: they cannot make B12 and must obtain them. Everything you need from their diet. In a study published today in PLOS Genetics researchers from Rice biochemist and cancer researcher Natasha Kirienko Lab described how B12 lacks diet to harm C. The health of the nematode at the cellular level reduces the ability of the worm to metabolize branched chain amino acids (BCAA). This study suggests that reduced ability to break down BCAAs leads to accumulation of toxicity of partially metabolized BCAA by-products, thereby damaging mitochondrial health.
The researchers studied the health of two worms, one of which had adequate diet in B12 and the other had too little B12 in the diet. Like the second worm, at least 10% of American adults consume too little B12 in their diet, a risk that increases with age.
"We use C. elegans to study the effects of diet on the host and find that a food can significantly increase resistance to a variety of stressors – such as heat and free radicals – as well as pathogens," Reisko said assistant professor of biological sciences and CPRIT scholar of Wright Cancer Research.
Kirienko, the lead scientist and co-author of the study, said that the discovery of B12 surprised her team, who first noticed the experiment aimed at investigating the pathogenesis of Pseudomonas aeruginosa (Pseudomonas aeruginosa). According to the Centers for Disease Control, worms and humans infect 51,000 American hospital patients every year, which is a fatal and deadly disease.
Her laboratory uses C like thousands of people around the world. Nematode is a model organism that studies the effects of diseases, drugs, toxins and other processes affecting humans and animals. In many C. Nematode The worm in the research laboratory is fed E. coli, a common human intestinal bacterium that is itself a model organism.
"We found that the conversion between E. coli strain OP50 and strain HT115 greatly changed the resistance of worms," Kirienko said. She said it took about two years of follow-up studies to isolate the biochemical mechanisms of stress and pathogen resistance. Her research team includes research co-author Alexey Revtovich and co-author Ryan Lee.
"The key difference between the two diets is the ability of HT115 and OP50 to acquire B12 from the environment," research scientist Revtovich said. "We found that HT115 is much more efficient in this respect, and that it requires about eight times more protein than the OP50 to harvest B12 protein."
Researchers used a large number of tests to confirm their results and ruled out other possible effects mechanisms. They also found that C. elegans on the HT115 diet has the ability to resist infection with another deadly human pathogen Enterococcus faecalis.
Rice is a student at Rice University, and he said the study emphasizes the need for C. Elegans Laboratories around the world are concerned about the different effects that diet can have on experimental results.
"Some laboratories use OP50 as a standard food, and other laboratories use HT115 or even another E. coli strain," Lee said. "Our findings suggest that there are significant metabolic differences between these diets, and these differences are likely to lead to large uncertainties in the results."
Kirienko joined Rice's faculty in 2015, benefiting from the Texas Cancer Prevention and Research Institute (CPRIT) recruitment grant, a state ballot program that was approved in 2007 to provide 30 Billions of dollars are used to support cancer research across the state. To date, CPRIT has provided $2.2 billion in grants to researchers, institutions, and organizations in Texas through its academic research, prevention, and product development research programs.
"This work is related to the significance of mitochondrial health," Kirienko said. "In this case, we are working to improve mitochondrial health to help fight infection. For CPRIT, we are trying to do the opposite. We want to destroy the mitochondria in cancer cells to kill them. So, actually, now We know that it is important that it provides another potential target for cancer cells."
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