Using accurate worms, one of the simplest animals in the world, Rice biosciences found the first direct link between diet and too much vitamin B12 and an increased risk of infection by two pathogens that may be dead.
Despite its simplicity, nematodes are called 1 millimeter in length Caenorhabditis elegans (C. elegans(b) sharing an important limitation with people: They cannot do a B12 and must get what they need from their diet. In a study published today PLOS geneticsNatasha Kirienko, researchers from the Rice biochemistry laboratory and cancer researcher, describe how a deficient diet in B12 is successful. C. elegansHealth at cellular level, reducing the ability of amino acids branched chain to metabolize acid (BCAA). The research showed that the reduced ability to break down BCAAs that damaged adverse health was partly due to the toxic buildup of metabolism by-products.
Researchers studied the health of two worm populations, one of which had a sufficient diet in Y12 and another that had too little B12 from their diet. Like the second population of worms, at least 10 per cent of adults with disabilities receive too little B12 in their diet, a risk that increases with age.
"We used." C. elegans study the impact of the diet on a host and find out that one type of food was able to greatly increase resistance against multipliers – such as heat and free radicals – and with pathogens, "said Kirienko, assistant professor the biosciences and CPRIT Scholar in Cancer Research at Rice.
Kirienko, chief scientist and author of the study, said that the B12 result surprised her team, which noted the effect in experiments designed to pseudomonas aeruginosa (P. aeruginosa) pathogenesis mechanisms to investigate diseases in worms and humans alike. Approximately 51,000 US hospital patients infect each year, according to the Centers for Disease Control.
Its laboratory, like thousands more around the world, uses it C. elegans as an organic model for the study of the effects of diseases, drugs, toxins and other processes affecting humans and animals. In many C. elegans research laboratories Escherichia coli (E. coli) worms, a common generation of bacteria that are their own organic specimens, are cultivated.
"We found that a change between E.-coli OP50 pressure and HT115 pressure stress tolerance of the worm changed greatly," Kirienko said. She said that it had taken two years of follow-up studies to isolate the biochemical mechanism of stress resistance and pathogen. Among her research team was Alexey Revtovich, the author who led the study and co-author Ryan Lee.
"The main difference between the two diets is the ability to obtain B115 and OP50 B12 from the environment," said Revtovich, a research scientist. "We have shown that HT115 is much more efficient at this time, and that eight of the protein it needs to remove B12 compared to OP50."
The researchers used many tests to confirm their results and to achieve other possible mechanisms for the effect. They also got that C. elegans HT115 diet had the potential for infection by other human pathogen, Enterococcus faecalis.
Lee, Rice undergraduate student, said that the study shows the need for C. elegans laboratories around the world to pay attention to the differential impacts that the diet may have on experimental results.
"Some laboratories use OP50 as their normal food, while others use HT115 or even another E. coli," said Lee. "Our findings show that there are significant metabolic differences between these diets, and these differences are likely to contribute to substantial uncertainty in research findings."
Kirienko joined Rice faculty in 2015 for a recruitment grant from the Texas Cancer Prevention and Research Institute (CPRIT), a state ballot initiative approved in 2007 to provide $ 3 billion to support cancer research across the country. To date, CPRIT has awarded grants of € 2.2 billion to researchers, institutions and Texas organizations through its research, prevention and product development research programs.
"This work is involved in that it focuses on mitochondrial health," Kirienko said. "In this case, we are working to improve mitochondrial health to combat infections. For CPRIT, we want to do the other thing. We want to damage mitochondria in cancer cells to kill them. it gives us another goal in cancer cells. "
Materials provided by University of Rice. The original was written by Jade Boyd. Note: Content can be edited for style and length.
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