If you take antibiotics, your doctor will warn you not to skip pills and continue treatment even after you start feel better. Indeed, the failure to kill insects that makes you sick can cause some of them to become resistant to antibiotics. Now, a new study explains how non-lethal concentrations of antibiotics can lead to resistance. Drugs cause the release of species referred to as reactive oxygen species (ROS) within bacteria which in turn cause mutations in the DNA of insects -. Including some who manage to cause resistance
Traditionally, the development of antibiotic resistance - a big and growing problem in medicine - was considered a passive phenomenon. random mutations occur in bacterial genomes, and the bacteria exchange random genetic elements. Occasionally, a mutation or some newly acquired DNA allows microbes to detoxify antibiotics, pumping out of cells, or render them harmless otherwise. When these bacteria are exposed to antibiotics, natural selection will allow them to replace those who do not resist.
But over the past six years, a different view has emerged, says microbiologist Jesús Blázquez of the Spanish National Research Council in Madrid. The researchers found that mutation rates in bacteria sometimes go in response to stress, in some cases, promoting resistance. Blázquez and the studies and others have shown that antibiotics themselves can cause this phenomenon, called hypermutability.
The new study, led by biologist James Collins systems Harvard University explains how this is possible. There are a few years, the group of Collins discovered that antibiotics can trigger the production of ROS, also known as free radicals, which can cause mutations in DNA. At high levels, the group found at the time, these changes have helped to kill germs. But what about non-lethal doses of antibiotics, the researchers wondered. Can they, for the release of ROS, trigger the same mutations that make them resistant bacteria?
To find out, the treated group Escherichia coli bacteria with low levels of antibiotics norfloxacin, ampicillin, and kanamycin. ROS levels of drugs increased, reports the team today Molecular Cell . Using a simple procedure for estimating the number of mutations that occur in a cell culture, the team found that higher levels of ROS leading to higher mutation rate in bacterial genomes - to increase eightfold in the case of norfloxacin. Then they showed that low-level treatments were indeed trigger resistance -. In many cases, not only against the drug itself, but a range of other antibiotics, as well
The likely explanation, said Collins, is that antibiotics are creating a "whole zoo of mutants "in a bacterial population -.. including some that are found to be resistant to one or more drugs the findings could have practical results, said Collins for example, if researchers could find molecules that prevent hypermutability, they could be combined with antibiotics to prevent or delay resistance.
the document provides more evidence that antibiotics are not only choosing certain mutations, but cause them, says molecular geneticist Susan Rosenberg at Baylor College of Medicine in Houston, Texas . "and they showed that the mechanism involved is the release of reactive oxygen species," she said. The document also reinforces how microbes are versatile, adds Blázquez. "Again, it seems that bacteria use adversity as a stimulant to fit almost everything," he said.
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