For years, public health officials have been sounding an alarm about the overuse of antibiotics, noting that the powerful drugs that can quash an infection with few side effects can also spur the rise of drug-resistant “superbugs.” It’s an argument that often seems to miss its mark, considering that about a fifth of doctor’s office visits in the United States result in a prescription for an antibiotic and every child receives, on average, one antibiotic prescription per year.
Now, a new study offers a different and more personal reason to think cautiously about the use of the drugs: they may harm our cells, too. Although no one with a good reason to take the drugs should be alarmed, researchers have found that certain antibiotics administered at the doses people receive clinically can cause mitochondria, the power plants within cells, to malfunction. Their tests so far are on human cells in a laboratory dish and in mice, but they have accumulated evidence that common antibiotics cause mitochondria to spew out factors that damage DNA, proteins, and other crucial components.
“That’s not killing the cell or causing a lot of damage, but it’s causing some damage,” said James J. Collins, a bioengineer at Boston University who led the work published Wednesday in the journal Science Translational Medicine. “Our paper points to the need to investigate it further; I guess the public health comment would be given there is a potential for harm, one needs to be sure to ask for and only take [these drugs] when needed.”
It was already known that antibiotics can have broad effects, including altering the population of good bacteria that dwell in our guts. Prolonged antibiotic use and particular drugs can cause risks, including hearing loss, tendinitis, or kidney problems. But the new study shows that several types of antibiotics, including ciprofloxacin, ampicillin, and kanamycin, spur the release of damaging factors called reactive oxygen species in mammalian cells.
The researchers were also able to show a possible solution: a particular antioxidant could be administered simultaneously to ameliorate the negative effect of the antibiotics on cells, seemingly without preventing the drugs’ ability to stop infections.
The work is early research and needs to be replicated in further experiments in laboratory animals and people to see if the same thing holds up. In any case, many mysteries remain about how, exactly, antibiotics even work. An earlier result from Collins’ laboratory had suggested that antibiotics kill bacteria by generating the damaging reactive oxygen species, but that interpretation has recently been contested by conflicting results generated by two laboratories.
The new results open even more questions about how antibiotics trigger the damaging factors and why some classes of the drugs do not have the effect, two outside scientists wrote in an accompanying essay.
The bottom line, however, may simply be that antibiotic use needs to be reevaluated more broadly as a treatment. If overused, the drugs may have negative effects not only at a public health level, but also—possibly—for individuals. Collins thinks some people may be at greater risk, including people who are immunocompromised, or have a genetic disease that affects the mitochondria. He also pointed out that drug resistant strains of bacteria that may cause recurrent infections raise the spectre of people being placed on antibiotics for longer terms of treatment, which could place them at greater risk for side effects.