Although ultraviolet light can wipe out several germs, the exact mechanisms that orchestrate the radiation’s damaging action have long been elusive. In a recent issue of PNAS, researchers at Texas A&M University in College Station reported that ultraviolet radiation creates holes in the microbes’ outer protective sheath by dislodging tryptophan, a molecule that is an important component of the bacteria’s outer covering. The investigators said that these holes provide gateways for ultraviolet radiation to enter the bacteria and disrupt its DNA, which then stops the microbes from replicating.
“Our study provides the science behind the germicidal action of ultraviolet light,” said Dr. Peter Rentzepis, TEES eminent professor in the department of electrical and computer engineering. “We’d like to use this knowledge to develop better ways to monitor bacteria inactivation in various settings, including the food industry and health care.”
Ultraviolet light is a highly energetic beam of radiation that has been harnessed for a variety of applications ranging from food contamination prevention to infection control. Although ultraviolet radiation has been used for more than five decades to kill bacteria, the means by which it enters microorganisms and then accesses their genetic material has not been clear.
To reach the interior of the bacterium, ultraviolet radiation must pass through the cell membrane. Attached to this membrane are tryptophan molecules, which anchor proteins made within the microbes onto the cell membrane. Consequently, the bacterial outer covering is studded with tryptophan molecules. When hit by ultraviolet light, tryptophan molecules absorb the radiation and get energized, and when they lose this absorbed energy, they re-emit a much weaker ultraviolet light, dubbed fluorescent light. Rentzepis and his team investigated whether these ultraviolet light–tryptophan interactions played a role in killing bacteria.
For their experiments, the researchers examined the fluorescent light emitted by tryptophan molecules in Escherichia coli and Bacillus subtilis after shining a beam of ultraviolet radiation on them. As expected, they found that, at the end of radiation, which typically lasted several minutes, the fluorescent light emitted by the tryptophan molecules was drastically reduced, indicating that the radiation was killing the bacteria. However, to their surprise, this decreased fluorescent light came after an initial increase, immediately after the radiation was turned on.
“The surge of the emitted ultraviolet light just after the radiation onset made us suspect that changes happening to tryptophan molecules before they are ultimately destroyed by ultraviolet light may be involved in how radiation gets into the bacteria,” said Rentzepis.
The researchers’ findings suggest that, in bacteria, ultraviolet light might unfold membrane proteins and detach tryptophan molecules, which may then cause the initial increase in the emitted light signal. With tryptophan plucked out of the cell membrane, the space left behind forms gaping holes for the ultraviolet light to enter and damage DNA, he said.