Scientists at University of Southern California (USC) are examining the toxicity of oxygen on human cells, research they believe could make deep sea diving safer and also lead to better understanding of neurological disorders.
USC chemical engineer Noah Malmstadt, PhD, believes we only think of oxygen as good for us. But studies show the corrosive and highly unstable gas can damage human cells. While oxygen therapy has benefits for treating burn victims, that’s not the case for general health, he explained.
“Oxygen … is a blessing and a curse,” Malmstadt, a chemical engineer and associate professor at the USC Viterbi School of Engineering who studies the physical chemistry of cell membrane oxidation, explained in a university release. “Oxygen is super dangerous; it’s a corrosive gas.”
Deep-sea divers, for example, can seize up and die if they experience oxygen toxicity. Malmstadt, in work funded by the Office of Naval Research, is trying to determine when and how that happens on the molecular level. Malmstadt and his team are among a few researchers nationwide who focus on how oxidation affects super-thin membranes called lipid bilayers, the architectural scaffolding that surround cells, the building blocks of biology.
Researchers still don’t know why oxygen becomes toxic, said Malmstadt. At a certain depth, nitrogen in conventional compressed air tanks becomes toxic, so a combination of oxygen and noble gases such as helium and xenon must be used. But breathing in that cocktail of air can lead to oxygen toxicity. Why and when that happens is unpredictable. Malmstadt hopes to come up with some answers.
“That’s why we’re studying it from the point of view of the structure and function of the cell membrane,” he said. “It’s a hard question to answer because oxygen does a lot of things to a cell membrane.”
To study oxygen toxicity on the human body, Malmstadt and his team have used basic chemicals to create simplified copies of real cells, according to the university release. By better understanding the physical chemistry of membrane oxidation, one of the things Malmstadt hopes to determine is how deep-sea divers can best avoid oxygen toxicity.
“One of the interesting things we have found is that just a tiny bit of oxidation can cause a radical increase in the permeability of a cell membrane,” Malmstadt said.
A membrane doesn’t need to be completely destroyed by oxygen for problems to occur — just a little bit changes the properties radically, he said.
By using artificial cells, Malmstadt can isolate and identify key physical and chemical aspects of cellular membrane permeability, said Jacob Schmidt, an associate professor in UCLA’s Department of Bioengineering who served as Malmstadt’s postdoctoral advisor.
“Only with this improved understanding can we begin to rationally develop preventative or therapeutic strategies to counter the effects of oxidation,” Schmidt said.
His research not only has implications for deep-sea diving, but also could provide a crucial window into how oxidation of cells plays a role in such neurological disorders as Parkinson’s and Alzheimer’s disease, as well as arteriosclerosis, the buildup of plaque in the arteries that feed the heart.