Investigating Arsenic-Induced Mitochondrial Toxicity in C. elegans


By Tanner Waters


In Dr. Joel Meyer’s laboratory, I’m studying the effects of arsenic on C. elegans with genetic deficiencies in their mitochondria. I am a junior at Duke University, majoring in Environmental Science and Earth & Ocean Sciences. I’m originally from South Florida and have been living in Durham for the past two years. The field of environmental toxicology lies at the intersection of my many interests: it allows me to take a biological/chemical approach to protecting the environment. I learned about the Duke Superfund Research Center from graduate students in the Meyer Lab, where I was working to cross different C. elegans strains.


In our research we are interested in the ‘bioenergetics,’ or energy relationships, in the organism. We are looking at how varying concentrations of arsenic can cause growth delays, lethality, or effects on mitochondrial respiration, among a variety of other things. After the exposures, we will know if the strains of C. elegans worms with the mutated DNA will be more sensitive to arsenite than the wild type C. elegans.


I have been working here for about two months, and in that time I have learned a lot about arsenic and mitochondria, as well as the nematode C.elegans. We use this organism as a model because of its high biological and genomic similarity to humans.  Mitochondria are organelles in the cells that create most of the body’s energy. In C. elegans, much like humans, the mitochondrial electron transport chain is composed of 5 complexes that use electrons to create energy. Genetic mutations may alter the genes that encode for these complexes and adversely affect mitochondria, which can lead to disease in humans. I hypothesize that these mutations may also result in greater sensitivity to arsenic. I study C. elegans with mutations in complex I, complex II, complex III and complex V of the electron transport chain. Since these complexes are preserved in humans, the C.elegans model shows that humans carrying similar genetic deficiencies may be especially sensitive to arsenic.


Our work has practical applications because millions of people are exposed to high levels of arsenic. Historically, arsenic was used in commercial products such as pesticides, wood preservatives, and even chicken feed. These human-made sources, in addition to the natural occurrence of arsenic in soil, rivers, and drinking water, increase the chance that people may be exposed to arsenic. For this reason, it is important to understand whether individuals who are afflicted with mitochondrial deficiencies are exposed, because they may be more vulnerable to the effects of arsenic exposure than the general population.


The experience I’ve gained as a Duke Superfund Research Center intern this summer will be helpful as I continue researching mitochondrial toxicity for my senior thesis.