Silver Nanoparticle-Induced Mitochondrial Toxicity in Caenorhabditis elegans

Tuesday, January 12, 2016

12:00 pm to 1:00 pm
Schiciano Auditorium Side A


Laura Maurer

Laura Maurer, Ph.D.
Postdoctoral Associate, Nicholas School of the Environment

Abstract: The quantity of consumer products containing engineered nanoparticles continues to increase, creating the potential for widespread exposure to human populations. Silver nanoparticles (AgNPs) are added to products such as wound dressings, children’s toys, textiles, appliances, and cosmetics as an antimicrobial agent. Because silver nanoparticles are widely used in consumer products as an antimicrobial agent, and mitochondria descended from bacteria in eukaryotic cells, the mitochondrion is a plausible intracellular target of silver nanoparticles. Mitochondria provide the majority of the energy required for proper cellular function, and damage to mitochondria resulting in decreased or inefficient energy production has the potential to hinder ATP-dependent cellular mechanisms. This study utilized C. elegans mutants deficient in mitochondrial homeostasis and metal homeostasis to assess mitochondrial dysfunction following AgNP exposure. AgNPs are one of the more toxic nanoparticles tested to date, and like many other nanoparticles, the toxicity of AgNPs depends on their physicochemical properties. The experiments described in this study allowed for analysis of a particle-size effect and particle-coating effect, and included 10nm and 30nm polyvinylpyrrolidone-coated and 6nm and 25nm gum arabic-coated AgNPs. Overall, mitochondria appear to be an intracellular target of AgNPs. However, the relationships between size, coating, and mitochondrial toxicity are not yet clear and require follow-up studies.