Faculty Advisor
Dominko, Tanja
Center
OTHER / Other location, not listed
Abstract
A large contributor to cellular aging is the decline in mitochondrial fitness. The mitochondrial oxidative phosphorylation pathway is responsible for producing adenosine triphosphate (ATP) and reactive oxygen species (ROS) within eukaryotic cells. Using NIH/3T3 mouse embryonic fibroblasts and H2O2 as a model of oxidative stress senescence-induced aging, it was found low levels of oxidative stress mimicked senesced traits, weakened mitochondrial and cellular membranes, and decreased levels of cellular ROS and ATP. By understanding the consequences of oxidative stress on mitochondria, insight may be gained for future studies and developments towards a reliable model of aging using more than H2O2 as oxidative stressors to replicate cellular aging, as more experimentation is needed.
Publisher
Worcester Polytechnic Institute
Date Accepted
January 2016
Major
Biology and Biotechnology
Project Type
Major Qualifying Project
Copyright Statement
All authors have granted to WPI a nonexclusive royalty-free license to distribute copies of the work, subject to other agreements. Copyright is held by the author or authors, with all rights reserved, unless otherwise noted.
Accessibility
Unrestricted
Advisor Department
Biology and Biotechnology