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.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Nguyen, Sunny Sang Huynh

Publisher

• Worcester Polytechnic Institute

Identifier

• E-project-012816-081816

Advisor

• Dominko, Tanja

Year

• 2016

Date created

• 2016-01-28

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright