Faculty Advisor

Dominko, Tanja

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

Accessibility

Unrestricted

Advisor Department

Biology and Biotechnology

Share

COinS