Symposium gathers experts on oxidative stress and mitochondria

Cutting-edge work on molecular mechanisms involved in the cellular response to stress was the focus at the 18th annual John B. Little Symposium, held Oct. 23-24 at Harvard T.H. Chan School of Public Health.

The symposium is hosted each year by the John B. Little (JBL) Center for Radiation Sciences. Both the symposium and the center are named for John B. Little, James Steven Simmons Professor of Radiobiology Emeritus, one of the first scholars to characterize problems in public health associated with radiation exposure.

Attendees packed the School’s Snyder auditorium to hear experts in the field discuss topics related to oxidative stress, which is caused by high levels of chemically reactive molecules containing oxygen (called reactive oxygen species, or ROS). Oxidative stress can cause damage to DNA, protein, and lipids, leading to myriad pathologies such as type 2 diabetes, Alzheimer’s disease, atherosclerosis, and cancer. Some speakers focused on mitochondria, the cell components that convert food and oxygen into energy and power metabolic activities. Mitochondria also generate ROS, and may overproduce it if their function is deregulated.

Work in this area provides important evidence toward advancing the JBL Center’s research mission in radiation sciences, said Director Zhi-Min Yuan, professor of radiobiology. Elucidating the process of oxidative stress — which can be induced by ionizing radiation — will help researchers understand mechanisms underlying the cellular response to ionizing radiation and how the biological system adapts, he said.