Abby Harris

UC Berkeley

“Cell-intrinsic mechanisms of oxidative stress tolerance in the Northern elephant seal”

The oxygen paradox holds that while oxygen is essential for aerobic respiration, it also generates reactive oxygen species (ROS) that can damage the cell. Some forms of ROS can lead to cell death, such as lipid peroxidation in ferroptosis. For an organism to survive these detrimental effects, it must evolve oxidative stress tolerance mechanisms to combat ROS. In some cases, rapid reoxygenation and ROS generation can cause irreversible tissue damage. During ischemia-reperfusion injury (IRI), a prolonged period of low oxygen in the blood followed by a sudden influx of oxygen can cause acute kidney and liver injury, ischemic stroke, and myocardial infarction in humans. Interestingly, diving mammals like the Northern elephant seal undergo hypoxemia regularly while diving yet are immune to reperfusion injury upon coming up to the surface to breathe. The reasons for this immunity are not well characterized. I aim to investigate the robust oxidative stress tolerance mechanisms in elephant seal cells and to translate what I learn from these cells to improve our understanding of potentially related mechanisms in human cells.


Northern elephant seals are uniquely resistant to ROS-induced tissue damage following hypoxemic dives of up to two hours in duration. My project aims to elucidate the cellular mechanisms responsible for oxidative stress resistance in this novel model organism and to develop a CRISPR screening platform in elephant seal cells.

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