Mechanisms of lampricide toxicity
Sea lamprey invaded the Great Lakes in the early 20th century, and continue to threaten populations of native fishes. Control of these parasitic invaders involves regular application of specialized pesticides - TFM and nicolsamide - to nursery streams containing lamprey larvae.
TFM and likely nicolsamide work by short-circuiting lamprey mitochondria, causing depletion of limited energetic stores and potentially exposing animals to oxidative stress. The full extent of the toxicological effects of these chemicals, especially nicolsamide, is an area of active investigation.
My postdoctoral work investigates how nicolsamide and nicolsamide-TFM mixes affect the mitochondria of native fish and sea lamprey. What is the mechanism of toxicity of these agents and what does it have to do with oxidative stress?
Adult sea lamprey
Mitochondria from a mammalian lung
Does hypoxia pattern matter?
Periods of low oxygen are a fact of life for many fishes, and physiologists have a good understanding of how fish cope with stable, long periods of low oxygen. However, we have much poorer understanding of how fish cope with repeated cycles between low and high oxygen, even though we know so called patterns of 'intermittent hypoxia' are very common in the wild.
My PhD research focuses on how killifish cope with low oxygen, and how these fish use different strategies to deal with daily cycles of hypoxia-reoxygenation compared to constant exposure to low oxygen conditions.
My key papers in this research area:
Killifish in a respirometer by B.G.B.
Killifish (Fundulus heteroclitus) by B.G.B.
I'm broadly interested in how animals, especially fish, cope with both natural and human-generated environmental challenges. Check out my Academic Publications to learn more about the cool side projects I've worked on!