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The Effects of Manganese Exposure on Mitochondrial Respiration and the Consequential Alteration of Mitochondrial Iron Uptake and Energy ProductionEPA Grant Number: U915989
Title: The Effects of Manganese Exposure on Mitochondrial Respiration and the Consequential Alteration of Mitochondrial Iron Uptake and Energy Production
Investigators: Pilsner, Jonathon R.
Institution: Columbia University
EPA Project Officer: Graham, Karen
Project Period: January 1, 2001 through January 1, 2003
Project Amount: $68,000
RFA: STAR Graduate Fellowships (2001) RFA Text | Recipients Lists
Research Category: Fellowship - Toxicology , Academic Fellowships , Health Effects
The objective of this research project will focus on the neurodegenerative effects of manganese exposure on cellular respiration and the possible relationship of the manifestation of Idiopathic Parkinson's Disease (IPD).Approach:
I will work in Dr. W. Zheng's Neurotoxicology laboratory at Columbia University, where my research will focus specifically on the effects of manganese exposure on mitochondrial respiration and the consequential alteration of mitochondrial iron uptake and energy production. It has been long known that over-exposure to manganese can cause neurodegenerative damage. More specifically, recent investigations have led to the theory that the dysregulation of iron in the mitochondria can cause IPD. Subcellular regulation of iron balance is so precise that the process is highly sensitive to any subtle changes in the elements involved. Thus, any disruption to this regulatory process could result in profound consequences in cellular iron balance, which could then contribute to the development of IPD. The results of my research will provide the U.S. Environmental Protection Agency with the necessary exposure information to ensure the protection of human health as well as the propagation of a viable environment.Supplemental Keywords:
fellowship, manganese exposure, mitochondrial respiration, mitochondrial iron uptake, Idiopathic Parkinson's Disease, IPD, neurodegenerative damage, iron balance, cellular respiration.