Articles by Brian
Activity
1K followers
Experience
Education
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University of Alabama at Birmingham
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Activities and Societies: Molecular and Cellular Pathology Graduate Program Presiding Officer, Graduate Student Association Senator, Center for Free Radical Biology Trainee
Graduate Student in the lab of Dr. Victor Darley-Usmar from 2005-2009. I studied the influence of oxidative stressors on the bioenergetics of intact cells.
Most Outstanding Graduate Student - Department of Pathology 2009
Dissertation entitled "Mitochondrial Bioenergetics and Cellular Stress" 2009 -
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Publications
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Alterations in bioenergetic function induced by Parkinson's disease mimetic compounds: lack of correlation with superoxide generation.
Journal of Neurochemistry
In vitro and in vivo models of Parkinson's disease (PD) suggest that increased oxidant production leads to mitochondrial dysfunction in dopaminergic neurons and subsequent cell death. However, it remains unclear if cell death in these models is caused by inhibition of mitochondrial function or oxidant production. The objective of this study was to determine the relationship between mitochondrial dysfunction and oxidant production in response to multiple PD neurotoxicant mimetics. MPP(+) caused…
In vitro and in vivo models of Parkinson's disease (PD) suggest that increased oxidant production leads to mitochondrial dysfunction in dopaminergic neurons and subsequent cell death. However, it remains unclear if cell death in these models is caused by inhibition of mitochondrial function or oxidant production. The objective of this study was to determine the relationship between mitochondrial dysfunction and oxidant production in response to multiple PD neurotoxicant mimetics. MPP(+) caused a dose-dependent decrease in the basal oxygen consumption rate in dopaminergic N27 cells, indicating a loss of mitochondrial function. In parallel, we found that MPP(+) only modestly increased oxidation of hydroethidine as a diagnostic marker of superoxide production in these cells. Similar results were found using rotenone as a mitochondrial inhibitor, or 6-hydroxydopamine (6-OHDA) as a mechanistically distinct PD neurotoxicant, but not with exposure to paraquat. In addition, the extracellular acidification rate, used as a marker of glycolysis, was stimulated to compensate for oxygen consumption rate inhibition after exposure to MPP(+) , rotenone, or 6-OHDA, but not paraquat. Together these data indicate that MPP(+) , rotenone, and 6-OHDA dramatically shift bioenergetic function away from the mitochondria and towards glycolysis in N27 cells.
Other authorsSee publication -
Assessing bioenergetic function in response to oxidative stress by metabolic profiling.
Free Radical Biology and Medicine
This article describes our approach to the study of bioenergetic function in cultured cells. We focus on the consequences of oxidant production using exposure to various toxicants, though the methods are applicable to many other scientific paradigms. The article ends with some best-practices and suggestions for accurate data analysis.
Other authorsSee publication
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