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Rotenone-mediated changes in intracellular coenzyme A thioester levels: implications for mitochondrial dysfunction.

Sankha S Basu¹, Ian A Blair

¹Centers for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-6160, United States.

Chemical Research in Toxicology

|September 29, 2011

Summary

Rotenone pesticide exposure alters cellular metabolism, decreasing succinyl-coenzyme A (CoA) and increasing beta-hydroxybutyryl-CoA. These findings reveal rotenone

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Area of Science:

Biochemistry
Neuroscience
Toxicology

Background:

Rotenone, a pesticide, is a known mitochondrial complex I inhibitor.
Rotenone exposure is linked to Parkinson-like neurodegeneration in animal models and implicated in human Parkinson's disease.

Purpose of the Study:

To investigate the metabolic effects of rotenone in human cell lines.
To elucidate the mechanisms underlying rotenone-induced mitochondrial dysfunction and neurotoxicity.

Main Methods:

Utilized stable isotope dilution liquid chromatography-mass spectrometry.
Performed CoA thioester isotopomer analysis on multiple human cell lines, including SH-SY5Y neuroblastoma cells.
Assessed the impact of rotenone on [U-(13)C(6)]-glucose-derived acetyl-CoA and succinyl-CoA biosynthesis.

Main Results:

Rotenone induced a dose-dependent decrease in succinyl-CoA and an increase in beta-hydroxybutyryl-CoA in human cell lines (IC(50) < 100 nM).
Rotenone inhibited the biosynthesis of acetyl-CoA and succinyl-CoA from glucose in SH-SY5Y cells.
Observed metabolic changes suggest a compensatory metabolic rearrangement in response to rotenone toxicity.

Conclusions:

Rotenone significantly disrupts cellular energy metabolism by altering key Coenzyme A metabolites.
The observed metabolic alterations provide insights into the mechanisms of rotenone's neurotoxicity.
Findings support the development of novel biomarkers for mitochondrial dysfunction in Parkinson's disease research.