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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Elevated neuronal nitric oxide synthase expression during ageing and mitochondrial energy production
Philip Y Lam1, Fei Yin, Ryan T Hamilton
1Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA 90089, USA.
Free Radical Research
|April 7, 2009
Summary
Aging impairs brain mitochondrial function through protein modifications. Key enzymes like F1-ATPase showed age-related nitration, decreasing activity and supporting apoptosis.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Aging is associated with cellular dysfunction, particularly in mitochondria.
- Mitochondrial dysfunction contributes to age-related neurological decline.
Purpose of the Study:
- To investigate the impact of aging on brain mitochondrial function.
- To identify age-related protein post-translational modifications in mitochondria.
- To determine the functional consequences of these modifications.
Main Methods:
- Liquid chromatography-tandem mass spectrometry (LC/MS/MS) for protein identification.
- Enzyme activity assays for mitochondrial function assessment.
- Analysis of protein expression and complex assembly.
Main Results:
- Neuronal nitric oxide synthase increased with age, leading to mitochondrial protein nitration.
- Succinyl-CoA-transferase and F1-ATPase were identified as nitrated proteins.
- Activities of succinyl-CoA-transferase, F1-ATPase, and cytochrome oxidase decreased with age.
- Decreased cytochrome oxidase activity was linked to reduced complex IV expression and assembly.
- Mitochondrial dysfunction was evidenced by reduced respiratory control ratios and cytochrome c release.
Conclusions:
- Age-related protein post-translational modifications contribute to impaired brain mitochondrial function.
- These modifications, including nitration, can affect enzyme activity and mitochondrial integrity.
- Mitochondrial dysfunction exacerbates apoptotic processes in aging brains.
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