Cited by 67Redox biology and oxidative stressMitochondrial Function and PathologyLiver Disease Diagnosis and Treatment

Increased nitroxidative stress promotes mitochondrial dysfunction in alcoholic and nonalcoholic fatty liver disease

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Song, Byoung-Joon, Abdelmegeed, Mohamed A., Henderson, Lauren E., Yoo, Seong-Ho, Wan, Jie, Purohit, Vishnudutt, Hardwick, James P., Moon, Kwan-Hoon·2013·Oxidative Medicine and Cellular Longevity

Abstract

Increased nitroxidative stress causes mitochondrial dysfunctions through oxidative modifications of mitochondrial DNA, lipids, and proteins. Persistent mitochondrial dysfunction sensitizes the target cells/organs to other pathological risk factors and thus ultimately contributes to the development of more severe disease states in alcoholic and nonalcoholic fatty liver disease. The incidences of nonalcoholic fatty liver disease continuously increase due to high prevalence of metabolic syndrome including hyperlipidemia, hypercholesterolemia, obesity, insulin resistance, and diabetes. Many mitochondrial proteins including the enzymes involved in fat oxidation and energy supply could be oxidatively modified (including S-nitrosylation/nitration) under increased nitroxidative stress and thus inactivated, leading to increased fat accumulation and ATP depletion. To demonstrate the underlying mechanism(s) of mitochondrial dysfunction, we employed a redox proteomics approach using biotin-N-maleimide (biotin-NM) as a sensitive biotin-switch probe to identify oxidized Cys residues of mitochondrial proteins in the experimental models of alcoholic and acute liver disease. The aims of this paper are to briefly describe the mechanisms, functional consequences, and detection methods of mitochondrial dysfunction. We also describe advantages and limitations of the Cys-targeted redox proteomics method with alternative approaches. Finally, we discuss various applications of this method in studying oxidatively modified mitochondrial proteins in extrahepatic tissues or different subcellular organelles and translational research.

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Authors
Song, B.-J., Abdelmegeed, M. A., Henderson, L. E., Yoo, S.-H., Wan, J., Purohit, V., Hardwick, J. P., & Moon, K.-H.
Affiliations
  • National Institutes of Health (US)
  • National Institute on Drug Abuse (US)
  • Northeast Ohio Medical University (US)
Corresponding author
Song, Byoung-Joon
Venue
Oxidative Medicine and Cellular Longevity
Published
2013
Volume
2013
Pages
1-14
ISSN
  • 1942-0994 (ISSN-L)
  • 1942-0900
OpenAlex
W2112596550
Cited by
67
References
148
Citations by year
2026: 4 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 3 · 2018: 4 · 2017: 10 · 2016: 5 · 2015: 9 · 2014: 3 · 2013: 4
FWCI
0.66
Type
journal article
Language
en
Open access
Locations
  • Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (Z99‐AA999999)
  • National Institute on Alcohol Abuse and Alcoholism (ZIAAA000036)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords
nitro-oxidative stress, mitochondrial dysfunction, alcoholic fatty liver, non-alcoholic fatty liver disease, S-nitrosylation, redox proteomics, cysteine oxidation, metabolic syndrome, fat oxidation, ATP depletion, acute liver disease
MeSH terms
Animals, Fatty Liver, Fatty Liver, Alcoholic, Humans, Mitochondria, Oxidative Stress, Reactive Nitrogen Species, Proteomics, Non-alcoholic Fatty Liver Disease

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