Oxidative stress in experimental liver microvesicular steatosis: Role of mitochondria and peroxisomes

Sathish Kumar Natarajan, Chundamannil E. Eapen, Anna B. Pullimood, Kunissery A. Balasubramanian

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Background: Hepatic microvesicular steatosis is a clinical manifestation seen in a number of liver diseases. Although the role of mitochondrial β-oxidation in the development of the disease has been well studied, information on lipid peroxidative damage in liver subcellular organelles is scarce. The present study looked at oxidative stress in hepatic peroxisomes and microsomes in microvesicular steatosis, using an animal model of the disease. Methods: Rats were given i.p. injections of sodium valproate (700 mg/kg bodyweight) to induce microvesicular steatosis, which was confirmed by histology. Results: Oxidative stress was evident in liver in steatosis, accompanied by structural and functional alterations in hepatic mitochondria. Alterations in lipid composition, with decreased phosphatidyl choline and ethanolamine and increased lysophosphatidyl choline and ethanolamine, were seen. An increase in triglyceride content was also seen. In addition, increased lipid peroxidation was also evident in peroxisomes and microsomes from steatotic rats. Pretreatment with clofibrate results in partial reversal of changes produced by valproate. Conclusions: These results suggest that in addition to impaired mitochondrial β-oxidation, oxidative stress is also seen in the hepatic peroxisomes and microsomes during microvesicular steatosis.

Original languageEnglish (US)
Pages (from-to)1240-1249
Number of pages10
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume21
Issue number8
DOIs
StatePublished - Aug 2006

Fingerprint

Peroxisomes
Fatty Liver
Mitochondria
Oxidative Stress
Microsomes
Liver
Valproic Acid
Lipids
Animal Disease Models
Clofibrate
Ethanolamine
Choline
Phosphatidylcholines
Organelles
Lipid Peroxidation
Liver Diseases
Histology
Triglycerides
Injections

Keywords

  • Microvesicular steatosis
  • Mitochondria
  • Oxidative stress
  • Peroxisome proliferators activator receptor alpha (PPARα)
  • Valproate

ASJC Scopus subject areas

  • Hepatology
  • Gastroenterology

Cite this

Oxidative stress in experimental liver microvesicular steatosis : Role of mitochondria and peroxisomes. / Natarajan, Sathish Kumar; Eapen, Chundamannil E.; Pullimood, Anna B.; Balasubramanian, Kunissery A.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 21, No. 8, 08.2006, p. 1240-1249.

Research output: Contribution to journalArticle

Natarajan, Sathish Kumar ; Eapen, Chundamannil E. ; Pullimood, Anna B. ; Balasubramanian, Kunissery A. / Oxidative stress in experimental liver microvesicular steatosis : Role of mitochondria and peroxisomes. In: Journal of Gastroenterology and Hepatology (Australia). 2006 ; Vol. 21, No. 8. pp. 1240-1249.
@article{f3ef9e86f124466691330a3bbfb9e631,
title = "Oxidative stress in experimental liver microvesicular steatosis: Role of mitochondria and peroxisomes",
abstract = "Background: Hepatic microvesicular steatosis is a clinical manifestation seen in a number of liver diseases. Although the role of mitochondrial β-oxidation in the development of the disease has been well studied, information on lipid peroxidative damage in liver subcellular organelles is scarce. The present study looked at oxidative stress in hepatic peroxisomes and microsomes in microvesicular steatosis, using an animal model of the disease. Methods: Rats were given i.p. injections of sodium valproate (700 mg/kg bodyweight) to induce microvesicular steatosis, which was confirmed by histology. Results: Oxidative stress was evident in liver in steatosis, accompanied by structural and functional alterations in hepatic mitochondria. Alterations in lipid composition, with decreased phosphatidyl choline and ethanolamine and increased lysophosphatidyl choline and ethanolamine, were seen. An increase in triglyceride content was also seen. In addition, increased lipid peroxidation was also evident in peroxisomes and microsomes from steatotic rats. Pretreatment with clofibrate results in partial reversal of changes produced by valproate. Conclusions: These results suggest that in addition to impaired mitochondrial β-oxidation, oxidative stress is also seen in the hepatic peroxisomes and microsomes during microvesicular steatosis.",
keywords = "Microvesicular steatosis, Mitochondria, Oxidative stress, Peroxisome proliferators activator receptor alpha (PPARα), Valproate",
author = "Natarajan, {Sathish Kumar} and Eapen, {Chundamannil E.} and Pullimood, {Anna B.} and Balasubramanian, {Kunissery A.}",
year = "2006",
month = "8",
doi = "10.1111/j.1440-1746.2006.04313.x",
language = "English (US)",
volume = "21",
pages = "1240--1249",
journal = "Journal of Gastroenterology and Hepatology (Australia)",
issn = "0815-9319",
publisher = "Wiley-Blackwell",
number = "8",

}

TY - JOUR

T1 - Oxidative stress in experimental liver microvesicular steatosis

T2 - Role of mitochondria and peroxisomes

AU - Natarajan, Sathish Kumar

AU - Eapen, Chundamannil E.

AU - Pullimood, Anna B.

AU - Balasubramanian, Kunissery A.

PY - 2006/8

Y1 - 2006/8

N2 - Background: Hepatic microvesicular steatosis is a clinical manifestation seen in a number of liver diseases. Although the role of mitochondrial β-oxidation in the development of the disease has been well studied, information on lipid peroxidative damage in liver subcellular organelles is scarce. The present study looked at oxidative stress in hepatic peroxisomes and microsomes in microvesicular steatosis, using an animal model of the disease. Methods: Rats were given i.p. injections of sodium valproate (700 mg/kg bodyweight) to induce microvesicular steatosis, which was confirmed by histology. Results: Oxidative stress was evident in liver in steatosis, accompanied by structural and functional alterations in hepatic mitochondria. Alterations in lipid composition, with decreased phosphatidyl choline and ethanolamine and increased lysophosphatidyl choline and ethanolamine, were seen. An increase in triglyceride content was also seen. In addition, increased lipid peroxidation was also evident in peroxisomes and microsomes from steatotic rats. Pretreatment with clofibrate results in partial reversal of changes produced by valproate. Conclusions: These results suggest that in addition to impaired mitochondrial β-oxidation, oxidative stress is also seen in the hepatic peroxisomes and microsomes during microvesicular steatosis.

AB - Background: Hepatic microvesicular steatosis is a clinical manifestation seen in a number of liver diseases. Although the role of mitochondrial β-oxidation in the development of the disease has been well studied, information on lipid peroxidative damage in liver subcellular organelles is scarce. The present study looked at oxidative stress in hepatic peroxisomes and microsomes in microvesicular steatosis, using an animal model of the disease. Methods: Rats were given i.p. injections of sodium valproate (700 mg/kg bodyweight) to induce microvesicular steatosis, which was confirmed by histology. Results: Oxidative stress was evident in liver in steatosis, accompanied by structural and functional alterations in hepatic mitochondria. Alterations in lipid composition, with decreased phosphatidyl choline and ethanolamine and increased lysophosphatidyl choline and ethanolamine, were seen. An increase in triglyceride content was also seen. In addition, increased lipid peroxidation was also evident in peroxisomes and microsomes from steatotic rats. Pretreatment with clofibrate results in partial reversal of changes produced by valproate. Conclusions: These results suggest that in addition to impaired mitochondrial β-oxidation, oxidative stress is also seen in the hepatic peroxisomes and microsomes during microvesicular steatosis.

KW - Microvesicular steatosis

KW - Mitochondria

KW - Oxidative stress

KW - Peroxisome proliferators activator receptor alpha (PPARα)

KW - Valproate

UR - http://www.scopus.com/inward/record.url?scp=33745844419&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33745844419&partnerID=8YFLogxK

U2 - 10.1111/j.1440-1746.2006.04313.x

DO - 10.1111/j.1440-1746.2006.04313.x

M3 - Article

C2 - 16872304

AN - SCOPUS:33745844419

VL - 21

SP - 1240

EP - 1249

JO - Journal of Gastroenterology and Hepatology (Australia)

JF - Journal of Gastroenterology and Hepatology (Australia)

SN - 0815-9319

IS - 8

ER -