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Acrolein-Induced Toxicity—Defective Mitochondrial Function as a Possible Mechanism

  • N.  Arumugam
  • J.  Thanislass
  • K.  Ragunath
  • S.  Niranjali Devaraj
  • H.  Devaraj

Abstract.

Administration of acrolein (2.5 mg/kg body weight/day) to rats for 45 days depleted the glutathione level in liver, which triggered an imbalance in the antioxidant defense, resulting in lipid peroxidation. Enhanced lipid peroxidation damaged the membranous structure of mitochondria, which was indicated by the loss of lamellae, and increased the oxidation of exogenously added NADH. Loss in membrane integrity altered the activities of the tricarboxylic acid cycle enzymes and levels of cytochromes. Decreased rate of ADP—stimulated oxygen uptake, respiratory coupling ratio, and ATP synthesis—were also observed. We report that the acrolein-induced toxicity is mediated through the depletion of GSH leading to impairment of rat liver mitochondrial function.

Keywords

Glutathione Lipid Peroxidation NADH Oxygen Uptake Antioxidant Defense 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag New York Inc. 1999

Authors and Affiliations

  • N.  Arumugam
    • 1
  • J.  Thanislass
    • 2
  • K.  Ragunath
    • 3
  • S.  Niranjali Devaraj
    • 4
  • H.  Devaraj
    • 1
  1. 1.Unit of Biochemistry, Department of Zoology, University of Madras, Gundy Campus, Chennai-600 025, India IN
  2. 2.Department of Biochemistry, Rajiv Gandhi College of Veterinary and Animal Sciences, Pondicherry—605 009, India IN
  3. 3.Cancer Institute (WIA), Adyar, India IN
  4. 4.Department of Biochemistry, University of Madras, Guindy Campus, Chennai—600 025, India IN

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