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Coenzyme Q10 or Creatine Counteract Pravastatin-Induced Liver Redox Changes in Hypercholesterolemic Mice

Ana C Marques1, Estela N B Busanello1, Diogo N de Oliveira1

  • 1Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, Brazil.

Frontiers in Pharmacology
|July 13, 2018
PubMed

Insights

Pravastatin, a statin, may cause liver damage by inducing mitochondrial oxidative stress in LDL receptor knockout mice. Co-treatment with antioxidants like CoQ10 or creatine effectively reversed these harmful effects.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Toxicology

Background:

  • Statins, like pravastatin, are primary treatments for hypercholesterolemia, acting by inhibiting cholesterol synthesis.
  • Previous research indicates statin use can lead to mitochondrial oxidative stress and membrane permeability transition (MPT).

Purpose of the Study:

  • To investigate potential hepatotoxicity induced by chronic pravastatin treatment in LDL receptor knockout (LDLr-/-) mice, a model for familial hypercholesterolemia.
  • To assess the impact of pravastatin on mitochondrial function, oxidative stress markers, and antioxidant defenses in the liver.

Main Methods:

  • LDLr-/- mice were treated with pravastatin for 3 months.
  • Evaluated liver mitochondrial respiration, reactive oxygen species (ROS) production, calcium-induced MPT, and activities of antioxidant enzymes.
  • Measured glutathione levels and oxidized lipid/protein species.

Main Results:

  • Pravastatin increased hydrogen peroxide (H2O2) production and susceptibility to Ca2+-induced MPT in liver mitochondria.
  • Aconitase activity decreased, while glucose-6-phosphate dehydrogenase (G6PD) activity and glutathione levels increased.
  • Oxidized lipid species were detected, but protein oxidation markers remained unchanged.

Conclusions:

  • Chronic pravastatin treatment induces liver mitochondrial redox imbalance, potentially explaining reported hepatic side effects in patients.
  • Co-administration with antioxidants (CoQ10 or creatine) fully mitigated pravastatin-induced mitochondrial dysfunction and oxidative stress.
Keywords:
LDL receptor knockout micecoenzyme Q10creatinemitochondriapravastatinreactive oxygen species

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