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Carnosine Mitigates Manganese Mitotoxicity in an In Vitro Model of Isolated Brain Mitochondria

Vahid Ghanbarinejad1,2, Asrin Ahmadi1, Hossein Niknahad1,2

  • 1Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Advanced Pharmaceutical Bulletin
|August 6, 2019
PubMed

Insights

Manganese (Mn) exposure damages brain mitochondria. Carnosine treatment effectively protected mitochondria from Mn-induced damage, suggesting carnosine

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • Manganese (Mn) is a neurotoxicant causing brain complications.
  • Mitochondria are key cellular targets of Mn toxicity.
  • Carnosine, a brain dipeptide, exhibits antioxidant and mitochondrial protective properties.

Purpose of the Study:

  • To investigate carnosine's protective effects against Mn-induced mitochondrial dysfunction.
  • To evaluate carnosine's impact on isolated brain mitochondria exposed to manganese.

Main Methods:

  • Isolated mouse brain mitochondria were exposed to varying Mn concentrations (10 µM-10 mM).
  • Carnosine (1 mM) was used as a protective agent.
  • Mitochondrial depolarization, reactive oxygen species (ROS) generation, enzyme activity, ATP content, swelling, and permeabilization were assessed.

Main Results:

  • Manganese exposure significantly impaired mitochondrial function, affecting all assessed indices.
  • Carnosine treatment effectively prevented Mn-induced mitochondrial damage and dysfunction.
  • Key mitochondrial parameters were restored by carnosine in the presence of manganese.

Conclusions:

  • Mitochondrial protection is a primary mechanism underlying carnosine's efficacy against manganese neurotoxicity.
  • Carnosine demonstrates potential therapeutic application for manganese neurotoxicity in various conditions, including liver cirrhosis.
Keywords:
BioenergeticsCirrhosisCognitive defectsLocomotor activityManganesePeptide

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