Mitochondrial function is altered in horse atypical myopathy

Area of Science:

• Veterinary Medicine
• Toxicology
• Biochemistry

Background:

• Equine atypical myopathy is a severe, often fatal, rhabdomyolysis syndrome in horses.
• It is caused by the ingestion of hypoglycin A, a toxin found in Acer pseudoplatanus (sycamore maple) seeds and seedlings.
• The disease significantly impacts muscle energy metabolism.

Purpose of the Study:

• To investigate acylcarnitine concentrations in serum.
• To assess muscle oxidative phosphorylation (OXPHOS) capacity in horses with atypical myopathy.
• To understand the biochemical alterations contributing to the high mortality rate.

Main Methods:

• Serum and muscle samples were collected from 15 horses diagnosed with atypical myopathy.
• Acylcarnitine concentrations were measured.
• Muscle mitochondrial respiratory capacity (OXPHOS) was determined and compared to 10 healthy controls.

Main Results:

• All but one measured acylcarnitine concentration were outside the normal reference range in affected horses.
• Muscle mitochondrial respiratory capacity was significantly decreased, up to 49%, compared to healthy controls.
• These findings indicate a severe disruption of energy metabolism.

Conclusions:

• Equine atypical myopathy is characterized by severe alterations in energy metabolism.
• Impaired muscle mitochondrial respiration is a key feature of the disease.
• These metabolic disturbances likely contribute to the high fatality rate of equine atypical myopathy.