Melatonin prevents mitochondrial dysfunctions and death in differentiated skeletal muscle cells

Area of Science:

• Cell Biology
• Muscle Physiology
• Biochemistry

Background:

• Oxidative stress contributes to cellular damage and apoptosis, implicated in sarcopenia and muscle disorders.
• Reactive oxygen species (ROS) play a key role in initiating these damaging pathways.
• Melatonin is recognized for its potent ROS scavenging capabilities.

Purpose of the Study:

• To investigate the protective effects of melatonin against oxidative stress and apoptosis in skeletal muscle cells.
• To determine if melatonin can modulate or prevent myotube death induced by specific chemical triggers.
• To explore the potential therapeutic applications of melatonin in skeletal muscle health.

Main Methods:

• Utilized differentiated C2C12 skeletal muscle cells.
• Treated cells with melatonin prior to exposure to apoptosis-inducing and oxidative stress-inducing chemicals.
• Conducted morpho-functional analyses, including ultrastructural observations, to assess cellular integrity and function.

Main Results:

• Melatonin demonstrated significant protection against apoptotic triggers, reducing membrane blebbing, chromatin condensation, and DNA cleavage.
• Ultrastructural analysis confirmed melatonin's ability to prevent myonuclei loss.
• Melatonin effectively prevented mitochondrial dysfunction in myotubes exposed to oxidative stress.

Conclusions:

• Melatonin effectively prevents apoptotic cell death in skeletal muscle fibers in vitro.
• The findings highlight melatonin's protective role against oxidative stress-induced damage in muscle cells.
• Melatonin presents a potential therapeutic agent for treating various skeletal muscle disorders.