Testosterone deficiency impairs cardiac interfibrillar mitochondrial function and myocardial contractility while...

Area of Science:

• Cardiovascular Biology
• Mitochondrial Physiology
• Endocrinology

Background:

• Low testosterone levels are linked to cardiovascular diseases.
• Oxidative metabolism is crucial for myocardial contractility.

Purpose of the Study:

• To investigate the impact of testosterone deficiency on cardiac mitochondria subpopulations (SSM and IFM).
• To assess the effects on myocardial contractility and mitochondrial function.

Main Methods:

• Male Wistar rats underwent orchidectomy to induce testosterone deficiency.
• Cardiac function and mitochondrial structure (SSM and IFM) were analyzed after 12 weeks.
• Mitochondrial function markers, protein expression, and oxidative stress indicators were measured.

Main Results:

• Testosterone deficiency reduced myocardial contractility and impaired interfibrillar mitochondrial oxidative phosphorylation.
• Changes included increased mitochondrial membrane potential and size in IFM, alongside reduced p-AMPK-α, PGC-1α, and TFAM.
• Increased NADPH oxidase (NOX) and ACE expression, with decreased Mn-SOD and catalase, were observed in IFM.

Conclusions:

• Testosterone deficiency impairs cardiac function and interfibrillar mitochondrial energetics.
• Reactive oxygen species, potentially from NOX, are implicated in this dysfunction.
• Testosterone replacement and apocynin treatment restored cardiac and mitochondrial function.