Curcumin Protects Mitochondria and Cardiomyocytes from Oxidative Damage and Apoptosis Induced by Hemiscorpius...

Area of Science:

• Toxicology
• Cardiovascular Biology
• Mitochondrial Medicine

Background:

• * Fish venom toxicity is a growing concern.
• * Understanding venom-induced cardio-toxicity is crucial for developing treatments.
• * Curcumin is a natural compound with known protective properties.

Purpose of the Study:

• * To elucidate the mechanisms of cardio-toxicity induced by H. lepturus venom.
• * To investigate the protective effects of curcumin against H. lepturus venom-induced cardiac damage.
• * To utilize isolated rat heart mitochondria and cardiomyocytes as experimental models.

Main Methods:

• * Assessed cytotoxicity and caspase 3 activation in cardiomyocytes.
• * Evaluated mitochondrial dysfunction markers: ROS levels, swelling, membrane potential (MMP), ATP levels, and outer membrane (MOM) rupture.
• * Measured cytochrome-c oxidase (complex IV) activity.
• * Administered curcumin to rats and re-evaluated the aforementioned parameters.

Main Results:

• * H. lepturus venom significantly increased cytotoxicity, caspase 3 activation, and mitochondrial dysfunction, including ROS production, swelling, MMP collapse, decreased complex IV activity, ATP depletion, and MOM rupture.
• * Curcumin administration significantly attenuated venom-induced cytotoxicity, caspase 3 activation, ROS formation, MMP collapse, mitochondrial swelling, and MOM rupture.
• * Venom disrupted the mitochondrial respiratory chain, particularly complexes II and IV.

Conclusions:

• * H. lepturus venom induces cardio-toxicity through mitochondrial dysfunction and activation of cell death pathways.
• * Curcumin demonstrates significant protective effects against H. lepturus venom-induced cardio-toxicity.
• * Curcumin's protective mechanism involves preserving mitochondrial integrity and function.