Protective effect of P. fraternus against ethanol-induced mitochondrial dysfunction

Area of Science:

• Biochemistry
• Pharmacology
• Toxicology

Background:

• Chronic ethanol consumption is known to induce cellular damage.
• Mitochondrial dysfunction is a key mechanism in alcohol-induced organ toxicity.
• Ethanol's impact on mitochondrial respiratory chain enzymes and cytochromes requires further elucidation.

Purpose of the Study:

• To investigate the effects of chronic ethanol consumption on mitochondrial respiration and enzyme activities.
• To evaluate the potential protective effects of Phyllanthus fraternus aqueous extract against ethanol-induced mitochondrial toxicity.

Main Methods:

• Rats were administered ethanol (10 g/kg) chronically.
• Mitochondrial respiration, P/O ratio, and respiratory control ratio (RCR) were measured.
• Activities of NADH dehydrogenase and cytochrome oxidase were assayed.
• Mitochondrial membrane potential and cytochrome content (b, c, aa3) were analyzed.
• The effects of Phyllanthus fraternus aqueous extract (100 mg/kg) co-administered with ethanol were assessed.

Main Results:

• Ethanol consumption significantly decreased respiration rate, P/O ratio, RCR, NADH dehydrogenase, and cytochrome oxidase activities.
• Ethanol administration led to a significant reduction in mitochondrial cytochromes b, c, and aa3.
• No significant changes were observed in the membrane potential of submitochondrial particles.
• Phyllanthus fraternus extract administration partially reversed ethanol-induced decreases in respiration, P/O ratio, RCR, and cytochrome content.

Conclusions:

• Chronic ethanol intake severely impairs mitochondrial respiratory function and reduces key electron transport chain components.
• Phyllanthus fraternus aqueous extract demonstrates partial protective effects against ethanol-induced mitochondrial damage.
• These findings suggest Phyllanthus fraternus may be a potential therapeutic agent for mitigating alcohol-related mitochondrial injury.