Oxidative Stress in Biotoxin-Induced Liver Injury: From ROS Generation to Cell Death and Therapeutic Intervention

Area of Science:

• Hepatology
• Toxicology
• Molecular Biology

Background:

• Biotoxins from fungi, plants, and algae pose significant global health risks.
• The liver is a primary target for biotoxin accumulation and injury due to its metabolic role.
• Mechanisms of oxidative stress in various liver injury phenotypes (necrosis, steatosis, fibrosis) are not fully understood.

Purpose of the Study:

• To establish oxidative stress as a unifying mechanism in biotoxin-induced liver injury.
• To explore the role of oxidative stress in different injury phenotypes and their molecular underpinnings.
• To summarize therapeutic strategies targeting oxidative stress for liver injury.

Main Methods:

• Systematic review of biotoxin-induced liver injury.
• Comparative analysis of representative toxins and their oxidative stress pathways.
• Examination of signaling cascades (Nrf2, NF-κB, MAPK) and cell death modes (apoptosis, ferroptosis, necroptosis).

Main Results:

• Oxidative stress is identified as a convergent mechanism in biotoxin-induced liver injury.
• Specific toxins activate distinct oxidative stress pathways leading to varied hepatic injury phenotypes.
• Signaling pathways like Nrf2, NF-κB, and MAPK are crucial in regulating cell death.

Conclusions:

• Oxidative stress is central to biotoxin-induced liver injury, irrespective of the toxin source.
• Understanding these pathways offers potential for broad-spectrum, redox-targeted therapies.
• Targeting oxidative stress pathways presents a promising strategy for treating biotoxin-induced liver damage.