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

Exposure to diverse naturally occurring biotoxins—originating from fungal, plant, and algal sources—poses a severe and escalating threat to global public health. The liver, due to its pivotal role in toxin metabolism, faces an increased risk of injury from toxin accumulation. Although extensive research has been conducted on toxin-induced hepatic injury, the heterogeneity of oxidative stress mechanisms across different injury phenotypes (such as necrosis, steatosis, and fibrosis) remains poorly understood. This review systematically addresses this gap by establishing oxidative stress as the central, convergent mechanism underlying biotoxin-induced liver injury. By critically comparing representative toxins, we examine the role of oxidative stress in various biotoxin-induced hepatic injury phenotypes and their underlying molecular mechanisms. Furthermore, we discuss the specific involvement of interconnected signaling cascades—specifically the Nrf2, NF-κB and MAPK pathways—in orchestrating different modes of cell death (including apoptosis, ferroptosis, and necroptosis), and summarize antagonistic strategies for biotoxin-induced hepatic injury from an oxidative stress perspective, highlighting their translational potential and providing a robust rationale for developing broad-spectrum, redox-targeted therapies.