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<p>Rapid industrialization and technological advancements have led to extensive environmental contamination of lead, disrupting the ecological balance and posing significant risks to biodiversity and ecosystem functionality. Lead remains a critical concern due to its high toxicity, persistence, and ability to bioaccumulate, which can elicit oxidative and metabolic disruptions. Lead toxicity impairs haematological, biochemical, and structural parameters, ultimately compromising hepatic, renal, neurological, and reproductive functions. This review integrates the current understanding of the mechanistic pathways involved in lead-induced toxicity, with a specific focus on oxidative stress and apoptosis. Lead exposure disrupts redox homeostasis, characterized by an increase in reactive oxygen species (ROS) and a reduction in antioxidant defenses, notably superoxide dismutase, catalase, and glutathione levels. Concurrently, it triggers apoptotic signalling via mitochondrial dysfunction, thereby elevating the expression of pro-apoptotic mediators (e.g., Bax, caspases) while suppressing the anti-apoptotic factor Bcl-2. Furthermore, this review discusses emerging strategies for prevention and therapy, highlighting the protective effects of natural phytochemicals and antioxidant-based interventions that may alleviate cellular and tissue damage associated with lead exposure.</p>

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Unravelling lead-induced toxicity in mammals: the role of oxidative stress and apoptosis and their modulation by emerging therapeutic strategies

  • 期刊论文

  • 发表日期：

    2026年2月22日

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  • Reena Sheoran,
  • Sunita Grewal,
  • Jagjeet Singh,
  • Vinay Malik

摘要

Rapid industrialization and technological advancements have led to extensive environmental contamination of lead, disrupting the ecological balance and posing significant risks to biodiversity and ecosystem functionality. Lead remains a critical concern due to its high toxicity, persistence, and ability to bioaccumulate, which can elicit oxidative and metabolic disruptions. Lead toxicity impairs haematological, biochemical, and structural parameters, ultimately compromising hepatic, renal, neurological, and reproductive functions. This review integrates the current understanding of the mechanistic pathways involved in lead-induced toxicity, with a specific focus on oxidative stress and apoptosis. Lead exposure disrupts redox homeostasis, characterized by an increase in reactive oxygen species (ROS) and a reduction in antioxidant defenses, notably superoxide dismutase, catalase, and glutathione levels. Concurrently, it triggers apoptotic signalling via mitochondrial dysfunction, thereby elevating the expression of pro-apoptotic mediators (e.g., Bax, caspases) while suppressing the anti-apoptotic factor Bcl-2. Furthermore, this review discusses emerging strategies for prevention and therapy, highlighting the protective effects of natural phytochemicals and antioxidant-based interventions that may alleviate cellular and tissue damage associated with lead exposure.