Pesticides have played a crucial role in modern agriculture, safeguarding crops and ensuring global food security. However, their widespread and often indiscriminate use has raised serious concerns about their long-term impact on human health and the environment. From acute poisoning cases to chronic diseases and biodiversity loss, toxic pesticides pose a complex and pressing challenge that requires urgent scientific and policy-driven solutions.

This Collection of Discover Toxicology explores the dual challenge of monitoring toxic pesticides and the mitigation of their harmful effects on the environment and human health, while promoting sustainable alternatives. We invite cutting-edge research and reviews on innovative diagnostic techniques for detecting pesticide exposure, the development of novel biopesticides, precision agriculture strategies, and policy interventions that can reduce reliance on hazardous chemicals. Key topics include:

• Advances in biomonitoring and early detection methods for pesticide-related toxicity

• Environmentally friendly pest management alternatives to toxic pesticides, such as biopesticides and integrated pest management (IPM)

• The role of nanotechnology and AI-driven approaches in the reduction of pesticides and pesticide toxicity

• Mechanistic insights into pesticide toxicity and their effects on human and ecosystem health

• Policy frameworks and regulatory strategies for toxic pesticides and transition to sustainable agricultural practices

By fostering interdisciplinary dialogue and highlighting pioneering research, this Collection aims to contribute to a future where food production is both safe and sustainable. We encourage contributions from science and industry experts working towards reducing the global burden of toxic pesticides.

Keywords: Agrochemicals; Biomonitoring; Ecotoxicology; Environmental Contamination; Human Health Impacts; Sustainable Pest Management; Toxicology

The interplay between toxicological mechanisms and redox biology is a critical area of research that underpins our understanding of how various environmental and biological factors influence health outcomes. Reactive oxygen species and other redox-active molecules, collectively called reactive species (RS) are central players in cellular signaling and homeostasis. However, their dysregulation can lead to oxidative stress, resulting in significant cellular damage. Toxicants, whether from environmental exposure or pharmaceutical sources, can profoundly alter redox states and disrupt normal biological functions, leading to a spectrum of adverse health effects.

Exposure to certain toxicants can lead to disease by compromising the body's antioxidant defenses. This disruption may occur through various direct and indirect mechanisms, including the generation of reactive species, interference with metal ion homeostasis, and alterations in gene expression, cellular signaling, antioxidant synthesis pathways and antioxidant activity. As a result, the body's ability to neutralize reactive species diminishes, allowing their accumulation and causing oxidative damage to vital biomolecules such as DNA, proteins, lipids, and carbohydrates. This oxidative stress can lead to mutations, impaired protein function, lipid peroxidation, and the formation of advanced glycation end-products (AGEs). These molecular alterations can trigger a cascade of inflammatory responses, further intensifying cellular damage and fostering chronic inflammation.

This Collection is motivated by the urgent need to integrate insights from toxicology and redox biology to better comprehend the mechanisms underlying toxicity and the biological responses to oxidative stress. Recent studies have revealed novel molecular targets and pathways that mediate the toxic effects of various compounds, highlighting the importance of redox signaling in these processes. By fostering interdisciplinary collaboration among toxicologists, biochemists, and molecular biologists, we aim to stimulate innovative research that addresses current challenges in the field. This Collection seeks to capture the momentum of recent discoveries and facilitate discussions on the implications of these findings for public health and environmental safety.

The purpose of this Collection is to provide a dedicated platform for researchers to share their findings on the mechanistic insights linking toxicology and redox biology. We invite submissions that explore the molecular mechanisms of toxicity, the role of oxidative stress in disease processes, and the potential for redox-based therapeutic strategies. By compiling a diverse array of studies, this Collection aims to enhance our understanding of how toxicants interact with biological systems and inform future research directions in both toxicology and redox biology.

Areas of interest encompass, but are not limited to, chemical analysis and studies conducted through in vitro, in vivo, ex vivo, in silico approaches:

Chemistry of reactive species generation and regulation. Toxicants can drive the overproduction of reactive species by promoting redox cycling or activating redox-active metals, while also weakening antioxidant defenses that normally neutralize these species. This imbalance leads to oxidative stress, a key contributor to cellular damage and disease. Understanding the chemical pathways through which toxicants directly or indirectly generate reactive species is essential for uncovering their role in toxicity and disease mechanisms.

Endogenous molecular targets of toxicants. These include direct interactions with cellular components, such as lipids, proteins, and DNA, as well as indirect effects like the inhibition of antioxidant enzymes or depletion of essential cofactors. Enzymes involved in antioxidant synthesis (e.g., glutathione peroxidase, superoxide dismutase), mitochondrial proteins, metal-binding proteins as well as small molecules (e.g., glutathione, neurotransmitters, cofactors). Toxicants may bind to or modify these targets causing post-translational protein, epigenetic changes, production of pro-inflammatory mediators (e.g., lipid peroxidation and AGE products), or redox modifications of small molecules, impairing their function and further exacerbating oxidative stress.

Toxicant-mediated redox signaling pathways and other oxidative stress mechanisms. These pathways regulate critical cellular functions such as proliferation, apoptosis, and immune responses. Toxicants can alter redox-sensitive transcription factors (e.g., Nrf2, NF-κB), leading to aberrant gene expression and contributing to disease pathogenesis. Such mechanisms compromise the cell’s ability to maintain redox homeostasis which is a complex and a dynamic process. Xenobiotics can modulate redox-sensitive signaling cascades, alter mitochondrial function, activate immune response, influence the expression of detoxifying genes and alter synthesis of endogenous antioxidants. These interactions not only affect cellular resilience to stress but also determine the long-term outcomes of toxicant exposure.

This Collection supports and amplifies research related to SDG 3.

Keywords: toxicology; redox biology; reactive oxygen species; ROS; oxidative stress; free radicals; oxidative damage; disease pathogenesis