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Reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive sulfur species (RSS)—collectively referred to as RONSS—are essential redox-active molecules that are involved in cellular communication and the initiation of oxidative stress in pathological circumstances. This chapter discusses the various roles of RONSS in modulating redox equilibrium and influencing disease processes in numerous chronic diseases. Although substantial research has been conducted on ROS and RNS separately, the combined functions with RSS in disease-specific pathophysiology and therapeutic potential are yet insufficiently investigated. The chapter delineates the molecular origins, interactions, and subsequent effects of RONSS in neurological illnesses, cardiovascular disorders, diabetes, cancer, and muscular dysfunctions. We emphasize mechanisms that include dysfunction in the mitochondria, free radical damage to nucleic acids and proteins, and inflammatory activation. Recent advancements in redox imaging, antioxidant modulation, and molecular targeting are examined as promising strategies for comprehending and addressing RONSS-related illness progression.

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Recent Advances in Oxidative Stress Associated Chronic Diseases

  • 章节

  • 发表日期：

    2026年

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  • Sana Firdous,
  • Meenakshi Prakash,
  • Shaikh Zaahid Iqbal,
  • Yash Banabakode,
  • R. Deepika,
  • Rebeccas Thomas,
  • T. Aravinth Karthik,
  • Sharine Priscilla,
  • S. Beer Mohamed,
  • Sahabudeen Sheik Mohideen

摘要

Reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive sulfur species (RSS)—collectively referred to as RONSS—are essential redox-active molecules that are involved in cellular communication and the initiation of oxidative stress in pathological circumstances. This chapter discusses the various roles of RONSS in modulating redox equilibrium and influencing disease processes in numerous chronic diseases. Although substantial research has been conducted on ROS and RNS separately, the combined functions with RSS in disease-specific pathophysiology and therapeutic potential are yet insufficiently investigated. The chapter delineates the molecular origins, interactions, and subsequent effects of RONSS in neurological illnesses, cardiovascular disorders, diabetes, cancer, and muscular dysfunctions. We emphasize mechanisms that include dysfunction in the mitochondria, free radical damage to nucleic acids and proteins, and inflammatory activation. Recent advancements in redox imaging, antioxidant modulation, and molecular targeting are examined as promising strategies for comprehending and addressing RONSS-related illness progression.