The article discusses the role of reactive oxygen species (ROS) in apoptosis induction, particularly in inflammatory cells. ROS, including various radicals and non-radical species, are generated by inflammatory cells and play dual roles: destructive and regulatory. They can induce apoptosis by triggering caspase activation through the release of cytochrome c from mitochondria, but they also have anti-apoptotic effects. The review highlights that ROS are involved in receptor-mediated signaling pathways and transcriptional activation. Specific studies show that hydrogen peroxide can induce apoptosis in neutrophils and eosinophils, which can be blocked by antioxidants like catalase and glutathione. ROS also influence the activation of death receptors, such as TNF and Fas, by contributing to mitochondrial events and generating ceramide. Additionally, nitric oxide (NO) has been shown to induce apoptosis in various cell types and can act as a survival factor, depending on its concentration. The mechanisms by which NO blocks apoptosis involve the induction of heat shock proteins, which increase intracellular glutathione levels, opposing the pro-apoptotic effects of ROS. Overall, the article emphasizes the complex and multifaceted role of ROS in regulating apoptosis.The article discusses the role of reactive oxygen species (ROS) in apoptosis induction, particularly in inflammatory cells. ROS, including various radicals and non-radical species, are generated by inflammatory cells and play dual roles: destructive and regulatory. They can induce apoptosis by triggering caspase activation through the release of cytochrome c from mitochondria, but they also have anti-apoptotic effects. The review highlights that ROS are involved in receptor-mediated signaling pathways and transcriptional activation. Specific studies show that hydrogen peroxide can induce apoptosis in neutrophils and eosinophils, which can be blocked by antioxidants like catalase and glutathione. ROS also influence the activation of death receptors, such as TNF and Fas, by contributing to mitochondrial events and generating ceramide. Additionally, nitric oxide (NO) has been shown to induce apoptosis in various cell types and can act as a survival factor, depending on its concentration. The mechanisms by which NO blocks apoptosis involve the induction of heat shock proteins, which increase intracellular glutathione levels, opposing the pro-apoptotic effects of ROS. Overall, the article emphasizes the complex and multifaceted role of ROS in regulating apoptosis.