This review article discusses the mechanisms of nanoparticle (NP)-induced oxidative stress and toxicity, focusing on metal-based nanoparticles and carbon nanotubes (CNT). The unique physicochemical properties of engineered nanoparticles make them valuable for various applications, but they also pose potential health risks due to their ability to generate reactive oxygen species (ROS), leading to oxidative stress. Oxidative stress can result from both extracellular factors such as particle surface characteristics and intracellular responses like mitochondrial dysfunction and immune cell activation. ROS-induced damage can lead to genotoxicity, inflammation, and fibrosis, highlighting the importance of understanding NP-induced oxidative stress for predicting toxicity. ROS are generated through various mechanisms, including intrinsic cellular processes and interactions with NP. Factors such as particle size, surface charge, and composition influence ROS production. Metal-based NP, in particular, can catalyze ROS generation via Fenton-type reactions, while CNT-induced oxidative stress is often linked to mitochondrial dysfunction. The prooxidant effects of NP are influenced by their surface properties and interactions with cellular components, leading to oxidative damage to DNA, lipids, and proteins. NP-induced oxidative stress activates signaling pathways such as NF-κB, AP-1, and MAPK, contributing to inflammation, cell death, and fibrosis. The role of ROS in NP-induced toxicity is further highlighted by their involvement in genotoxic effects, inflammatory responses, and fibrosis. Metal-based NP and CNT can induce oxidative stress through various mechanisms, including mitochondrial damage and activation of redox-sensitive pathways. The review emphasizes the importance of characterizing NP properties to understand and mitigate their toxic effects, with a focus on oxidative stress as a key mechanism in NP-induced toxicity. Understanding these mechanisms is crucial for developing strategies to reduce the health risks associated with NP exposure.This review article discusses the mechanisms of nanoparticle (NP)-induced oxidative stress and toxicity, focusing on metal-based nanoparticles and carbon nanotubes (CNT). The unique physicochemical properties of engineered nanoparticles make them valuable for various applications, but they also pose potential health risks due to their ability to generate reactive oxygen species (ROS), leading to oxidative stress. Oxidative stress can result from both extracellular factors such as particle surface characteristics and intracellular responses like mitochondrial dysfunction and immune cell activation. ROS-induced damage can lead to genotoxicity, inflammation, and fibrosis, highlighting the importance of understanding NP-induced oxidative stress for predicting toxicity. ROS are generated through various mechanisms, including intrinsic cellular processes and interactions with NP. Factors such as particle size, surface charge, and composition influence ROS production. Metal-based NP, in particular, can catalyze ROS generation via Fenton-type reactions, while CNT-induced oxidative stress is often linked to mitochondrial dysfunction. The prooxidant effects of NP are influenced by their surface properties and interactions with cellular components, leading to oxidative damage to DNA, lipids, and proteins. NP-induced oxidative stress activates signaling pathways such as NF-κB, AP-1, and MAPK, contributing to inflammation, cell death, and fibrosis. The role of ROS in NP-induced toxicity is further highlighted by their involvement in genotoxic effects, inflammatory responses, and fibrosis. Metal-based NP and CNT can induce oxidative stress through various mechanisms, including mitochondrial damage and activation of redox-sensitive pathways. The review emphasizes the importance of characterizing NP properties to understand and mitigate their toxic effects, with a focus on oxidative stress as a key mechanism in NP-induced toxicity. Understanding these mechanisms is crucial for developing strategies to reduce the health risks associated with NP exposure.