This review article explores the mechanisms of nanoparticle (NP)-induced oxidative stress and toxicity, focusing on metal-based nanoparticles and carbon nanotubes (CNT). It highlights the role of reactive oxygen species (ROS) in NP toxicity, emphasizing their generation through physicochemical properties of NPs, such as surface reactivity, size, composition, and presence of transition metals. ROS can be generated intrinsically or extrinsically, leading to oxidative stress, which is linked to various pathophysiological effects including genotoxicity, inflammation, and fibrosis. The article discusses the generation of ROS through different NP characteristics and their interaction with cellular components, leading to oxidative damage. It also examines the role of ROS in NP-induced inflammation, genotoxicity, and fibrosis, highlighting the involvement of signaling pathways such as NF-κB, MAPK, and AP-1. The review emphasizes the importance of understanding oxidative stress as a key determinant of NP-induced toxicity and the need for systematic toxicity screening using oxidative stress as a predictive model. The article also discusses the prooxidant effects of metal oxide nanoparticles, their interaction with cellular components, and the resulting oxidative damage. It concludes by emphasizing the importance of understanding the molecular and cellular mechanisms of NP-induced oxidative stress to develop strategies for mitigating NP toxicity. The review underscores the need for rigorous characterization of NPs and the establishment of stringent procedures for testing their oxidative potential prior to commercialization.This review article explores the mechanisms of nanoparticle (NP)-induced oxidative stress and toxicity, focusing on metal-based nanoparticles and carbon nanotubes (CNT). It highlights the role of reactive oxygen species (ROS) in NP toxicity, emphasizing their generation through physicochemical properties of NPs, such as surface reactivity, size, composition, and presence of transition metals. ROS can be generated intrinsically or extrinsically, leading to oxidative stress, which is linked to various pathophysiological effects including genotoxicity, inflammation, and fibrosis. The article discusses the generation of ROS through different NP characteristics and their interaction with cellular components, leading to oxidative damage. It also examines the role of ROS in NP-induced inflammation, genotoxicity, and fibrosis, highlighting the involvement of signaling pathways such as NF-κB, MAPK, and AP-1. The review emphasizes the importance of understanding oxidative stress as a key determinant of NP-induced toxicity and the need for systematic toxicity screening using oxidative stress as a predictive model. The article also discusses the prooxidant effects of metal oxide nanoparticles, their interaction with cellular components, and the resulting oxidative damage. It concludes by emphasizing the importance of understanding the molecular and cellular mechanisms of NP-induced oxidative stress to develop strategies for mitigating NP toxicity. The review underscores the need for rigorous characterization of NPs and the establishment of stringent procedures for testing their oxidative potential prior to commercialization.