<p>Extensive growth in the production of nanoparticles (NPs) together with increased usage in a variety of consumer products has introduced potential health risks amongst organisms, humans and ecosystems. Unique physico-chemical properties of nanoparticles facilitate their entry, bioaccumulation and subsequent interaction with biounterfaces in diverse cellular systems. These nano bio-interfaces occur in different cells/organ systems and contribute to selective toxicity through a cross talk amongst couple of mechanisms viz. oxidative stress, inflammation, apoptosis, DNA damage and redox signaling pathways. Present review describes the role of these mechanisms especially in teratogenicity induced by metallic nanoparticles. Available data suggests that generation of ROS and oxidative stress are the predominant mechanisms of NP induced materno—fetal toxicity. They do trigger inflammatory responses in the fetus and lead to structural abnormalities. Exposure to NPs induces apoptosis and DNA damage that result in fetal cytotoxicity. Autophagy has been recognized as a major form of cell death encountered during pregnancy in NP treated models. It may involve oocytogenesis, implantation, placentation, embryogenesis and preterm delivery. Vascular signaling and toll like receptors are also involved in the feto-toxicity of NPs. It is concluded that mechanism based high throughput in vitro screening of NPs can predict the genesis of teratogenicity. A better understanding of teratogenicity induced by NPs is not only essential for health risk assessment but also for the design and synthesis of novel and safer nanomaterials.</p>