Hindawi Publishing Corporation ISRN Toxicology Volume 2013, Article ID 316075, 8 pages http://dx.doi.org/10.1155/2013/316075 Research Article Nanosized Zinc Oxide Induces Toxicity in Human Lung Cells Devashri Sahu, 1 G. M. Kannan, 1 R. Vijayaraghavan, 2 T. Anand, 3 and Farhath Khanum 3 1 Pharmacology and Toxicology Division, Defence Research and Development Establishment, Jhansi Road, Gwalior 474001, India 2 Saveetha University, Chennai 600077, India 3 Biochemistry and Nutrition Discipline, Defence Food Research Laboratory, Mysore 570011, India Correspondence should be addressed to Devashri Sahu; devashree.sahu@gmail.com Received 27 May 2013; Accepted 14 July 2013 Academic Editors: G. Ramesh and G. S. Shukla Copyright © 2013 Devashri Sahu et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Zinc oxide nanoparticles (ZnO-NPs) are increasingly used in sunscreens, biosensors, food additives, pigments, rubber manufacture, and electronic materials. With the wide application of ZnO-NPs, concern has been raised about its unintentional health and environmental impacts. Tis study investigates the toxic efects of ZnO-NPs in human lung cells. In order to assess toxicity, human lung epithelial cells (L-132) were exposed to dispersion of 50 nm ZnO-NPs at concentrations of 5, 25, 50, and 100 g/mL for 24 h. Te toxicity was evaluated by observing changes in cell morphology, cell viability, oxidative stress parameters, DNA damage analysis, and gene expression. Exposure to 50 nm ZnO-NPs at concentrations between 5 and 100 g/mL decreased cell viability in a concentration-dependent manner. Morphological examination revealed cell shrinkage, nuclear condensation, and formation of apoptotic bodies. Te oxidative stress parameters revealed signifcant depletion of GSH level and increase in ROS levels suggesting generation of oxidative stress. ZnO-NPs exposure caused DNA fragmentation demonstrating apoptotic type of cell death. ZnO- NPs increased the expression of metallothionein gene, which is considered as a biomarker in metal-induced toxicity. To summarize, ZnO-NPs cause toxicity in human lung cells possibly through oxidative stress-induced apoptosis. 1. Introduction Over the past decade the ability to engineer and produce materials at the nano- or near-atomic scale has triggered rapid product development due to their new interesting properties that were not previously seen at scales above the micrometer. Industrial applications using nanoparticles have resulted in an almost exponentially growing demand for nanosized materials. Due to increasing use of nanoparticles in variety of consumer goods, humans are constantly exposed to such nanomaterials besides exposure at production sites [1–5]. Unintended exposure to nanomaterials may occur via inhalation, dermal exposure, or gastrointestinal tract absorption and may pose a great risk [6, 7]. Despite their wide application, little is known about their efect on human health and environment. Zinc oxide (ZnO) is among the most commonly utilized group of nanomaterials and has wide-ranging applications [8]. As a well-known photocatalyst, ZnO has received much attention in the degradation and complete mineralization of environmental pollutants [9, 10]. ZnO nanoparticles (ZnO- NPs) are used in industrial products including cosmetics, paints, and medical materials. ZnO-NPs have external uses as antibacterial agents in ointments, lotions, mouthwashes, and surface coatings to prevent microorganism growth [11]. ZnO- NPs have also been used as a dietary supplement in human and livestock because zinc can stimulate the immune system and act in an anti-infammatory way [12, 13]. Many in vitro studies demonstrated that ZnO-NPs are toxic to mammalian cells and are even more toxic than other nanoscale structures of metallic oxide [14–16]. In combination with UV exposure, ZnO-NPs are known to generate reactive oxygen species (ROS) like hydroxyl radicals or hydrogen peroxide in aqueous solutions leading to efcient decomposition of organic compounds [17]. Brunner et al. [18] showed that a three-day exposure of human mesothelioma and rodent fbroblast cell to ZnO-NPs (19 nm) caused DNA and mitochondrial damages. Te human lung is a vulnerable organ for nanoparticle invasion as there is approximately 2300 km of airways and