Akademik Veri Yönetim Sistemi
Journal of Trace Elements in Medicine and Biology, cilt.83, 2024 (SCI-Expanded)
Background: Nickel oxide nanoparticles (NiONPs) are used as industrial photoelectric and recording materials, catalysts, and sensors. It has been increasingly used in many industrial sectors. Lungs are the important biological barrier that comes into contact with nanomaterials in the inhaled air. This study aimed to compare the effects of nickel oxide (NiO) microparticles and NiONPs on rat lung tissues in different dose administrations, such as oral, intraperitoneal, and intravenous. Methods: The mature male Wistar rats (n = 42) were divided into seven groups with six animals: Group I (control), Group II NiO gavage (150 mg/kg), Group III NiO intraperitoneally (20 mg/kg), Group IV NiO intravenously (1 mg/kg), Group V NiONP gavage (150 mg/kg), Group VI NiONP intraperitoneal (20 mg/kg), and Group VII NiONP intravenous (1 mg/kg) for 21 days. Oxidative stress (MDA, CAT, SOD, GPx, and GST), apoptotic marker (p53) gene expression, and histopathological changes were determined comparatively. Results: Our data showed that NiO and NiONPs caused an exposure-related increase in the incidence of alveolar/bronchiolar pathological changes, oxidative damage, and p53 gene expression in male rats. Intravenous exposure to NiONPs produces statistically (p < 0.05) more oxidative damage and histopathological changes than exposure to NİO. It also induces higher upregulation of the pro-apoptotic p53 gene. Conclusion: NiO and NiONPs induce oxidative damage, histopathological alterations and p53 gene expression in rat lungs. Thus, exposure to NiO and NiONPs, especially intravenously, may indicate more toxicity and carcinogenicity.