Metallic and metallic oxide nanoparticles toxicity primarily targets the mitochondria of hepatocytes and renal cells.
Autor: | Jarrar B; Nanobiology Unit, Faculty of Sciences, Jerash University, Jordan., Almansour M; College of Science, King Saud University, Riyadh, Saudi Arabia., Al-Doaiss A; Department of Biology, College of Science, King Khalid University, Abha, Saudi Arabia., Lee SY; Faculty of Health and Life Sciences, INTI International University, Nilai, Malaysia., Melhem W; School of Medicine, King Faisal University, Saudi Arabia., Jarrar Q; Department of Applied Pharmaceutical Sciences and Clinical Pharmacy, Faculty of Pharmacy, Isra University, Jordan., Sewelam A; Department of Human Anatomy and Embryology, Faculty of Medicine, Zagazig University, Egypt. |
---|---|
Jazyk: | angličtina |
Zdroj: | Toxicology and industrial health [Toxicol Ind Health] 2024 Dec; Vol. 40 (12), pp. 667-678. Date of Electronic Publication: 2024 Sep 17. |
DOI: | 10.1177/07482337241282860 |
Abstrakt: | Nanoparticles (NPs) are utilized in various applications, posing potential risks to human health, tissues, cells, and macromolecules. This study aimed to investigate the ultrastructural alterations in hepatocytes and renal tubular cells induced by metallic and metal oxide NPs. Adult healthy male Wistar albino rats ( Rattus norvegicus ) were divided into 6 ( n = 7) control and 6 treated groups ( n = 7). The rats in the treated groups exposed daily to silver NPs, gold NPs, zinc oxide NPs, silicon dioxide NPs, copper oxide NPs, and ferric oxide NPs for 35 days. The members of the control group for each corresponding NPs received the respective vehicle. Liver and kidney tissue blocks from all rats were processed for Transmission Electron Microscopy (TEM) examinations. The hepatocytes and renal tubular cells of all NPs-treated rats demonstrated mitochondrial ultrastructural alterations mainly cristolysis, swelling, membrane disruption, lucent matrices, matrices lysis, and electron-dense deposits. However, other organelles demonstrated injury but to a lesser extent in the form of shrunken nuclei, nuclear membrane indentation, endoplasmic reticulum fragmentation, cellular membranes enfolding, brush border microvilli disruption, lysosomal hyperplasia, ribosomes dropping, and peroxisome formation. One may conclude from the findings that the hepatocytes and the renal tubular cells mitochondria are the main targets for nanoparticles toxicity ending in mitochondrial disruption and cell injury. Further studies taking into account the relation of mitochondrial ultrastructural damage with a weakened antioxidant defense system induced by chronic exposure to nanomaterials are needed. Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. |
Databáze: | MEDLINE |
Externí odkaz: |