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氧化钇纳米颗粒可改善氢氧化钙和钛酸钙纳米颗粒引起的基因组 DNA 和线粒体损伤、ROS 生成和炎症。

Yttrium oxide nanoparticles ameliorates calcium hydroxide and calcium titanate nanoparticles induced genomic DNA and mitochondrial damage, ROS generation and inflammation.

机构信息

Zoology Department, Faculty of Science, Cairo University, Giza, Egypt.

Faculty of Biotechnology, October University for Modern Sciences and Arts, 6 Ocober, Egypt.

出版信息

Sci Rep. 2024 Jun 6;14(1):13015. doi: 10.1038/s41598-024-62877-4.

DOI:10.1038/s41598-024-62877-4
PMID:38844752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11156978/
Abstract

Calcium hydroxide (Ca(OH)NPs), calcium titanate (CaTiONPs) and yttrium oxide (YONPs) nanoparticles are prevalent in many industries, including food and medicine, but their small size raises concerns about potential cellular damage and genotoxic effects. However, there are very limited studies available on their genotoxic effects. Hence, this was done to investigate the effects of multiple administration of Ca(OH)NPs, CaTiONPs or/and YONPs on genomic DNA stability, mitochondrial membrane potential integrity and inflammation induction in mouse brain tissues. Mice were orally administered Ca(OH)NPs, CaTiONPs or/and YONPs at a dose level of 50 mg/kg b.w three times a week for 2 weeks. Genomic DNA integrity was studied using Comet assay and the level of reactive oxygen species (ROS) within brain cells was analyzed using 2,7 dichlorofluorescein diacetate dye. The expression level of Presenilin-1, tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6) genes and the integrity of the mitochondrial membrane potential were also detected. Oral administration of Ca(OH)NPs caused the highest damage to genomic DNA and mitochondrial membrane potential, less genomic DNA and mitochondrial damage was induced by CaTiONPs administration while administration of YONPs did not cause any remarkable change in the integrity of genomic DNA and mitochondrial membrane potential. Highest ROS generation and upregulation of presenilin-1, TNF-α and IL-6 genes were also observed within the brain cells of mice administrated Ca(OH)NPs but YONPs administration almost caused no changes in ROS generation and genes expression compared to the negative control. Administration of CaTiONPs alone slightly increased ROS generation and the expression level of TNF-α and IL-6 genes. Moreover, no remarkable changes in the integrity of genomic DNA and mitochondrial DNA potential, ROS level and the expression level of presenilin-1, TNF-α and IL-6 genes were noticed after simultaneous coadministration of YONPs with Ca(OH)NPs and CaTiONPs. Coadministration of YONPs with Ca(OH)NPs and CaTiONPs mitigated Ca(OH)NPs and CaTiONPs induced ROS generation, genomic DNA damage and inflammation along with restoring the integrity of mitochondrial membrane potential through YONPs scavenging free radicals ability. Therefore, further studies are recommended to study the possibility of using YONPs to alleviate Ca(OH)NPs and CaTiONPs induced genotoxic effects.

摘要

氢氧化钙 (Ca(OH)NPs)、钛酸钙 (CaTiONPs) 和氧化钇 (YONPs) 纳米颗粒广泛存在于食品和医药等许多行业中，但它们的小尺寸引起了人们对潜在细胞损伤和遗传毒性的关注。然而，关于它们的遗传毒性影响的研究非常有限。因此，本研究旨在探讨多次给予 Ca(OH)NPs、CaTiONPs 或/和 YONPs 对小鼠脑组织中基因组 DNA 稳定性、线粒体膜电位完整性和炎症诱导的影响。将小鼠以 50mg/kg bw 的剂量经口给予 Ca(OH)NPs、CaTiONPs 或/和 YONPs，每周 3 次，共 2 周。使用彗星试验研究基因组 DNA 的完整性，并使用 2,7-二氯二氢荧光素二乙酸酯染料分析脑细胞内活性氧 (ROS) 的水平。还检测了早老素-1、肿瘤坏死因子-α (TNF-α) 和白细胞介素-6 (IL-6) 基因的表达水平以及线粒体膜电位的完整性。结果表明，口服给予 Ca(OH)NPs 导致基因组 DNA 和线粒体膜电位损伤最严重，给予 CaTiONPs 导致的基因组 DNA 和线粒体损伤较少，而给予 YONPs 则未导致基因组 DNA 和线粒体膜电位完整性发生显著变化。还观察到给予 Ca(OH)NPs 的小鼠脑细胞中 ROS 生成和早老素-1、TNF-α 和 IL-6 基因的表达水平最高，但与阴性对照组相比，给予 YONPs 后，ROS 生成和基因表达几乎没有变化。单独给予 CaTiONPs 可轻微增加 ROS 生成以及 TNF-α 和 IL-6 基因的表达水平。此外，同时给予 YONPs 与 Ca(OH)NPs 和 CaTiONPs 后，未观察到基因组 DNA 和线粒体 DNA 完整性、ROS 水平以及早老素-1、TNF-α 和 IL-6 基因的表达水平发生显著变化。YONPs 通过清除自由基的能力减轻了 Ca(OH)NPs 和 CaTiONPs 诱导的 ROS 生成、基因组 DNA 损伤和炎症，同时恢复了线粒体膜电位的完整性。因此，建议进一步研究使用 YONPs 来减轻 Ca(OH)NPs 和 CaTiONPs 诱导的遗传毒性的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/82ed762c83d4/41598_2024_62877_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/20ad0d691164/41598_2024_62877_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/7d8fe0d1ce35/41598_2024_62877_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/f16797bfd183/41598_2024_62877_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/82ed762c83d4/41598_2024_62877_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/20ad0d691164/41598_2024_62877_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/7d8fe0d1ce35/41598_2024_62877_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/f16797bfd183/41598_2024_62877_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/11156978/82ed762c83d4/41598_2024_62877_Fig4_HTML.jpg

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