Waseem Mohd, Kaushik Pooja, Dutta Shamita, Chakraborty Rohan, Hassan Md Imtaiyaz, Parvez Suhel
Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi 110062, India.
Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India.
ACS Omega. 2022 Jan 21;7(4):3192-3202. doi: 10.1021/acsomega.1c04740. eCollection 2022 Feb 1.
Titanium dioxide (TiO) nanoparticles are among the largely manmade nanomaterials worldwide and are broadly used as both industrial and user products. The primary target site for several nanoparticles is the liver, including TiO nanoparticles (TNPs), exposed directly or indirectly through ingestion of contaminated water, food, or animals and elevated environmental contamination. Oxidative stress is a known facet of nanoparticle-induced toxicity, including TNPs. Mitochondria are potential targets for nanoparticles in several types of toxicity, such as hepatotoxicity. Nevertheless, its causal mechanism is still controversial due to scarcity of literature linking the role of mitochondria-mediated TNP-induced hepatotoxicity. The objective of the current study was to evaluate the relation of mitochondrial oxidative stress and respiratory chain mechanisms with TNP-induced mitochondrial dysfunction , and explore the hepatoprotective effect of quercetin (QR), which is a polyphenolic flavonoid abundant in fruits and vegetables with known antioxidant properties, on TNP-induced mitochondrial oxidative stress and disturbance in respiratory chain complex enzymes in the liver of rats. : Enzymatic and non-enzymatic antioxidant levels, oxidative stress markers, and mitochondrial complexes were assessed with regard to TNP-induced hepatotoxicity. The depleted lipid peroxidation levels and protein carbonyl content, in mitochondria, induced by TNPs were restored significantly by pretreatment with QR. QR modulated the altered non-enzymatic and enzymatic antioxidants and mitochondrial complex enzymes. Based on the findings, we conclude that QR, which mitigates oxidative stress caused by mitochondrial dysfunction, holds promising capability to potentially diminish TNP-induced adverse effects in the liver.
二氧化钛（TiO）纳米颗粒是全球大量人造纳米材料之一，广泛用作工业产品和消费产品。包括二氧化钛纳米颗粒（TNPs）在内的几种纳米颗粒的主要靶器官是肝脏，其可通过摄入受污染的水、食物或动物直接或间接接触，并因环境污染加剧而暴露。氧化应激是纳米颗粒诱导毒性的一个已知方面，包括TNPs。线粒体是纳米颗粒在几种毒性类型（如肝毒性）中的潜在靶点。然而，由于将线粒体介导的TNP诱导肝毒性的作用联系起来的文献稀缺，其因果机制仍存在争议。 本研究的目的是评估线粒体氧化应激和呼吸链机制与TNP诱导的线粒体功能障碍之间的关系，并探讨槲皮素（QR）对TNP诱导的大鼠肝脏线粒体氧化应激和呼吸链复合酶紊乱的肝保护作用。QR是一种在水果和蔬菜中含量丰富的具有已知抗氧化特性的多酚类黄酮。：针对TNP诱导的肝毒性评估了酶促和非酶促抗氧化剂水平、氧化应激标志物和线粒体复合物。TNPs诱导的线粒体中脂质过氧化水平和蛋白质羰基含量的降低通过QR预处理得到显著恢复。QR调节了改变的非酶促和酶促抗氧化剂以及线粒体复合酶。 基于这些发现，我们得出结论，QR可减轻线粒体功能障碍引起的氧化应激，具有潜在减轻TNP诱导的肝脏不良反应的能力。
