Silver and titanium dioxide nanoparticles alter oxidative/inflammatory response and renin–angiotensin system in brain

Krawczyńska, Agata; Dziendzikowska, Katarzyna; Gromadzka-Ostrowska, Joanna; Lankoff, Anna; Herman, Andrzej Przemysław; Oczkowski, Michał; Królikowski, Tomasz; Wilczak, Jacek; Wojewódzka, Maria; Kruszewski, Marcin

doi:10.1016/j.fct.2015.08.005

Cited by 46 publications

(27 citation statements)

References 80 publications

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“…They concluded that apoptosis was initiated by NP-induced OS in the brain. After rats were administered TiO 2 and Ag NPs through a single injection, there was a change in the expression of OS-related genes in the rat brain [ 72 ]. At the same time, the antioxidant capability as well as the renin-angiotensin system in the brain was disrupted.…”

Section: Reviewmentioning

confidence: 99%

Is Neurotoxicity of Metallic Nanoparticles the Cascades of Oxidative Stress?

et al. 2016

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With the rapid development of nanotechnology, metallic (metal or metal oxide) nanoparticles (NPs) are widely used in many fields such as cosmetics, the food and building industries, and bio-medical instruments. Widespread applications of metallic NP-based products increase the health risk associated with human exposures. Studies revealed that the brain, a critical organ that consumes substantial amounts of oxygen, is a primary target of metallic NPs once they are absorbed into the body. Oxidative stress (OS), apoptosis, and the inflammatory response are believed to be the main mechanisms underlying the neurotoxicity of metallic NPs. Other studies have disclosed that antioxidant pretreatment or co-treatment can reverse the neurotoxicity of metallic NPs by decreasing the level of reactive oxygen species, up-regulating the activities of antioxidant enzymes, decreasing the proportion of apoptotic cells, and suppressing the inflammatory response. These findings suggest that the neurotoxicity of metallic NPs might involve a cascade of events following NP-induced OS. However, additional research is needed to determine whether NP-induced OS plays a central role in the neurotoxicity of metallic NPs, to develop a comprehensive understanding of the correlations among neurotoxic mechanisms and to improve the bio-safety of metallic NP-based products.

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Section: Reviewmentioning

confidence: 99%

Is Neurotoxicity of Metallic Nanoparticles the Cascades of Oxidative Stress?

et al. 2016

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“…AgNPs were reported to alter the expression of oxidative stress-related genes (Rahman et al 2009; Krawczyńska et al 2015), as well as biochemical parameters (Skalska et al 2016). …”

Section: Discussionmentioning

confidence: 99%

“…As mentioned above, there is evidence indicating the ability of AgNPs to induce oxidative stress in many organs of exposed animals, including brain, which is more vulnerable to excessive reactive oxygen or nitrogen species (ROS/RNS) than other organs (Friedman 2011). AgNPs were reported to alter the expression of oxidative stress-related genes (Rahman et al 2009; Krawczyńska et al 2015), as well as biochemical parameters (Skalska et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Prolonged Exposure to Silver Nanoparticles Results in Oxidative Stress in Cerebral Myelin

et al. 2018

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Currently, silver nanoparticles (AgNPs) are frequently used in a wide range of medical and consumer products. Substantial usage of AgNPs is considered to create substantive risks to both the environment and the human health. Since there is increasing evidence that the main mechanism of toxicity of AgNPs relates to oxidative stress, in the current study we investigate oxidative stress-related biochemical parameters in myelin isolated from adult rat brain subjected to a low dose of AgNPs. Animals were exposed for 2 weeks to 0.2 mg/kg b.w. of small (10 nm) AgNPs stabilized in citrate buffer or silver citrate established as a control to compare the effects of particulate and ionic forms of silver. We observe enhanced peroxidation of lipids and decreased concentrations of protein and non-protein –SH groups in myelin membranes. Simultaneously, expression of superoxide dismutase, a free radical scavenger, is increased whereas the process of protein glutathionylation, being a cellular protective mechanism against irreversible oxidation, is found to be inefficient. Results indicate that oxidative stress-induced alterations in myelin membranes may be the cause of ultrastructural disturbances in myelin sheaths.

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“…These changes indicated that OS was involved in neurological lesions induced by TiO 2 NPs. In further studies, Krawczynska et al [ 22 ] injected rats with TiO 2 NPs intravenously. Twenty-eight days after injection, the level of aromatase was reduced and glutathione peroxidase and reductase activities were suppressed, implying that the regulation of oxidative stress in the brain was disturbed.…”

Section: Reviewmentioning

confidence: 99%

Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms

Song¹,

Liu²,

Feng³

et al. 2016

Beilstein J. Nanotechnol.

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SummaryTitanium dioxide nanoparticles (TiO2 NPs) possess unique characteristics and are widely used in many fields. Numerous in vivo studies, exposing experimental animals to these NPs through systematic administration, have suggested that TiO2 NPs can accumulate in the brain and induce brain dysfunction. Nevertheless, the exact mechanisms underlying the neurotoxicity of TiO2 NPs remain unclear. However, we have concluded from previous studies that these mechanisms mainly consist of oxidative stress (OS), apoptosis, inflammatory response, genotoxicity, and direct impairment of cell components. Meanwhile, other factors such as disturbed distributions of trace elements, disrupted signaling pathways, dysregulated neurotransmitters and synaptic plasticity have also been shown to contribute to neurotoxicity of TiO2 NPs. Recently, studies on autophagy and DNA methylation have shed some light on possible mechanisms of nanotoxicity. Therefore, we offer a new perspective that autophagy and DNA methylation could contribute to neurotoxicity of TiO2 NPs. Undoubtedly, more studies are needed to test this idea in the future. In short, to fully understand the health threats posed by TiO2 NPs and to improve the bio-safety of TiO2 NPs-based products, the neurotoxicity of TiO2 NPs must be investigated comprehensively through studying every possible molecular mechanism.

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Silver and titanium dioxide nanoparticles alter oxidative/inflammatory response and renin–angiotensin system in brain

Cited by 46 publications

References 80 publications

Is Neurotoxicity of Metallic Nanoparticles the Cascades of Oxidative Stress?

Is Neurotoxicity of Metallic Nanoparticles the Cascades of Oxidative Stress?

Prolonged Exposure to Silver Nanoparticles Results in Oxidative Stress in Cerebral Myelin

Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms

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