Penetration, distribution and brain toxicity of titanium nanoparticles in rodents' body: a review

Zeman, Tomáš; Loh, El Wui; Čierný, Daniel; Šerý, Omar

doi:10.1049/iet-nbt.2017.0109

Cited by 28 publications

(26 citation statements)

References 74 publications

(114 reference statements)

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“…Many authors studied the serum biochemical parameters, pathology changes, and the biodistribution of TiO 2 -NP in the liver, kidneys, lung, spleen, and brain tissue by facilitating a variety of methods including blood biomarker assays, histopathological examination, etc. The dependence of experiment results on the intake (inhalation, oral administration, intraperitioneal/intravenous injection), dosages, and different sizes of nanoparticles was also discussed [21, 26–33].…”

Section: Resultsmentioning

confidence: 99%

“…Animal experiments, especially in rodents, are being conducted to study the effects of titanium oxide nanoparticles on the human body. In these experiments, titanium was overdosed in rats and the distribution of titanium in the liver, spleen, bone marrow, lungs, brain, and kidneys and titanium-related problems were found in each tissue [32, 33, 90]. In particular, lung problems, cytotoxic reactions, inflammation reactions, fibrosis, and tumors were observed.…”

Section: Discussionmentioning

confidence: 99%

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General review of titanium toxicity

et al. 2019

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Background Titanium is a commonly used inert bio-implant material within the medical and dental fields. Although the use of titanium is thought to be safe with a high success rate, in some cases, there are rare reports of problems caused by titanium. In most of these problematic reports, only individual reports are dominant and comprehensive reporting has not been performed. This comprehensive article has been prepared to review the toxicity of titanium materials within the medical and dental fields. Methods We used online searching tools including MEDLINE (PubMed), Embase, Cochrane Library, and Google Scholar by combining keywords such as “titanium implant toxicity,” “titanium implant corrosion,” “titanium implant allergy,” and “yellow nail syndrome.” Recently updated data has been collected and compiled into one of four categories: “the toxicity of titanium,” “the toxicity of titanium alloys,” “the toxicity of titanium implants,” and “diseases related to titanium.” Results Recent studies with regard to titanium toxicity have been increasing and have now expanded to the medical field in addition to the fields of environmental research and basic science. Problems that may arise in titanium-based dental implants include the generation of titanium and titanium alloy particles and ions deposited into surrounding tissues due to the corrosion and wear of implants, resulting in bone loss due to inflammatory reactions, which may lead to osseointegration failure of the dental implant. These titanium ions and particles are systemically deposited and can lead to toxic reactions in other tissues such as yellow nail syndrome. Additionally, implant failure and allergic reactions can occur due to hypersensitivity reactions. Zirconia implants can be considered as an alternative; however, limitations still exist due to a lack of long-term clinical data. Conclusions Clinicians should pay attention to the use of titanium dental implants and need to be aware of the problems that may arise from the use of titanium implants and should be able to diagnose them, in spite of very rare occurrence. Within the limitation of this study, it was suggested that we should be aware the rare problems of titanium toxicity.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

General review of titanium toxicity

et al. 2019

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“…particles. Both are phagocytized, [25,[35][36][37][38][39] the TiO2 also by microglia [20,40]. In mice, activation of microglial NLRP3 inflammasome by misfolded α-synuclein causes the death of proximal dopaminergic neurons.…”

Section: Discussionmentioning

confidence: 99%

“…[33,34] Both COD and TiO2 are phagocytized, [25,[35][36][37][38][39] TiO2 also by microglia. [40] Both activate the NLRP3 inflammasome. [24,25,38,[41][42][43][44][45][46][47] Crystalline COD is associated with human lesions [31,33,34,[48][49][50] and has been reported in the human brain, [51] particularly when patients are lethally poisoned by the antifreeze ethylene glycol.…”

Section: Introductionmentioning

confidence: 99%

Submicron Crystals of the Parkinson’s Disease Substantia nigra: Calcium Oxalate, Titanium Dioxide and Iron Oxide

Heller¹,

Coffman²

2019

Preprint

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Parkinson's disease (PD) results of the death of dopaminergic neurons of the substantia nigra. When activated, the NLRP3 inflammasome of phagocytes releases inflammatory agents, their release resulting in the death of proximal cells. The hallmark protein of PD, aggregated α-synuclein, is phagocytized and activates the NLRP3 inflammasome. Because crystalline particles are known to activate the NLRP3 inflammasome, to enhance α-synuclein expression and aggregation in dopaminergic neurons and because their facets may mis-template adsorbed α-synuclein, we probe here, by transmission electron microscopy (TEM), four human PD substantia nigra specimens for their crystalline particles. Samples weighing 5 mg of PD stages 1, 2, 4 and 5 were processed by proteolysis and centrifugation. TEM-grids were dipped in the centrifugate diluted to 1 mL and the dried films were searched for crystalline particles. Two types of crystalline particles, known to activate the NLRP3 inflammasome were found. Endogenous calcium oxalate, a downstream product of ascorbate and dopamine oxidation-produced hydrogen peroxide; and TiO2, the with pigment of foods and medications. The number-density of the NLRP-inflammasome activating crystalline particles found approached the reported about-equal number-densities of microglia and neuronal cells in the brain.The observations of COD and protein-coated TiO2 support two putative feedback loops, both leading to dopaminergic neuron death. In one, polymeric oxidized-dopamine catalyst accelerates H2O2-generation, the H2O2 indirectly oxidizing ascorbate in an ascorbate-fueled, oxalate-generating, loop the excess oxalate precipitating the subsequently inflammasome-activating COD crystals; In the second, protein-adsorbing facets of TiO2 mis-template the aggregation of α-synuclein to produce inflammasome-activating misfolded α-synuclein.

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“…Once TNPs enter the brain, they may accumulate there and cause damage to the brain, leading to dysfunctions. Damage to the brain is usually irreversible and severe, and therefore any potential cause of damage should be investigated [11].…”

Section: Introductionmentioning

confidence: 99%

Nec-1 Attenuates Neurotoxicity Induced by Titanium Dioxide Nanomaterials on Sh-Sy5y Cells Through RIP1

Zhou

Huang

et al. 2020

Nanoscale Res Lett

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Titanium dioxide nanomaterials are applied in numerous fields due to their splendid physicochemical characteristics, which in turn poses a potential threat to human health. Recently, numerous in vivo studies have revealed that titanium dioxide nanoparticles (TNPs) can be transported into animal brains after exposure through various routes. Absorbed TNPs can accumulate in the brain and may disturb neuronal cells, leading to brain dysfunction. In vitro studies verified the neurotoxicity of TNPs. The mechanisms underlying the neurotoxicity of TNPs remains unclear. Whether necroptosis is involved in the neurotoxicity of TNPs is unknown. Therefore, we performed an in vitro study and found that TNPs induced inflammatory injury in SH-SY5Y cells in a dose-dependent way, which was mitigated by necrostatin-1 (Nec-1) pretreatment. Since receptor-interacting protein kinase 1 (RIP1) is reported to be the target of Nec-1, we silenced it by siRNA. We exposed mutant and wild-type cells to TNPs and assessed inflammatory injury. Silencing RIP1 expression inhibited inflammatory injury induced by TNPs exposure. Taken together, Nec-1 ameliorates the neurotoxicity of TNPs through RIP1. However, more studies should be performed to comprehensively assess the correlation between the neurotoxicity of TNPs and RIP1.

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Penetration, distribution and brain toxicity of titanium nanoparticles in rodents' body: a review

Cited by 28 publications

References 74 publications

General review of titanium toxicity

General review of titanium toxicity

Submicron Crystals of the Parkinson’s Disease Substantia nigra: Calcium Oxalate, Titanium Dioxide and Iron Oxide

Nec-1 Attenuates Neurotoxicity Induced by Titanium Dioxide Nanomaterials on Sh-Sy5y Cells Through RIP1

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