Investigations on the inflammatory and genotoxic lung effects of two types of titanium dioxide: untreated and surface treated

Rehn, B.; Seiler, Frank; Rehn, Steffeni; Bruch, Joachim; Maier, Monika

doi:10.1016/s0041-008x(03)00092-9

Cited by 166 publications

(82 citation statements)

References 46 publications

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“…At the doses tested, the induced inflammation in the animals' lungs was reversible. A significant difference in the effects of the two different titanium dioxide samples was not found in this study (Rehn et al 2003).…”

Section: Acute Toxicitycontrasting

confidence: 73%

“…The inflammation parameters were found to be permanently increased in the quartz control group. The 8-oxoguanine level in the lungs of the animals treated with titanium dioxide was not higher than that of the controls (Rehn et al 2003).…”

Section: In Vivomentioning

confidence: 59%

“…Particles with a diameter of 20 nm are expected to be deposited in the alveoli to a particularly large extent. According to Rehn et al (2003), there are, however, no free ultrafine titanium dioxide particles present in commercial products (P25, untreated hydrophilic surface, and T805, silanized hydrophobic surface), but only agglomerates and aggregates, which are considerably larger than the primary particles and, in the opinion of Rehn et al (2003), could not be destroyed even by ultrasound in an aqueous phospholipid lecithin suspension. The authors conclude from this that the agglomerates and aggregates therefore do not disintegrate into primary particles in the alveoli.…”

Section: Comparison Of the Properties Of Fine And Ultrafine Particlesmentioning

confidence: 99%

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Titanium dioxide (respirable fraction) [MAK Value Documentation, 2009]

2014

The MAK‐Collection for Occupational Health and Safety

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Published in the series Occupational Toxicants , 2014 The article contains sections titled: Toxic Effects and Mode of Action Mechanism of Action Toxicokinetics and Metabolism Absorption, distribution, elimination Metabolism Effects in Humans Single exposures Repeated exposure Local effects on skin and mucous membranes Allergenic effects Reproductive toxicity Genotoxicity Carcinogenicity Animal Experiments and in vitro Studies Acute toxicity Subacute, subchronic and chronic toxicity Local effects on skin and mucous membranes Allergenic effects Reproductive toxicity Genotoxicity Carcinogenicity Other effects Manifesto (MAK value/characterization)

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Section: Acute Toxicitycontrasting

confidence: 73%

Section: In Vivomentioning

confidence: 59%

Section: Comparison Of the Properties Of Fine And Ultrafine Particlesmentioning

confidence: 99%

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Titanium dioxide (respirable fraction) [MAK Value Documentation, 2009]

2014

The MAK‐Collection for Occupational Health and Safety

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“…Another study found sustained elevations (in weeks) in PL and SP-A in response to silica [16]. Several other studies found silica-induced increases in PL and SP [17,18] including specific increases in SP-A [19,20], SP-D [19,21], Vitamin E [22], and phosphotidyl inositol [23]. In contrast, Seiler et al, found a dose-dependent decrease in phospotidyl glycerol in response to silica [23].…”

Section: Effect Of Silica Exposure On Lung Surfactantmentioning

confidence: 97%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

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Inhalation of the crystalline form of silica is associated with a variety of pathologies from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silicainduced toxicity on the cellular level. Based on experimental results, several rationales have been developed on exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica) triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species (RNS) are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, where silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis is described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

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“…Nowadays, a large number of nanoparticles are entering into our environment due to their usage due to advances in nanotechnology, thus, causing concern as they have potential impacts on human and environmental health [3]. The conventional toxicological experiments has revealed that, TiO 2 NPs can produce free radicals with strong oxidizing ability which thus induce oxidative stress and finally resulted in apoptotic cell death, fibrosis, DNA damage and pulmonary inflammation [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Evaluating Metabolic Responses in Mice to Nanosized Titanium Dioxide Particles Using Gas Chromatography- Mass Spectrometry Based Metabolomics

Mudiam¹

2017

Austin J Anal Pharm Chem

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Titanium dioxide nanoparticle (TiO 2 NP) is one of the most commonly used engineered nanoparticles. It has attracted lot of interest to analytical toxicologists in recent past due to its toxicity on human health and environment. The present study was aimed to explore the GC-MS based metabolomics as a tool to investigate the toxicity of TiO 2 NP in comparison to TiO 2 BP with doses of 300, 600, 1200 mg/kg respectively in both gender(s) of Swiss Albino mice for 7 and 14 days. Serum biochemistry and histopathology parameters were performed. Chemometric analysis by supervised PLS-DA was performed to identify the discrimination/classification between exposed and non-exposed samples due to metabolic perturbations. The morphological, biochemical, haematological and metabolomic analysis revealed that, TiO 2 NP has induced toxicological effects to both female and male mice. The results showed that metabolomics along with biochemical analysis can be employed as a comprehensive tool to identify the toxicity of NPs in the model organisms at molecular level.

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Investigations on the inflammatory and genotoxic lung effects of two types of titanium dioxide: untreated and surface treated

Cited by 166 publications

References 46 publications

Titanium dioxide (respirable fraction) [MAK Value Documentation, 2009]

Titanium dioxide (respirable fraction) [MAK Value Documentation, 2009]

Silica binding and toxicity in alveolar macrophages

Evaluating Metabolic Responses in Mice to Nanosized Titanium Dioxide Particles Using Gas Chromatography- Mass Spectrometry Based Metabolomics

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