Mechanism of effects of nickel or nickel compounds on intestinal mucosal barrier

Huang, Lijing; He, Fang; Wu, Biao

doi:10.1016/j.chemosphere.2022.135429

Cited by 18 publications

(2 citation statements)

References 113 publications

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“…The mechanical barrier consists of intact intestinal epithelial cells and tight connections between cells. Goblet cells in the intestinal epithelium secrete mucus to form the intestinal mucus barrier, which is an important component of the chemical barrier [ 49 , 50 ]. The intestinal mucus layer covers almost the entire intestinal cavity surface; it lubricates, resists bacterial invasion, and protects the intestinal tract from mechanical damage and pathogenic bacteria [ 51 , 52 ].…”

Section: Introductionmentioning

confidence: 99%

Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice

Jia

Han²,

Liu³

et al. 2023

Toxics

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Extensive environmental pollution by microplastics has increased the risk of human exposure to plastics. However, the biosafety of polypropylene microplastics (PP-MPs), especially of PP particles < 10 μm, in mammals has not been studied. Thus, here, we explored the mechanism of action and effect of exposure to small and large PP-MPs, via oral ingestion, on the mouse intestinal tract. Male C57BL/6 mice were administered PP suspensions (8 and 70 μm; 0.1, 1.0, and 10 mg/mL) for 28 days. PP-MP treatment resulted in inflammatory pathological damage, ultrastructural changes in intestinal epithelial cells, imbalance of the redox system, and inflammatory reactions in the colon. Additionally, we observed damage to the tight junctions of the colon and decreased intestinal mucus secretion and ion transporter expression. Further, the apoptotic rate of colonic cells significantly increased after PP-MP treatment. The expression of pro-inflammatory and pro-apoptosis proteins significantly increased in colon tissue, while the expression of anti-inflammatory and anti-apoptosis proteins significantly decreased. In summary, this study demonstrates that PP-MPs induce colonic apoptosis and intestinal barrier damage through oxidative stress and activation of the TLR4/NF-κB inflammatory signal pathway in mice, which provides new insights into the toxicity of MPs in mammals.

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Section: Introductionmentioning

confidence: 99%

Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice

Jia

Han²,

Liu³

et al. 2023

Toxics

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“…It is known that metals, such as nickel [ 14 ], and to a lesser extent titanium [ 15 ], can increase the release of free radicals. However, to the best of our knowledge it is not known to date whether nitinol affects the free radical production in bronchial epithelial cells.…”

Section: Resultsmentioning

confidence: 99%

Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling

Pouwels

Sigaeva

Boer

et al. 2023

J Mater Sci: Mater Med

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Endoscopic implantation of medical devices for the treatment of lung diseases, including airway stents, unidirectional valves and coils, is readily used to treat central airway disease and emphysema. However, granulation and fibrotic tissue formation impairs treatment effectiveness. To date little is known about the interaction between implanted devices, often made from metals, such as nickel, titanium or nitinol, and cells in the airways. Here, we study the response of lung epithelial cells and fibroblasts to implant device materials. The adhesion and proliferation of bronchial epithelial cells and lung fibroblasts upon exposure to 10 × 3 × 1 mm pieces of nickel, titanium or nitinol is examined using light and scanning electron microscopy. Pro-inflammatory cytokine mRNA expression and release, signaling kinase activity and intracellular free radical production are assessed. Nitinol, and to a lesser extent nickel and titanium, surfaces support the attachment and growth of lung epithelial cells. Nitinol induces a rapid and significant alteration of kinase activity. Cells directly exposed to nickel or titanium produce free radicals, but those exposed to nitinol do not. The response of lung epithelial cells and fibroblasts depends on the metal type to which they are exposed. Nitinol induces cellular surface growth and the induction of kinase activity, while exposure of lung epithelial cells to nickel and titanium induces free radical production, but nitinol does not. Graphical Abstract

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Deep eutectic solvent-based simultaneous complexation and preconcentration of nickel in Antarctic lake water samples for determination by flame atomic absorption spectrometry

Tan

Kılınç

Zaman

et al. 2023

Environ Monit Assess

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Mechanism of effects of nickel or nickel compounds on intestinal mucosal barrier

Cited by 18 publications

References 113 publications

Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice

Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice

Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling

Deep eutectic solvent-based simultaneous complexation and preconcentration of nickel in Antarctic lake water samples for determination by flame atomic absorption spectrometry

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