Ingestion of titanium dioxide nanoparticles: a definite health risk for consumers and their progeny

Cornu, Raphaël; Béduneau, Arnaud; Martin, Hélène

doi:10.1007/s00204-022-03334-x

Cited by 19 publications

(12 citation statements)

References 128 publications

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“…An obvious question is what mechanism(s) is responsible for the protective effect of the short-term application of fructose? Several mechanisms may be responsible for the protective effects of fructose: [ 1 ] iron binding and prevention of the Fenton reaction [ 40 ]; [ 2 ] stabilization of the glutathione pool in the cell [ 42 ]; [ 3 ] upregulation of the pentose phosphate pathway producing NADPH [ 44 ] and [ 4 ] production of fructose-1,6-bisphosphate that mediates cytoprotective and antioxidant mechanisms [ 40 , 46 ].…”

Section: Discussionmentioning

confidence: 99%

“…Some nanoparticles may have detrimental effects on reproductive tissues and fetal development because they are smaller and have a larger surface area to volume ratios than the original chemical compounds, allowing them to enter cells and stimulate catalytic and biological activities [ 3 ]. Titanium dioxide nanoparticles (TiO 2 NPs) are natural, highly insoluble, thermally stable and widely manufactured particles [ 4 – 6 ]. They are integrated into numerous industries and products such as paints, plastics, papers, cosmetics, clothing, electronics, toothpastes, food colorants, and sunscreens [ 7 – 9 ].…”

Section: Introductionmentioning

confidence: 99%

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Fructose improves titanium dioxide nanoparticles induced alterations in developmental competence of mouse oocytes

Elmetwally,

Helmy,

Balboula

et al. 2024

BMC Vet Res

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Aims We investigated the effects of intraperitoneal injections of titanium dioxide nanoparticles (TiO2 NPs, 100 mg/kg) for 5 consecutive days on the developmental competence of murine oocytes. Furthermore, study the effects of TiO2 NPs on antioxidant and oxidative stress biomarkers, as well as their effects on expression of apoptotic and hypoxia inducing factor-1α (HIF1A) protein translation. Moreover, the possible ameliorating effects of intraperitoneal injections of fructose (2.75 mM/ml) was examined. Materials and methods Thirty sexually mature (8–12 weeks old; ~ 25 g body weight) female mice were used for the current study. The female mice were assigned randomly to three treatment groups: Group1 (G1) mice were injected intraperitoneal (ip) with deionized water for 5 consecutive days; Group 2 (G2) mice were injected ip with TiO2 NPs (100 mg/kg BW) for 5 consecutive days; Group 3 (G3) mice were injected ip with TiO2 NPs (100 mg/kg BW + fructose (2.75 mM) for 5 consecutive days. Results Nano-titanium significantly decreased expression of GSH, GPx, and NO, expression of MDA and TAC increased. The rates of MI, MII, GVBD and degenerated oocytes were significantly less for nano-titanium treated mice, but the rate of activated oocytes was significantly greater than those in control oocytes. TiO2 NPs significantly increased expression of apoptotic genes (BAX, Caspase 3 and P53) and HIF1A. Intraperitoneal injection of fructose (2.75 mM/kg) significantly alleviated the detrimental effects of TiO2 NPs. Transmission electron microscopy indicated that fructose mitigated adverse effects of TiO2 NPs to alter the cell surface of murine oocytes. Conclusion Results of this study suggest that the i/p infusion of fructose for consecutive 5 days enhances development of murine oocytes and decreases toxic effects of TiO2 NPs through positive effects on oxidative and antioxidant biomarkers in cumulus-oocyte complexes and effects to inhibit TiO2-induced increases in expression of apoptotic and hypoxia inducing factors.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fructose improves titanium dioxide nanoparticles induced alterations in developmental competence of mouse oocytes

Elmetwally,

Helmy,

Balboula

et al. 2024

BMC Vet Res

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“…The relationship between air pollution, sleep, neurodegeneration, depression, and suicide (210,211) should encourage health workers to know about combustion and friction UFPM sources and engineered NPs (food products, cosmetics, toothpaste, sun protectors, surface disinfectants, paints, and e-waste). The presence of zinc, silver, copper, gold, selenium, and calcium NPs as potential food additives for animals (212), nanoplastics in drinking water (213), the massive presence of nanometric particle fraction of TiO 2 in the food industry, and Fe 3 O 4 magnetic nanoparticles from food production, processing, storage, and detection, make constant exposures to NPs a serious health issue (76,214).…”

Section: Neurodegeneration Spectrum Heterogeneity Quadruple Neural Ab...mentioning

confidence: 99%

“…The detrimental impact of NPs on the brain includes high production of reactive oxygen species, neural inflammation, depletion of anti-oxidative enzymes, DNA damage, apoptosis, structural cell damage, including organelles, nuclei, tight junctions, adherens junctions, endothelial damage, and dysfunction (5,55,59,62,64,70,(75)(76)(77)(78).…”

Section: Introductionmentioning

confidence: 99%

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option

Calderón‐Garcidueñas

Torres‐Jardón²,

Greenough³

et al. 2023

Front. Neurol.

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Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM2.5), including combustion and friction ultrafine PM (UFPM) and industrial nanoparticles (NPs) starting in utero, are linked to early pediatric and young adulthood aberrant neural protein accumulation, including hyperphosphorylated tau (p-tau), beta-amyloid (Aβ1 − 42), α-synuclein (α syn) and TAR DNA-binding protein 43 (TDP-43), hallmarks of Alzheimer's (AD), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). UFPM from anthropogenic and natural sources and NPs enter the brain through the nasal/olfactory pathway, lung, gastrointestinal (GI) tract, skin, and placental barriers. On a global scale, the most important sources of outdoor UFPM are motor traffic emissions. This study focuses on the neuropathology heterogeneity and overlap of AD, PD, FTLD, and ALS in older adults, their similarities with the neuropathology of young, highly exposed urbanites, and their strong link with sleep disorders. Critical information includes how this UFPM and NPs cross all biological barriers, interact with brain soluble proteins and key organelles, and result in the oxidative, endoplasmic reticulum, and mitochondrial stress, neuroinflammation, DNA damage, protein aggregation and misfolding, and faulty complex protein quality control. The brain toxicity of UFPM and NPs makes them powerful candidates for early development and progression of fatal common neurodegenerative diseases, all having sleep disturbances. A detailed residential history, proximity to high-traffic roads, occupational histories, exposures to high-emission sources (i.e., factories, burning pits, forest fires, and airports), indoor PM sources (tobacco, wood burning in winter, cooking fumes, and microplastics in house dust), and consumption of industrial NPs, along with neurocognitive and neuropsychiatric histories, are critical. Environmental pollution is a ubiquitous, early, and cumulative risk factor for neurodegeneration and sleep disorders. Prevention of deadly neurological diseases associated with air pollution should be a public health priority.

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“…Analysis of US grocery store data suggested that the dietary intake of TiO 2 could be as high as 5 mg/kg body weight per day from food products (Putra et al, 2022). Moreover, the European Food Safety Authority (EFSA) estimated that the maximum level of exposure to E171, a food‐grade TiO 2 , occurs in children between the ages of 3 to 9, who ingest an average of 1.9 to 11.5 mg/kg body weight per day (Cornu et al, 2022). Owing to the extensive production and the broad potential for exposure inherent to TiO 2 NPs, this material presents a multitude of potential health hazards.…”

Section: Introductionmentioning

confidence: 99%

Titanium dioxide nanoparticles induce apoptosis through ROS‐Ca²⁺‐p38/AKT/mTOR pathway in TM4 cells

Wang,

Yang,

et al. 2024

J of Applied Toxicology

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Titanium dioxide nanoparticles (TiO2 NPs) can cause apoptosis in TM4 cells; however, the underlying mechanism has not been entirely elucidated. The purpose of this study was to investigate the effects of TiO2 NPs on ROS, Ca2+ level, p38/AKT/mTOR pathway, and apoptosis in TM4 cells and to evaluate the role of Ca2+ in p38/AKT/mTOR pathway and apoptosis. After exposure to different concentrations (0, 50, 100, 150, and 200 μg/mL) of TiO2 NPs for 24 h, cell viability, ROS, Ca2+ level, Ca2+‐ATPase activity, p38/AKT/mTOR pathway‐related proteins, apoptosis rate, and apoptosis‐related proteins (Bax, Bcl‐2, Caspase 3, Caspase 9, and p53) were detected. The ROS scavenger NAC was used to determine the effect of ROS on Ca2+ level. The Ca2+ chelator BAPTA‐AM was used to evaluate the role of Ca2+ in p38/AKT/mTOR pathway and apoptosis. TiO2 NPs significantly inhibited cell viability, increased ROS level, and elevated Ca2+ level while suppressing Ca2+‐ATPase activity. TiO2 NPs regulated the p38/AKT/mTOR pathway via increasing p‐p38 level and decreasing p‐AKT and p‐mTOR levels. TiO2 NPs significantly enhanced the apoptosis. NAC attenuated Ca2+ overload and reduction in Ca2+‐ATPase activity caused by TiO2 NPs. BAPTA‐AM alleviated TiO2 NPs‐induced abnormal expression of p38/AKT/mTOR pathway‐related proteins. BAPTA‐AM assuaged the apoptosis caused by TiO2 NPs. Altogether, this study revealed that TiO2 NPs elevated intracellular Ca2+ level through ROS accumulation. Subsequently, the heightened intracellular Ca2+ level was observed to exert regulation over the p38/AKT/mTOR pathway, ultimately culminating in apoptosis. These results provides a complementary understanding to the mechanism of TiO2 NPs‐induced apoptosis in TM4 cells.

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Ingestion of titanium dioxide nanoparticles: a definite health risk for consumers and their progeny

Cited by 19 publications

References 128 publications

Fructose improves titanium dioxide nanoparticles induced alterations in developmental competence of mouse oocytes

Fructose improves titanium dioxide nanoparticles induced alterations in developmental competence of mouse oocytes

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option

Titanium dioxide nanoparticles induce apoptosis through ROS‐Ca²⁺‐p38/AKT/mTOR pathway in TM4 cells

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Ingestion of titanium dioxide nanoparticles: a definite health risk for consumers and their progeny

Cited by 19 publications

References 128 publications

Fructose improves titanium dioxide nanoparticles induced alterations in developmental competence of mouse oocytes

Fructose improves titanium dioxide nanoparticles induced alterations in developmental competence of mouse oocytes

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option

Titanium dioxide nanoparticles induce apoptosis through ROS‐Ca2+‐p38/AKT/mTOR pathway in TM4 cells

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Titanium dioxide nanoparticles induce apoptosis through ROS‐Ca²⁺‐p38/AKT/mTOR pathway in TM4 cells