Acute Oral Administration of Cerium Oxide Nanoparticles Suppresses Lead Acetate–Induced Genotoxicity, Inflammation, and ROS Generation in Mice Renal and Cardiac Tissues

Mohamed, Hanan R. H.

doi:10.1007/s12011-021-02914-9

Cited by 8 publications

(5 citation statements)

References 54 publications

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“…In response to a variety of cellular stressors such as oxidative stress, hypoxia, DNA damage, ribonucleotide depletion, and oncogene activation, the tumor suppressor p53 gene is activated and overexpressed motivating apoptosis 36 – 39 . Consequently, the augmentation of TiO 2 NPs induced apoptosis noticed in this study may be due to the high increases demonstrated in the expression level of p53 after coadministration of acrylamide with TiO 2 NPs compared to its expression in mice given TiO 2 NPs or acrylamide separately.…”

Section: Discussionmentioning

confidence: 99%

Estimation of genotoxicity, apoptosis and oxidative stress induction by TiO2 nanoparticles and acrylamide subacute oral coadministration in mice

Safwat

Mohamed

2022

Sci Rep

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Acrylamide is used in the industry and can be a by-product of high-temperature food processing which has toxic potential in various tissues, and titanium dioxide nanoparticles (TiO2NPs) are widely used in toothpaste, sweets, food perseveration, chewing gum and medicines. Consequently, humans are daily exposed to large amounts of acrylamide and TiO2NPs mainly through food intake. However, limited studies are available on the effect of simultaneously intake of acrylamide and TiO2NPs on the integrity of genomic DNA and the induction of apoptosis in brain tissues. Therefore, this study estimated the influence of acrylamide coadministration on TiO2NPs induced genomic instability and oxidative stress in the brain tissues of mice. To achieve this, mice were orally administrated acrylamide (3 mg/kg b.w) or/and TiO2NPs (5 mg/kg b.w) for two successive weeks (5 days per week). The comet assay results showed that concurrent oral administration of acrylamide and TiO2NPs strongly induced single- and double stranded DNA breaks, and that the level of reactive oxygen species (ROS) was also highly elevated within neural cells after simultaneous oral intake of acrylamide and TiO2NPs compared to those observed after administration of acrylamide or/TiO2NPs alone. Moreover, oral co-administration of acrylamide with TiO2NPs increased apoptotic DNA damage to neurons by upregulating the expression levels of P53, TNF-α, IL-6 and Presenillin-1 genes compared to groups administered TiO2NPs. Therefore, from these results, the present study concluded that coadministration of acrylamide renders TiO2NPs more genotoxic and motivates apoptotic DNA damage and oxidative stress induced by TiO2NPs in brain cells, and thus it is recommended to avoid concurrent oral acrylamide administration with TiO2NPs.

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Section: Discussionmentioning

confidence: 99%

Estimation of genotoxicity, apoptosis and oxidative stress induction by TiO2 nanoparticles and acrylamide subacute oral coadministration in mice

Safwat

Mohamed

2022

Sci Rep

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“…MDA(nmol/g) DNA breaks particularly double-stranded DNA breaks are one of the most lethal and dangerous types of DNA damage since one double-stranded DNA break is sufficient to destabilize the genetic integrity of the cell until it is killed [45][46][47] . Alkaline comet assay is very sensitive for detecting single and double DNA breaks 32 .…”

Section: Discussionmentioning

confidence: 99%

Suppression of tumor growth and apoptosis induction by pomegranate seed nano-emulsion in mice bearing solid Ehrlich carcinoma cells

Mohamed

Tulbah

El-Ghor

et al. 2023

Sci Rep

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Despite the high antioxidant and penetration ability of pomegranate seed oil (PSO), the in vivo antitumor activity of PSO nano-emulsion has not been well investigated. Therefore, this study was undertaken to estimate the antitumor activity and safety of PSO nano-emulsion in mice bearing Ehrlich solid carcinoma cells. For tumor inoculation, about 2 × 106 viable Ehrlich tumor cells (200 µl) were implanted intramuscularly in the left thigh of hind leg. Once a solid tumor appears on the 10th day of transplantation; the mice were randomly divided into five groups (5 animals/group). Characterization of the PSO nano-emulsion using a Zeta sizer Malvern instrument and transmission electron microscope (TEM) revealed that the PSO nano-droplets were well dispersed with an average particle size of 8.95 nm and a spherical shape. Treatment with PSO nano-emulsions caused a significant reduction in the tumor size and weight, in a dose dependent manner, compared to tumor control group. Marked dose dependent elevations in the DNA damage level together with significant increases in the tumor suppressor p53, Bax and Caspase genes and reductions in the anti-apoptotic Bcl2 gene were also observed in the tumor tissue of mice given PSO nano-emulsions. Histological examination also revealed apoptosis and necrosis of tumor cells and tumor infiltration with inflammatory cells after PSO nano-emulsion treatment. However, high DNA damage was noticed in the liver and kidney tissues of mice given the highest dose of PSO nano-emulsion (400 mg/kg). Therefore, we concluded that PSO nano-emulsion exhibited a potent antitumor activity through induction of DNA breaks that triggers apoptosis of tumor cells but the highest dose caused genotoxicity to liver and kidney tissues, thus it is recommended to use doses lower than 400 mg/kg of PSO nano-emulsion as an alternative drugs for chemotherapy.

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“…Tese results indicate the existence of a common apoptotic pathway among all astrocytes, and U-87MG cells might be a suitable in vitro model besides primary astrocytes [46][47][48]. In response to various cellular stressors, such as oxidative stress, hypoxia, DNA damage, RNA consumption, and oncogene activation, the tumor suppressor gene p53 may be activated and overexpressed, promoting cell apoptosis [49]. Te latest research shows the increased apoptosis induced by AA may be due to the high increase of the p53 expression level [50].…”

Section: Acrylamide Induces Apoptosis In Nervous Related Cellsmentioning

confidence: 91%

Research Progress of Programmed Cell Death Induced by Acrylamide

Wang

et al. 2023

Journal of Food Quality

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Acrylamide exposure through environment pollution and diet is very common in daily life. With the deepening of the study on the toxicity of acrylamide, it has attracted widespread attention for the effects of acrylamide on multiple organs through affecting a variety of programmed cell death. Multiple studies have shown that acrylamide could exert its toxic effect by inducing programmed cell death, but its specific molecular mechanism is still unclear. In this review, the research on the main forms of programmed cell death (apoptosis, autophagy, and programmed necrosis) induced by acrylamide and their possible mechanisms are reviewed. This review may provide basic data for further research of acrylamide and prevention of its toxicity.

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Acute Oral Administration of Cerium Oxide Nanoparticles Suppresses Lead Acetate–Induced Genotoxicity, Inflammation, and ROS Generation in Mice Renal and Cardiac Tissues

Cited by 8 publications

References 54 publications

Estimation of genotoxicity, apoptosis and oxidative stress induction by TiO2 nanoparticles and acrylamide subacute oral coadministration in mice

Estimation of genotoxicity, apoptosis and oxidative stress induction by TiO2 nanoparticles and acrylamide subacute oral coadministration in mice

Suppression of tumor growth and apoptosis induction by pomegranate seed nano-emulsion in mice bearing solid Ehrlich carcinoma cells

Research Progress of Programmed Cell Death Induced by Acrylamide

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