p53, MAPKAPK-2 and caspases regulate nickel oxide nanoparticles induce cell death and cytogenetic anomalies in rats

Saquib, Quaiser; Attia, Sabry M.; Ansari, Sabiha M.; Al-Salim, Abdullah; Faisal, Mohammad; Alatar, Abdulrahman A.; Musarrat, Javed; Zhang, Xiaowei; Al-Khedhairy, Abdulaziz A.

doi:10.1016/j.ijbiomac.2017.07.032

Cited by 34 publications

(22 citation statements)

References 53 publications

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“…NiO NPs when ingested through oral route for 14 days, induced genotoxicity and enzymatic imbalance that triggered apoptosis in male Wistar rats. This study further indicated that the NiO NPs have the potential to induce multi-organ toxicity after oral exposure (Saquib et al, 2017). However, the potential adverse effects after 28 days repeated oral exposure to NiO NPs has not been performed.…”

Section: Introductionmentioning

confidence: 71%

Repeated oral dose toxicity study of nickel oxide nanoparticles in Wistar rats: a histological and biochemical perspective

Dumala

Mangalampalli

Kamal

et al. 2019

J of Applied Toxicology

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Despite the increasing use of nickel oxide (NiO) nanoparticles (NPs), limited information is available on their toxicological effects. Health consequences of 28 days repeated oral exposure to NiO NPs have not been explored thoroughly. Hence, toxicity investigations were performed after 28‐day daily exposure in albino Wistar rats with NiO NPs following Organization for Economic Co‐operation and Development test guideline 407. Histopathology, biochemical indices including oxidative stress and biodistribution patterns were evaluated to decipher the toxicological impact of NiO NPs. NiO NP characterization by transmission electron microscopy showed an average size of 12.9 (±3.4) nm. Histological studies depicted a prominent impact on the vital organs of the rats. A dose‐dependent rise in both aminotransferase enzyme values was recorded in the homogenates of liver and kidney tissues. A significant decrease in superoxide dismutase activity and increase in catalase activity was noted. Further, a dose‐dependent decrease in reduced glutathione content was recorded in rats, which suggested generation of reactive oxygen species and oxidative stress. Increase in the malondialdehyde levels was observed with an increase in the dose substantiating the antioxidant enzyme activity profiles. Biodistribution studies indicated maximum accumulation of Ni content in liver followed by kidney. Excretion of Ni was predominantly through feces and a little through renal clearance. Our study indicated that NiO NPs adversely alter the biochemical profile of the rats and cause histological damage. Further investigations are warranted to address the mechanism by which physiological path these NiO NPs exhibit their toxic nature in in vivo.

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Section: Introductionmentioning

confidence: 71%

Repeated oral dose toxicity study of nickel oxide nanoparticles in Wistar rats: a histological and biochemical perspective

Dumala

Mangalampalli

Kamal

et al. 2019

J of Applied Toxicology

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“…The main mechanism for the cell damage caused by NiNPs is through inducing oxidative stress (Patlolla et al,2019;Ahmad et al, 2015). Specifically, NiNPs were found to induce DNA damage (Abudayyak et al, 2017) , inflammation, cell degeneration (Razavipour et al, 2015),cell cycle arrest (Ahmad et al, 2015) , and cytogenetic alterations (Saquib et al, 2017). The present investigation aimed to focus on the hepatotoxicity of NiNPs in rats using different doses.…”

Section: Introductionmentioning

confidence: 90%

Hepatotoxicity of nickel nanoparticles in rats

Abdulqadir

Aziz

2019

IJAR

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Nanoparticles (NPs) are increasingly used nowadays for nanomedicine purposes, although they have been found to induce harmful effects on human health and living species in the environment. The current study investigated the impact of different doses of nickel nanoparticles (NiNPs) on the rats liver. Intraperitoneal (i.p.) administration of (0, 5, 20, 100mg/kg/BW/day) NiNPs for four weeks showed dose dependent elevation of malondialdehyde (MDA, lipid peroxidation marker), liver function enzymes (ALT, AST and ALP) and bilirubin. While, superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPX) and catalase (CAT) recorded significant reduction in their activity. NiNPs were found to cause several histopathological changes and ultrastructural alterations in liver such as appearance of inflammatory infiltrated leucocytes, sinusoid dilatation, fatty changes and degeneration of hepatocytes. The present findings suggest that administration of NiNPs may induce dose dependent hepatotoxicity.

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“…Several studies revealed the detrimental health impacts of Ni NPs both in human and experimental animals such as skin allergies, lung fibrosis, lung cancer, cardiovascular diseases, hepatotoxicity [13][14][15][16][17], reproductive toxicity [18], and zebrafish fetal toxicity [19]. Many previous studies reported that NiO NPs when ingested through oral exposure, induced genotoxicity [20,21], multi-organ toxicity [22] in male rats. Increasing uses of NiO NPs make it widely distributed in our environment, especially in the wastewater.…”

Section: Introductionmentioning

confidence: 99%

Maternal and Fetal Toxicity-Induced by Nickel Oxide Nanoparticles Administration in Albino Rats During Gestation

Hamdi

2020

Asian J Pharm Clin Res

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Objective: Despite the widespread of nickel oxide nanoparticles (NiO NPs) and their benefits in all fields, they have many negative effects on human life, especially expectant mothers and their fetus. The purpose of this study was to investigate the possible maternal and developmental toxicity-induced by NiO NPs administration during gestation. Methods: Three groups of pregnant rats were administered orally during days 5–19 of gestation, the pregnant rats were haphazardly designed into three groups (six rat/group), as follows: Control group and NiO NPs administered groups, low (4 mg/kg), and high (8 mg/kg) doses. Results: NiO NPs administration resulted in severe maternal and developmental toxicity which included reduction in uterine weight, mother weight gain, the average weight of placenta, the number corpora lutea, implantation sites, and the number of live fetuses. Furthermore, high pre/ postimplantation, fetal growth retardation, and morphological and skeletal anomalies, an elevation in liver and brain DNA damage in both mother and fetus, and histopathological alterations in different tissues (placenta, liver, kidney, and brain) of pregnant rats and fetuses. Lipid peroxidation showed a significant elevation in maternal, fetal liver, and brain tissues of NiO NPs ‐administered rats. Furthermore, glutathione content and catalase activity were decreased in both tissues of NiO NPs‐administered rats. Conclusion: Finally, the detrimental impacts of NiO NPs in dams and fetuses probably through its potential generation of reactive oxygen species.

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p53, MAPKAPK-2 and caspases regulate nickel oxide nanoparticles induce cell death and cytogenetic anomalies in rats

Cited by 34 publications

References 53 publications

Repeated oral dose toxicity study of nickel oxide nanoparticles in Wistar rats: a histological and biochemical perspective

Repeated oral dose toxicity study of nickel oxide nanoparticles in Wistar rats: a histological and biochemical perspective

Hepatotoxicity of nickel nanoparticles in rats

Maternal and Fetal Toxicity-Induced by Nickel Oxide Nanoparticles Administration in Albino Rats During Gestation

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