Acute toxicity of nickel nanoparticles in rats after intravenous injection

Magaye, Ruth; Xia, Yunlong; Zou, Baobo; Shi, Hang; Yu, Hongsheng; Kui, Liu; Lin, Xiaohui; Xu, Jin; Yang, Chengyue; Wu, Aiguo; Zhao, Jinshun

doi:10.2147/ijn.s56212

Cited by 54 publications

(18 citation statements)

References 32 publications

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“…Cytotoxic effects were reported when exposed to materials containing nickel [32–34]. Therefore, CS porous Nitinol with resistance to Ni leaching is crucial to its biocompatibility and use as implants.…”

Section: Resultsmentioning

confidence: 99%

Combustion Synthesis Porous Nitinol for Biomedical Applications

Aihara¹,

Zider²,

Fanton

et al. 2019

International Journal of Biomaterials

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Porous Nitinol with a three-dimensional anisotropic interconnective open pore structure has been successfully produced by the combustion synthesis (CS) of elemental Ni and Ti powders. The resulting product can be tailored to closely match the stiffness of cancellous bone to minimize stress shielding. The average elastic modulus was approximately 1 GPa for a porosity of 60 vol% and the average pore size of 100-500 µm. The low elastic modulus meets the basic demand for orthopedic bone ingrowth applications. Furthermore, porous Nitinol was composed of cubic (austenitic) and monoclinic (martensitic) NiTi compounds without the presence of Ni metal or Ni-rich phases. The resulting product exhibits excellent corrosion resistance with breakdown potentials above 750mV. An ovine study in cortical sites of the tibia demonstrated rapid osseointegration into the porous strucutre as early as two weeks and complete bone growth across the implant at six weeks. A separate ovine study showed complete through-growth of bone at four months using a lumbar interbody fusion model, substantiating the use of porous Nitinol as an implant material for applications in the spine. Porous Nitinol is thus a promising biomaterial with proven biocompatibility and exceptional osseointegration performance which may enhance the healing process and promote long-term fixation, making it a strong candidate for a wide range of orthopedic implant applications.

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Section: Resultsmentioning

confidence: 99%

Combustion Synthesis Porous Nitinol for Biomedical Applications

Aihara¹,

Zider²,

Fanton

et al. 2019

International Journal of Biomaterials

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“…These findings are consistent with previous studies that found liver toxicity for cobalt, manganese, and nickel nanoparticles. 8, 45, 46 Liu et al also reported that exposure of BRL 3A rat derived liver cells to Co nanoparticles reduced cell viability and LDH release, which was accompanied by ROS generation and DNA damage. 45 Similar induction of LDH release was found for micron-size MnO 2 particles in the same liver cell line.…”

Section: Discussionmentioning

confidence: 96%

Toxicological Profiling of Metal Oxide Nanoparticles in Liver Context Reveals Pyroptosis in Kupffer Cells and Macrophages versus Apoptosis in Hepatocytes

et al. 2018

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The liver and the mononuclear phagocyte system are a frequent target for engineered nanomaterials, either as a result of particle uptake and spread from primary exposure sites or systemic administration of therapeutic and imaging nanoparticles. In this study, we performed a comparative analysis of the toxicological impact of 29 metal oxide nanoparticles (NPs), some commonly used in consumer products, in transformed or primary Kupffer cells (KCs) and hepatocytes. We not only observed differences between KCs and hepatocytes, but also differences in the toxicological profiles of transition-metal oxides (TMOs, e. g., CoO) versus rare-earth oxide (REO) NPs ( e. g., GdO). While pro-oxidative TMOs induced the activation of caspases 3 and 7, resulting in apoptotic cell death in both cell types, REOs induced lysosomal damage, NLRP3 inflammasome activation, caspase 1 activation, and pyroptosis in KCs. Pyroptosis was accompanied by cell swelling, membrane blebbing, IL-1β release, and increased membrane permeability, which could be reversed by knockdown of the pore forming protein, gasdermin D. Though similar features were not seen in hepatocytes, the investigation of the cytotoxic effects of REO NPs could also be seen to affect macrophage cell lines such as J774A.1 and RAW 264.7 cells as well as bone marrow-derived macrophages. These phagocytic cell types also demonstrated features of pyroptosis and increased IL-1β production. Collectively, these findings demonstrate important mechanistic considerations that can be used for safety evaluation of metal oxides, including commercial products that are developed from these materials.

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“…These changes may be because of the interference of the NPs in the process of erythropoiesis (Morsy, El-Ala, & Ali, 2016). Ni NPs significantly increased the WBC count in rats after intravenous administration (Magaye et al, 2014).…”

Section: Ni Biodistributionmentioning

confidence: 99%

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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Acute toxicity of nickel nanoparticles in rats after intravenous injection

Cited by 54 publications

References 32 publications

Combustion Synthesis Porous Nitinol for Biomedical Applications

Combustion Synthesis Porous Nitinol for Biomedical Applications

Toxicological Profiling of Metal Oxide Nanoparticles in Liver Context Reveals Pyroptosis in Kupffer Cells and Macrophages versus Apoptosis in Hepatocytes

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

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