Biochemical alterations induced by nickel oxide nanoparticles in female Wistar albino rats after acute oral exposure

The extensive use of copper oxide nanoparticles (CuO‐NPs) in various industries and their wide range of applications have led to their accumulation in different ecological niches of the environment. This excess exposure raises the concern about its potential toxic effects on various organisms including humans. However, the hazardous potential of CuO‐NPs in the literature is elusive, and it is essential to study its toxicity in different biological models. Hence, we have conducted single acute dose (2000 mg/kg) and multiple dose subacute (30, 300 and 1000 mg/kg daily for 28 days) oral toxicity studies of CuO‐NPs in female albino Wistar rats following OECD guidelines 420 and 407 respectively. Blood analysis, tissue aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and acetylcholinesterase, superoxide dismutase, catalase, lipid malondialdehyde and reduced glutathione assays, and histopathology of the tissues were carried out. The higher dose treatments of the acute and subacute study caused significant alterations in biochemical and antioxidant parameters of the liver, kidney and brain tissues of the rat. In addition, histopathological evaluation of these three organs of treated rats showed significantly high abnormalities in their histoarchitecture when compared to control rats. We infer from the results that the toxicity observed in the liver, kidney and brain of treated rats could be due to the increased generation of reactive oxygen species by CuO‐NPs.

Section: Discussionsupporting

confidence: 81%

“…Similar findings were also reported in a study conducted on MgO‐NPs by Mangalampalli et al (). A similar type of increased liver, serum enzyme activities and decreased kidney enzyme actvities was observed in an acute study with NiO‐NPs administartion (Dumala, Mangalampalli, Kalyan Kamal, & Grover, ).…”

Section: Discussionsupporting

confidence: 70%

Acute and subacute oral toxicity of copper oxide nanoparticles in female albino Wistar rats

Bugata

Venkata

Gundu

et al. 2019

“…Furthermore, reports have shown the ability of NiO‐NPs to induce genotoxicity and substantial physicochemical perturbation on Allium cepa , which confirmed that these NPs are hazardous to the environment (Manna & Bandyopadhyay, , ). NiO‐NPs were shown to cause biochemical alterations (Dumala, Mangalampalli, Kalyan Kamal, & Grover, ) and genotoxicity in Wistar rats when exposed to acute doses via an oral route (Dumala et al, ). Moreover, there is evidence of induced cell death and cytogenetic anomalies in rats exposed orally for 14 days to NiO‐NPs.…”

Section: Introductionmentioning

confidence: 99%

Retracted: In vitro genotoxicity assessment of nickel(II) oxide nanoparticles on lymphocytes of human peripheral blood

Dumala

Mangalampalli

Grover

2019

Self Cite

The current study was intended to elucidate the cytotoxicity, genotoxicity ability of nickel oxide (NiO) nanoparticles (NPs) and assessment of preliminary mechanism of the toxicity. Characterization studies showed that NiO‐NPs have a particle size of 17.94 (±3.48) nm. The particle size of the NPs obtained by dynamic light scattering method in Milli‐Q and RPMI 1640 media was 189.9 (±17.1) and 285.9 (±19.6) nm, respectively. The IC50 concentration for NiO‐NPs after 24 hours of treatment was estimated as 23.58 μg/mL. Comet and cytokinesis‐block micronucleus assays revealed a significant dose‐ and time‐dependent genotoxic potential of NiO‐NPs. Morphological assessment of the lymphocytes upon exposure to NiO‐NPs showed that the mechanism of toxicity was apoptosis. Reactive oxygen species analysis and lipid peroxidation patterns were aligned with the cytotoxicity and genotoxicity endpoints. Thus, the preliminary mechanism of NiO‐NPs for cytotoxicity on lymphocytes was assumed to be oxidative stress‐mediated apoptosis and DNA damage. Furthermore, these NiO‐NPs are considered a potentially hazardous substance at environmentally significant levels. Further investigations are suggested to understand the immunotoxic effects of NiO‐NPs.

“…Although Ni and its compounds were classified as class 1 carcinogens (IARC, ), increase in the use of NiO NPs makes it necessary to have a clear understanding of their probable effect on the health of humans and the environment. Acute oral dose toxicity study of NiO NPs on Wistar rats showed significant genotoxicity and biochemical alterations (Dumala et al, ; Dumala, Mangalampalli, Kalyan Kamal, & Grover, ). NiO NPs when ingested through oral route for 14 days, induced genotoxicity and enzymatic imbalance that triggered apoptosis in male Wistar rats.…”

Section: Introductionmentioning

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

Self Cite

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.