Genotoxicity and oxidative stress induced by the orally administered nanosized nickel and cobalt oxides in male albino rats

Abstract

Background: Nanoparticles (NPs) are extensively used in many areas of our daily life. Thus, human exposure to a mixture of the NPs is likely to occur. However, most of the previous studies have investigated the toxicity of the individual NPs. Therefore, the current study investigated the genotoxicity and oxidative stress induced by an acute oral administration of the nano-sized nickel oxide (NiO) and/or cobalt oxide (Co 3 O 4) in the brain, liver, and kidney of the rats. Results: After 1 day of an administration with NiO-NPs or Co 3 O 4-NPs, at the dose levels of 0.5 and 1.0 g/kg, remarkable elevations in malondialdehyde (MDA) levels, percentage of DNA damage (%DNA), tail length (TL), and tail moment (TM), accompanied by marked reductions in the levels of zinc (Zn), glutathione (GSH) as well as the activities and expression levels of the superoxide dismutase (SOD) were recorded in all the studied groups, as compared to the controls. The changes in the levels of all the studied parameters were in a time-and dose-dependent manner. Excessive productions of the reactive oxygen species (ROS) associated with the genomic DNA fragmentation were observed in the experimental groups, as compared to the controls. However, in the groups administered with NiO-NPs and Co 3 O 4-NPs together, the alterations in all the studied parameters were improved as compared to those administered NiO-NPs or Co 3 O 4-NPs solely. Conclusion: The NiO-NPs and Co 3 O 4-NPs antagonized each other leading to an alleviation of the genotoxicity induced by each of them.

Ameliorative effects of glycine on cobalt chloride‐induced hepato‐renal toxicity in rats

“…In this study, the deleterious effects of CoCl 2 on hepatic and renal tissues manifested as increased biomarkers of oxidative stress including H 2 O 2 generation and MDA content, and reduction in the activities of GPx, GST, SOD, and GSH content. Our observations in this study corroborated an earlier report by Ali et al, 26 who described remarkable elevations in MDA levels accompanied by significant depletions in the GSH content and SOD activity in the brain, liver, and kidney of rats. Furthermore, there are several reports that cobalt mediates organ specific injuries in mammals and nonmammalian organisms via the induction of oxidative processes 27,28 …”

Protective effects of gallic acid against nickel-induced kidney injury: impact of antioxidants and transcription factor on the incidence of nephrotoxicity

“…Nickel oxide nanoparticles have also been found to cause cytogenetic changes and apoptosis [ 13 ]. Moreover, they have been discovered to cause kidney damage by reducing both enzymatic and nonenzymatic antioxidant activities [ 14 ] and by suppressing the immune system or activating various inflammatory mediators [ 15 ]. Fischer et al.…”