Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice

Abstract

The overexposure to nickel due to the extensive use of it in modern technology remains a major public health concern. The mechanisms of pathological effects of this metal remain elusive. The present study was devoted to evaluate the effect of nickel on the oxidative state of the brain cells of mice and to assess whether zinc as redox state modulator could efficiently protect cells against nickel’s neurotoxicity. As oxidative stress biomarkers in the present study, we have measured the concentrations of reduced glutathione, metallothioneins, and malondialdehyde and the activity of the enzyme δ-aminolevulinate dehydratase. For the single metal exposure, mice were i.p. injected once with solutions of NiCl2 and/or ZnSO4; repeated exposure was performed i.p. injecting metal salt solutions for 14 days (once a day). The control mice received i.p. injections of saline. Results of our study demonstrate that single and 14 days of Ni2+ exposure decreased reduced glutathione and increased malondialdehyde contents in the brain of mice. Repeated Ni2+ administration significantly inhibited δ-aminolevulinate dehydratase while increasing brain metallothionein concentration at both exposure periods. Zinc exhibited a protective effect against nickel-induced glutathione and lipid peroxidation in brain cells of mice at both intervals of time, while repeated exposure to this metal significantly raised the brain metallothionein content. Repeated Zn2+ pretreatment protected δ-aminolevulinate dehydratase from Ni2+-induced inhibition and significantly increased metallothionein concentration at both investigated time intervals.

Toxicity of organic and inorganic nickel in pancreatic cell cultures: Comparison to cadmium

“…In vivo models using injections of moderately high Ni doses resulted in increased expression/activity of various biomarkers. These biomarkers are associated with oxidative stress such as alkaline phosphatase, aspartate transaminase, oxidized lipids, malondialdehyde, or glutathione reduction (20,49,50). A study by Chen et al (18) generation of free radicals following NiCl2 administration showed that dichlorofluorescein fluorescence was not elevated until a concentration of 1 mM was used.…”

The Combination of Zinc and Melatonin Enhanced Neuroprotection and Attenuated Neuropathy in Oxaliplatin-Induced Neurotoxicity

“…Although, the reduction was not significant; all the treatment groups increased its level when compared to the OXL group. This effect could be attributed to the neuroprotective effect of each of zinc 56 and melatonin. 57 …”

“…increased its level when compared to the OXL group. This effect could be attributed to the neuroprotective effect of each of zinc 56 and melatonin. 57 Oxaliplatin increased the levels of the inflammatory markers and the treatment combination of zinc and melatonin demonstrated a better effect in this regard.…”

Metal Nanoparticles with Antimicrobial Properties: The Toxicity Response in Mouse Mesenchymal Stem Cells

“…The Comet assay which detects both the ssDNA and dsDNA breaks revealed significant changes, particularly after the Ag NP and CuO NP exposure. The effects of ZnO NP were minimal; this result might be linked with the possible protective role of Zn against oxidative stress [ 54 ]. In contrast, micronuclei formation, which corresponds to dsDNA breaks, was very limited in some significant data for the highest tested doses of NP.…”