Neurobehavioural and biochemical responses associated with exposure to binary waterborne mixtures of zinc and nickel in rats

Adedara, Isaac A.; Adegbosin, Adedayo N.; Abiola, Michael Abayomi; Odunewu, Ajibola A.; Owoeye, Olatunde; Owumi, Solomon E.; Farombi, Ebenezer O.

doi:10.1016/j.etap.2019.103294

Cited by 11 publications

(5 citation statements)

References 66 publications

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“… CAT and SOD significantly decreased, while NO and LPO in the hippocampus significantly increased Lamtai et al (2018) 6 Comparison between the effects of NiO and NiO NPs in brain at doses of 10, 25, and 50 mg/kg intraperitoneally for 8 days on oxidative stress biomarkers Rat brain Increased levels of MDA, GST and CAT enzymes and decreased GSH and TAC in both NiO and NiO NPs exposed groups Alteration of oxidative stress biomarkers Marzban et al (2020) 7 Ultrastructural changes to neurons in hippocampus, striatum and cortex of the brain after NiCl 2 treatment (10 or 20 mg/kg for 4 weeks) Rat brain Ultrastructural alterations in neurons of hippocampus, striatum and cortex Apoptotic pathway via caspase-3 action and perturbation of α-synuclein expression in Ni-induced neurodegeneration. Ijomone et al (2018b) 8 Impact of exposure to waterborne NiCl 2 concentrations (75 and 150 μg/L).on neurobehavioral performances of rats Rat brain Adverse motor activities; negative geotaxis, grooming, grip strength and body rotation Significant elevation in RONS, LPO, MPO, NO, IL-1β and TNF-α levels in cerebrum and cerebellum of treated rats Adedara et al (2020) 9 Effects of Ni exposure through drinking water (10 mg/L, 12 weeks) on neurobehavioral performances and dendrite complexity Male mice Learning and memory impairment in mice, and reduction of dendrite complexity in mouse hippocampi Reduction of histone acetylation (especially at H3K9) and downregulation of H3K9-modulated gene expression Zhou et al (2021) 10 Nickel-induced neurobehavioral alterations in male and female rats after NiCl 2 treatment (1 mg/kg for 60 days) Male and female rats Increased anxiety-like and depression-like behaviour in rats. Cognitive behaviour on the Morris water maze resulted compromised LPO and NO formation with a decrease in SOD and CAT activities Lamtai et al (2020) 11 Neuroprotective potential of melatonin on Ni-induced neurobehavioral alterations in male and female rats C. elegans Functional changes in locomotion and basal slowing response Increasing degeneration of cholinergic, dopaminergic and GABAergic neurons Ijomone et al (2020b) 12 Effects of Ni 2+ on neurotoxic outcomes PC12 cells Changes...…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review

Anyachor¹,

Dooka²,

Orish³

et al. 2022

IBRO Neuroscience Reports

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Section: Resultsmentioning

confidence: 99%

“…Elevated hippocampal and striatal levels of caspase-3 expression the main executioner enzyme in the apoptotic pathway have been reported in nickel exposed rats ( Ijomone et al, 2018b , Adedara et al, 2020 ). Some investigations reported that nickel treatment downregulates neuronal caspase 3 expression ( Deniz and Altun, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review

Anyachor¹,

Dooka²,

Orish³

et al. 2022

IBRO Neuroscience Reports

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“…Oxygen free radical was the effector of inflammatory response, and the excessive production of oxygen free radical could also induce inflammatory response ( 34 – 36 ). It had previously been observed that NiCl 2 -mediated reductions in antioxidant enzyme activity and increases in TNF-α and IL-1β levels were significantly abrogated by zinc in rat brain and liver ( 37 ). Study have demonstrated that Equisetum hyemale Linnaeus can mitigate the elevation of TNF-α, IL-6, and IL-8, thereby reducing the inflammatory response ( 38 ).…”

Section: Discussionmentioning

confidence: 98%

N-acetyl-L-cysteine alleviated the oxidative stress-induced inflammation and necroptosis caused by excessive NiCl2 in primary spleen lymphocytes

Zhang

et al. 2023

Front. Immunol.

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IntroductionNickel (Ni) is widely used in industrial manufacturing and daily life due to its excellent physical and chemical properties. However, Ni has the potential to harm animals' immune system, and spleen is a typical immune organ. Therefore, it is crucial to understand the mechanism of NiCl2 damage to the spleen. The purpose of this study is to investigate the effects of different concentrations of NiCl2 exposure and intervening with strong antioxidants on spleen lymphocytes to better understand the damage mechanism of Ni on spleen lymphocytes.MethodsIn this experiment, mice spleen lymphocytes were used as the research object. We first measured the degree of oxidative stress, inflammation, and necroptosis caused by different NiCl2 concentrations. Subsequently, we added the powerful antioxidant N-acetyl-L-cysteine (NAC) and used hydrogen peroxide (H2O2) as the positive control in subsequent experiments.ResultsOur findings demonstrated that NiCl2 could cause spleen lymphocytes to produce a large number of reactive oxygen species (ROS), which reduced the mRNA level of antioxidant enzyme-related genes, the changes in GSH-PX, SOD, T-AOC, and MDA, the same to the mitochondrial membrane potential. ROS caused the body to produce an inflammatory response, which was manifested by tumor necrosis factor (TNF-α) in an immunofluorescence experiment, and the mRNA level of related inflammatory genes significantly increased. In the case of caspase 8 inhibition, TNF-α could cause the occurrence of necroptosis mediated by RIP1, RIP3, and MLKL. AO/EB revealed that spleen lymphocytes exposed to NiCl2 had significant necroptosis, and the mRNA and protein levels of RIP1, RIP3, and MLKL increased significantly. Moreover, the findings demonstrated that NAC acted as an antioxidant to reduce oxidative stress, inflammation, and necroptosis caused by NiCl2 exposure.DiscussionOur findings showed that NiCl2 could cause oxidative stress, inflammation, and necroptosis in mice spleen lymphocytes, which could be mitigated in part by NAC. The study provides a point of reference for understanding the toxicological effect of NiCl2. The study suggests that NAC may be useful in reducing the toxicological effect of NiCl2 on the immune system. The research may contribute to the development of effective measures to prevent and mitigate the toxicological effects of NiCl2 on the immune system.

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“…The concurrent exposure effects can be categorized as antagonistic effects, synergistic effects, and additive effects [ 35 , 36 ]. Andrade et al [ 37 ] investigated the neurological and behavioral effects of nickel (Ni) and zinc (Zn) co-exposure on rats, and found that Zn attenuated the motor impairment caused by Ni, indicating antagonistic effects. It was found that co-exposure of mercury (Hg) and Cd inhibited the development of follicles in the human ovary, thereby reducing the number of human oocytes, indicating synergistic effects [ 38 ].…”

Section: Introductionmentioning

confidence: 99%

Enhanced Uptake of Arsenic Induces Increased Toxicity with Cadmium at Non-Toxic Concentrations on Caenorhabditis elegans

Pei

Sun

Zhao

et al. 2022

Toxics

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Cadmium (Cd) and arsenic (As) are widely distributed pollutants that co-exist in the environment; however, their joint toxicity on living organisms is still largely unknown. In this study, we explored the joint toxicity of concurrent exposure to Cd and different As species at low concentrations on Caenorhabditis elegans (C. elegans) in comparison to single exposures. Endpoints such as germ cell apoptosis, the number of oocytes, brood size, and the life span were employed to evaluate the combined effects of Cd and As on exposed C. elegans from L3 or L4 stages. Our results showed that concurrent exposure to non-toxic concentrations of Cd and As caused the synergy of reproductive and developmental toxicity. The presence of Cd promoted the accumulation of As in both germline and intestine detected by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS). Although a conversion of As(III) to As(V) was detected as dependent on pH according to the microenvironment of the intestine in the worm, there was no significant difference of toxicity in C. elegans concurrently exposed to Cd and different As species. Using loss-of-function mutant strains, As was deemed responsible for the enhanced joint toxicity, and in which gcs-1 played a key protective role. These data help to better evaluate the comprehensive adverse effects of concurrent exposure of heavy metals at low concentrations on living organisms in the environment.

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Neurobehavioural and biochemical responses associated with exposure to binary waterborne mixtures of zinc and nickel in rats

Cited by 11 publications

References 66 publications

Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review

Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review

N-acetyl-L-cysteine alleviated the oxidative stress-induced inflammation and necroptosis caused by excessive NiCl2 in primary spleen lymphocytes

Enhanced Uptake of Arsenic Induces Increased Toxicity with Cadmium at Non-Toxic Concentrations on Caenorhabditis elegans

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