Nickel Oxide Nanoparticles Trigger Caspase- and Mitochondria-Dependent Apoptosis in the Yeast <i>Saccharomyces cerevisiae</i>

Sousa, Cátia A.; Soares, Helena; Soares, Eduardo V.

doi:10.1021/acs.chemrestox.8b00265

Cited by 9 publications

(4 citation statements)

References 61 publications

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“…Instead of being bactericidal or algicidal (i.e., killing bacteria or microalgae), relatively low to intermediate concentrations of nano‐Ni appear to more commonly be bacteriostatic or algistatic (i.e., nano‐Ni slows or halts the cell cycle, thus slowing or halting cell division and population growth; Argueta‐Figueroa et al 2014; Sousa et al 2018b). However, high concentrations of nano‐Ni can cause cell death (e.g., see the sequence of events in the yeast Saccharomyces cerevisiae in Figure 6 in Sousa et al 2019).…”

Section: Resultsmentioning

confidence: 99%

Toxicity of Nanoparticulate Nickel to Aquatic Organisms: Review and Recommendations for Improvement of Toxicity Tests

Meyer¹,

Lyons-Darden²,

Garman³

et al. 2020

Environmental Toxicology and Chemistry

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We reviewed the literature on toxicity of nanoparticulate nickel (nano-Ni) to aquatic organisms, from the perspective of relevance and reliability in a regulatory framework. Our main findings were 1) much of the published nano-Ni toxicity data is of low or medium quality in terms of reporting key physical-chemical properties, methodologies, and results, compared with published dissolved nickel studies; and 2) based on the available information, some common findings about nanoparticle (NP) toxicity are not supported for nano-Ni. First, we concluded that nanoparticulate elemental nickel and nickel oxide, which differ in chemical composition, generally did not differ in their toxicity. Second, there is no evidence that the toxicity of nano-Ni increases as the size of the NPs decreases. Third, for most organisms tested, nano-Ni was not more toxic on a mass-concentration basis than dissolved Ni. Fourth, there is conflicting evidence about whether the toxicity is directly caused by the NPs or by the dissolved fraction released from the NPs. However, no evidence suggests that any of the molecular, physiological, and structural mechanisms of nano-Ni toxicity differ from the general pattern for many metal-based nanomaterials, wherein oxidative stress underlies the observed effects. Physical-chemical factors in the design and conduct of nano-Ni toxicity tests are important, but often they are not adequately reported (e.g., characteristics of dry nano-Ni particles and of wetted particles in exposure waters; exposure-water chemistry).

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Section: Resultsmentioning

confidence: 99%

Toxicity of Nanoparticulate Nickel to Aquatic Organisms: Review and Recommendations for Improvement of Toxicity Tests

Meyer¹,

Lyons-Darden²,

Garman³

et al. 2020

Environmental Toxicology and Chemistry

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“…NiCl 2 -induced perturbation of electrolyte balance in the present study was characterized by increased plasma Na + and Cl − with a concomitant decrease in K + . The cellular mechanism by which nickel affects electrolyte balance is not completely understood, but it may be secondary to its effects on mitochondria including depletion of ATP that may impair active transport of ions [54,55]. Also, NiCl 2 may alter tubular permeability or interfere with transporters including Na/K ATPase.…”

Section: Discussionmentioning

confidence: 99%

Ethanol extract of Nigella sativa has antioxidant and ameliorative effect against nickel chloride-induced hepato-renal injury in rats

et al. 2020

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Background: Nickel exposure causes hepato-renal toxicity via oxidative stress. Medicinal plants with antioxidants properties are being explored as treatment options. In this study, the effect of ethanol extract of Nigella sativa (ENS) on nickel chloride (NiCl 2)-induced hepato-renal damage was evaluated by monitoring biochemical and oxidative stress markers. Additionally, the antioxidant capacity and phytochemical constituents of ENS were quantified using HPLC and GC-MS. Result: NiCl 2 significantly increased (p < 0.05) aspartate aminotransferase, creatinine, sodium ion, chloride ion and malondialdehyde levels, while antioxidant enzymes were decreased in the organs except for kidney glutathione-Stransferase when compared to the control. However, ENS exerted inhibitory effect against NiCl 2 toxicity in both organs by reversing the biomarkers towards control levels. ENS has a high antioxidant capacity and is rich in antioxidants including gallic acid, quercetin, eucalyptol and levomenthol that may have accounted for the improvement of hepato-renal health in co-exposed rats. Conclusion: Our result suggests that amelioration of nickel chloride-induced hepato-renal pathology by ethanol extract of Nigella sativa was related to its antioxidant properties. Therefore, Nigella sativa could be valuable in the management of nickel-induced toxicity.

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“…Evaluation of the yeast cells' apoptosis was performed according to [57] with some modifications. Annexin V-FITC (fluorescein isothiocyanate) -conjugated that specifically binds to phosphatidylserine (PS) residues, was used to detect the externalization of PS which is an apoptosis marker.…”

Section: Detection Of Apoptosis and Necrosismentioning

confidence: 99%

Acrylamide-Derived Ionome, Metabolic, and Cell Cycle Alterations Are Alleviated by Ascorbic Acid in the Fission Yeast

et al. 2022

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Acrylamide (AA), is a chemical with multiple industrial applications, however, it can be found in foods that are rich in carbohydrates. Due to its genotoxic and cytotoxic effects, AA has been classified as a potential carcinogen. With the use of spectrophotometry, ICP-OES, fluorescence spectroscopy, and microscopy cell growth, metabolic activity, apoptosis, ROS production, MDA formation, CAT and SOD activity, ionome balance, and chromosome segregation were determined in Schizosaccharomyces pombe. AA caused growth and metabolic activity retardation, enhanced ROS and MDA production, and modulated antioxidant enzyme activity. This led to damage to the cell homeostasis due to ionome balance disruption. Moreover, AA-induced oxidative stress caused alterations in the cell cycle regulation resulting in chromosome segregation errors, as 4.07% of cells displayed sister chromatid non-disjunction during mitosis. Ascorbic acid (AsA, Vitamin C), a strong natural antioxidant, was used to alleviate the negative impact of AA. Cell pre-treatment with AsA significantly improved AA impaired growth, and antioxidant capacity, and supported ionome balance maintenance mainly due to the promotion of calcium uptake. Chromosome missegregation was reduced to 1.79% (44% improvement) by AsA pre-incubation. Results of our multiapproach analyses suggest that AA-induced oxidative stress is the major cause of alteration to cell homeostasis and cell cycle regulation.

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Nickel Oxide Nanoparticles Trigger Caspase- and Mitochondria-Dependent Apoptosis in the Yeast Saccharomyces cerevisiae

Cited by 9 publications

References 61 publications

Toxicity of Nanoparticulate Nickel to Aquatic Organisms: Review and Recommendations for Improvement of Toxicity Tests

Toxicity of Nanoparticulate Nickel to Aquatic Organisms: Review and Recommendations for Improvement of Toxicity Tests

Ethanol extract of Nigella sativa has antioxidant and ameliorative effect against nickel chloride-induced hepato-renal injury in rats

Acrylamide-Derived Ionome, Metabolic, and Cell Cycle Alterations Are Alleviated by Ascorbic Acid in the Fission Yeast

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