Nickel Release, ROS Generation and Toxicity of Ni and NiO Micro- and Nanoparticles

Latvala, Siiri; Hedberg, Jonas; Bucchianico, Sebastiano Di; Möller, Lennart; Wallinder, Inger Odnevall; Elihn, Karine; Karlsson, Hanna

doi:10.1371/journal.pone.0159684

Cited by 130 publications

(117 citation statements)

References 42 publications

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“…Soesetijo et al have recently demonstrated enhanced apoptosis of gingival fibroblasts induced by nickel released from nickel-chromium alloys [1]. Latvala et al found that nickel can enhance reactive oxygen species generation, cytotoxicity and genotoxicity in human alveolar epithelial cell line A549 [14]. Our present and previous results [13] are in concordance with the aforementioned data.…”

Section: Discussionsupporting

confidence: 93%

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Caspase-3 as an important factor in the early cytotoxic effect of nickel on oral mucosa cells in patients treated orthodontically

Buczko¹,

Szarmach²,

Grycz³

et al. 2017

Folia Histochem Cytobiol.

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Introduction. The effect of fixed orthodontic appliances on biochemical changes in saliva and pathophysiological status of the oral cavity is not clear. Recent data showed that nickel (Ni) released from orthodontic appliances can decrease cellular viability, induce DNA damage and apoptosis in oral mucosa cells. Since the mechanism of these Ni effects is unknown, the aim of our study was to analyze the expression of caspase-3 in epithelial cells of oral mucosa in healthy individuals treated orthodontically. Material and methods. Twenty-eight volunteers participated in the study. Epithelial cells were collected from oral mucosa directly before appliance insertion, one week after the insertion, and 24 weeks after the insertion of fixed appliances. Cellular identification and measurements were conducted by light microscopy. Caspase-3 expression was evaluated immunohistochemically. Nickel concentration in saliva was also determined. Results. A significantly higher number of oral epithelial cells with caspase-3 immunoreactivity was found one week, but not 24 weeks, after orthodontic treatment. The enhanced expression of caspase-3 was accompanied by increased nickel concentration in saliva. Conclusions. Our data suggests that nickel released from orthodontic appliances can activate caspase-3 and this mechanism may be partially responsible for the cytotoxic action of nickel in the oral cavity of orthodontically-treated individuals.

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Section: Discussionsupporting

confidence: 93%

“…It has been well established that orthodontic appliances release nickel into the artificial saliva and into the saliva of oral cavity [1,6,7,14]. Indeed, Faccioni et al found a higher nickel concentration in the oral mucosa cells of patients treated orthodontically in comparison to controls [6].…”

Section: Discussionmentioning

confidence: 99%

Caspase-3 as an important factor in the early cytotoxic effect of nickel on oral mucosa cells in patients treated orthodontically

Buczko¹,

Szarmach²,

Grycz³

et al. 2017

Folia Histochem Cytobiol.

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“…In the cell viability assay, Ni concentrations of 0.15 and 0.32 μg cm −2 induced substantially decreased viability (approximately 45%) after 48 hours post‐exposure in ALI, when compared to the control. In comparison with a previous study (Latvala et al, ), these results suggest that ALI exposure may result in more sensitive conditions when compared to submerged exposures, although different cell types were used.…”

Section: Discussioncontrasting

confidence: 42%

In vitro genotoxicity of airborne Ni‐NP in air–liquid interface

Latvala

Vare

Karlsson

et al. 2017

J of Applied Toxicology

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Studies using advanced toxicological methods enabling in vitro conditions that are more realistic are currently needed for understanding the risks of pulmonary exposure to airborne nanoparticles. Owing to the carcinogenicity of certain nickel compounds, the increased production of nickel nanoparticles (Ni‐NPs) raises occupational safety concerns. The aim of this study was to investigate the genotoxicity of airborne Ni‐NPs using a recently developed air–liquid interface exposure system. The wild‐type Chinese hamster lung fibroblast cell line (V79) was used and cytotoxicity, DNA damage and mutagenicity were studied by testing colony forming efficiency, alkaline DNA unwinding and HPRT mutation assays, respectively. Additionally, co‐exposure to a PARP‐1 inhibitor was performed to test possible involvement of base excision repair (BER) in repair of Ni‐induced DNA damage. The results showed that cell viability was reduced significantly (to 45% and 46%) after 48 hours Ni‐NP exposure at concentrations of 0.15 and 0.32 μg cm−2. DNA damage was significantly increased after Ni‐NP exposure in the presence of the BER inhibitor indicating that Ni‐NP‐induced DNA damages are subsequently repaired by BER. Furthermore, there was no increased HPRT mutation frequency following Ni‐NP exposure. In conclusion, this study shows that Ni‐NP treatment of lung fibroblasts in an air–liquid interface system that mimics real‐life exposure, results in increased DNA strand breaks and reduced cellular viability. These DNA lesions were repaired with BER in an error‐free manner without resulting in mutations. This study also underlines the importance of appropriate quantification of the actual exposure concentrations during air–liquid interface exposure studies.

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“…is the final product of lipid peroxidation process [25] and is still routinely used as a marker for oxidative stress induced by different toxicants [26]. Several works conclusions have agreed about the mechanism of NiNPs in inducing the toxicity in vivo [19] and in vitro [22]- [18] which is the inducting oxidative stress through elevating the levels of reactive oxygen species (ROS). In the present investigation, NiNPs have caused a significant (P≤0.05) dose dependent elevation of serum creatinine in comparison to the control (Fig.2).…”

Section: Resultsmentioning

confidence: 99%

“…The increased production of Ni-containing nanoparticles necessitates a thorough assessment of their toxicological properties [22].…”

Section: Introductionmentioning

confidence: 99%

Nephrotoxicity of nickel nanoparticles in rat: Effect of different doses

2018

CBEMS-18,DMCCIA-18,EHSSM-18,BLEIS-18,ICLTET-18 March 21-23, 2018 Istanbul (Turkey)

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Abstract-The present investigation was dealt with the study of the effect of different doses of Nickel nanoparticles (NiNPs) (particle size equal to 20nm) on the kidney of rat. Intraperitoneal administration of NiNPs (0,5,10,20, 50 and 100mg/kg bw) was achieved for 28 days and the kidney samples were homogenized to estimate the level of malondialdehyde (MDA) as lipid peroxidation marker while creatinine was estimated in serum as well as studying the histopathological changes. Significant dose dependent elevation of MDA in kidney homogenate and a significant dose dependent increase of serum creatinine were detected. The most histopathological feature was the appearance of inflammatory aggregations of infiltrated leucocytes.

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Nickel Release, ROS Generation and Toxicity of Ni and NiO Micro- and Nanoparticles

Cited by 130 publications

References 42 publications

Caspase-3 as an important factor in the early cytotoxic effect of nickel on oral mucosa cells in patients treated orthodontically

Caspase-3 as an important factor in the early cytotoxic effect of nickel on oral mucosa cells in patients treated orthodontically

In vitro genotoxicity of airborne Ni‐NP in air–liquid interface

Nephrotoxicity of nickel nanoparticles in rat: Effect of different doses

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