Assessment of the toxicity of silver nanoparticles in vitro: A mitochondrial perspective

Teodoro, João S.; Simões, Anabela M.; Duarte, Filipe V.; Rolo, Anabela P.; Murdoch, Richard C.; Hussain, Saber M.; Palmeira, Carlos M.

doi:10.1016/j.tiv.2011.01.004

Cited by 206 publications

(127 citation statements)

References 35 publications

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“…This characteristic of response was similar in all cells. Thus, it is thought that mitochondria might be important target of nanosilver cytotoxicity (Teodoro et al, 2011). It seems that diminished SOD2 gene expression, which was confirmed in the present study, involve in dysfunction of mitochondria.…”

Section: Discussionsupporting

confidence: 84%

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

Hassanpour

Mirshokraei

Sadrabad

et al. 2015

Animal

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To evaluate effects of different concentrations of nanosilver colloid on the cell culture of Sertoli cells, the proportion of lipid peroxidation, antioxidant capacity, nitric oxide (NO) production and genes expression of superoxide dismutases (SOD1 and SOD2) and nitric oxide synthases (eNOS and iNOS) were measured. Sertoli cells were incubated at concentrations of 25, 75 and 125 ppm nanosilver for 48 h. There was progressive lipid peroxidation in treatments according to increasing of nanosilver. Lipid peroxidation, as indicated by malondialdehyde levels, was significantly elevated by the highest concentration of silver colloid (125 ppm), although antioxidant capacity, as measured by ferric ion reduction, was unaffected. Nitrite, as an index of NO production was reduced only in 125 ppm of nanosilver. Expression of SOD1 gene was reduced in nanosilver-treated cells at all concentrations, whereas expression of SOD2 gene was reduced only in cells treated with 125 ppm nanosilver. Expression of iNOS gene was progressively increased with higher concentrations of nanosilver. Expression of eNOS gene was also increased in 125 ppm of nanosilver. In conclusion, toxic effects of nanosilver could be due to high lipid peroxidation and suppression of antioxidant mechanisms via reduced expression of SOD genes and increased expression of NOS genes.

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Section: Discussionsupporting

confidence: 84%

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

Hassanpour

Mirshokraei

Sadrabad

et al. 2015

Animal

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“…Thus, MPT induction is a catastrophic event that can lead to apoptosis (Eaton and Klaassen, 2001). According to previous studies, many types of chemicals such as methylmercury, silver nanoparticles, and ionic liquids can induce MPT and lead to mitochondrial dysfunction (Polunas et al, 2011;Teodoro et al, 2011;Li et al, 2012b). Our results reveal that resveratrol may promote the opening of MPTPs and induce MPT in the treated QGY-7701 cells, causing mitochondrial depolarization and ATP depletion.…”

Section: Discussionsupporting

confidence: 68%

Mitochondrial dysfunction in resveratrol-induced apoptosis in QGY-7701 cells

Chen

2016

Genet. Mol. Res.

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ABSTRACT. This study aims to evaluate the cytotoxicity of resveratrol on QGY-7701 cells via a cell viability assay, and determine the cytological alterations and damages that result. Resveratrol was found to inhibit QGY-7701 cell growth and decrease their viability in a remarkably dosedependent manner. Resveratrol exposure also induced an increase in Caspase-3 activity and a decrease in Bcl-2, which caused an increase in membrane permeability, and the opening of mitochondrial permeability transition pores and mitochondrial depolarization. Cellular ATP is thus exhausted, and apoptosis is induced via the change in mitochondrial membrane permeability and mitochondrial dysfunction.

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“…95 Additionally, Teodoro, et al, found that AgNP exposure resulted in decreased state 3 and state 4 respiration in isolated liver mitochondria. 96 Costa et al found that brain, heart, and muscle mitochondria displayed differing patterns of ETC enzyme inhibition, despite being tissues of commonly high metabolic demand: complex I and III were more sensitive to inhibition than II and IV in brain; complex I, II, III, and IV in heart were in general less sensitive than in brain and muscle, with complex I the least sensitive; and in muscle, complex III and IV were the most sensitive to inhibition, complex II exhibited intermediary sensitivity, and complex I was most resistant to inhibition by AgNPs. 95 While the contribution of silver ions themselves were not assessed in ETC enzyme inhibition, the dissolution of AgNPs likely plays a role, as silver ions bind readily to thiol groups.…”

Section: Mitochondrial Depolarizationmentioning

confidence: 99%

A systematic review of evidence for silver nanoparticle-induced mitochondrial toxicity

Maurer

Meyer

2016

Environ. Sci.: Nano

106

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Assessment of the toxicity of silver nanoparticles in vitro: A mitochondrial perspective

Cited by 206 publications

References 35 publications

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

Mitochondrial dysfunction in resveratrol-induced apoptosis in QGY-7701 cells

A systematic review of evidence for silver nanoparticle-induced mitochondrial toxicity

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