Nanotoxicity of pure silica mediated through oxidant generation rather than glutathione depletion in human lung epithelial cells

Akhtar, Mohd Javed; Ahamed, Maqusood; Kumar, Sudhir; Siddiqui, Huma; Patil, Govil; Ashquin, Mohd; Ahmad, Iqbal

doi:10.1016/j.tox.2010.07.010

Cited by 161 publications

(109 citation statements)

References 64 publications

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“…Taken together, treatment of MNP@ SiO 2 induced cytotoxicity and enhanced DNA damage in L5178Y cell. nanoparticles were found to induce oxidative stress indicated by induction of reactive oxygen species generation, and membrane lipid peroxidation (Akhtar et al, 2010), and the toxicity were confi rmed in recent studies (Nabeshi et al, 2010;Yang et al, 2010;Ye et al, 2010). It seems that these discrepancy of toxicities may be associated with nano characteristics such as size, shape, surface chemistry and degree of aggregation infl uenced the production of free radicals and oxidative stress (Aillon et al, 2009 (Yoon et al, 2005;.…”

Section: Introductionmentioning

confidence: 70%

“…As confocal microscope fi ndings showed that MNP@SiO 2 could enter the cell after treatment, irrespective of size, it may be owing to early cellular entry of MNP@SiO 2 . Base on recent reports that toxicity of silica nanoparticles was mediated through oxidant generation (Akhtar et al, 2010), and treatment of silica nanoparticles induced infl ammation (Hamilton et al, 2008) and enhanced infl ammatory cytokines (Nishimori et al, 2009), they could induce cellular toxicity even in larger size as well as small size.…”

Section: Discussionmentioning

confidence: 99%

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Cytotoxicity and DNA Damage Induced by Magnetic Nanoparticle Silica in L5178Y Cell

Kang¹,

Yum²,

Park³

2011

Biomolecules and Therapeutics

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Section: Introductionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Cytotoxicity and DNA Damage Induced by Magnetic Nanoparticle Silica in L5178Y Cell

Kang¹,

Yum²,

Park³

2011

Biomolecules and Therapeutics

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“…GSH, a ubiquitous and abundant cellular antioxidant tripeptide, was found to be strongly depleted in response to NP treatment. 59 GR is an important enzyme in recycling the GSSH back to GSH. The activity of GPx can provide important clues about the consumption rate of GSH during detoxification of organic hydroperoxides by it.…”

Section: Discussionmentioning

confidence: 99%

Zinc oxide nanoparticles selectively induce apoptosis in human cancer cells through reactive oxygen species

Akhtar¹,

Ahamed²,

Kumar³

et al. 2012

IJN

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260

105

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Background: Zinc oxide nanoparticles (ZnO NPs) have received much attention for their implications in cancer therapy. It has been reported that ZnO NPs induce selective killing of cancer cells. However, the underlying molecular mechanisms behind the anticancer response of ZnO NPs remain unclear. Methods and results:We investigated the cytotoxicity of ZnO NPs against three types of cancer cells (human hepatocellular carcinoma HepG2, human lung adenocarcinoma A549, and human bronchial epithelial BEAS-2B) and two primary rat cells (astrocytes and hepatocytes). Results showed that ZnO NPs exert distinct effects on mammalian cell viability via killing of all three types of cancer cells while posing no impact on normal rat astrocytes and hepatocytes. The toxicity mechanisms of ZnO NPs were further investigated using human liver cancer HepG2 cells. Both the mRNA and protein levels of tumor suppressor gene p53 and apoptotic gene bax were upregulated while the antiapoptotic gene bcl-2 was downregulated in ZnO NPtreated HepG2 cells. ZnO NPs were also found to induce activity of caspase-3 enzyme, DNA fragmentation, reactive oxygen species generation, and oxidative stress in HepG2 cells. Conclusion:Overall, our data demonstrated that ZnO NPs selectively induce apoptosis in cancer cells, which is likely to be mediated by reactive oxygen species via p53 pathway, through which most of the anticancer drugs trigger apoptosis. This study provides preliminary guidance for the development of liver cancer therapy using ZnO NPs.

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“…Among the possible mechanisms of nanoparticle toxicity, reactive oxygen species (ROS) generation and oxidative stress remain an important area of consideration (Nel et al, 2006;Ahamed et al, 2010aAhamed et al, , 2010bAhamed et al, , 2010cAhamed et al, , 2011aAhamed et al, , 2011bAhamed et al, and 2011cAkhtar et al, 2010aAkhtar et al, , 2010b. Our previous publication also demonstrated the oxidative stress mediated genotoxicity of CuO NPs in human lung epithelial (A549) cells (Ahamed et al, 2010c).…”

Section: Introductionmentioning

confidence: 98%

Protective effect of sulphoraphane against oxidative stress mediated toxicity induced by CuO nanoparticles in mouse embryonic fibroblasts BALB 3T3

et al. 2012

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-Despite the great interest in nanoparticles (NPs) safety, no comprehensive test paradigm has been developed. Oxidative stress has been implicated as an explanation behind the toxicity of NPs. It is reported that sulphoraphane (SFN) present in cruciferous vegetables like cauliflower and broccoli has potential to protect cells from oxidative damage and inflammation. However, protective role of SFN in nanotoxicity is not explored. We investigated the protective effect of SFN against the toxic response of copper oxide (CuO) NPs in mouse embryonic fibroblasts (BALB 3T3). Results showed that CuO NPs induced dose-dependent (5-15 μg/ml) cytotoxicity in BALB 3T3 cells demonstrated by MTT and lactate dehydrogenase (LDH) assays. CuO NPs were also found to induce oxidative stress in dose-dependent manner indicated by induction of reactive oxygen species (ROS) and lipid peroxidation (LPO) and depletion of glutathione and glutathione reductase. Co-treatment of BALB 3T3 cells with SFN (6 μM) significantly attenuated the cytotoxicity, ROS generation and oxidative stress caused by CuO NPs. Moreover, we found that co-treatment of another antioxidant N-acetyl-cysteine (NAC) (2 mM) also significantly attenuated glutathione depletion caused by CuO NPs but protection from the loss of cell viability due to CuO NPs exposure was not significant. We believe this is the first report showing that SFN significantly protected the BALB 3T3 cells from CuO NPs toxicity, which is mediated through generation of oxidants and depletion of antioxidants. Consequently, protective mechanism of SFN against CuO NPs toxicity was different from NAC that should be further investigated.

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Nanotoxicity of pure silica mediated through oxidant generation rather than glutathione depletion in human lung epithelial cells

Cited by 161 publications

References 64 publications

Cytotoxicity and DNA Damage Induced by Magnetic Nanoparticle Silica in L5178Y Cell

Cytotoxicity and DNA Damage Induced by Magnetic Nanoparticle Silica in L5178Y Cell

Zinc oxide nanoparticles selectively induce apoptosis in human cancer cells through reactive oxygen species

Protective effect of sulphoraphane against oxidative stress mediated toxicity induced by CuO nanoparticles in mouse embryonic fibroblasts BALB 3T3

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