Toxic responses in primary rat hepatocytes exposed with occupational dust collected from work environment of bone-based industrial unit

Ahmad, Iqbal; Siddiqui, Huma; Akhtar, Mohd Javed; Khan, Mohammad Imran; Patil, Govil; Ashquin, Mohd; Patel, Devendra Kumar; Arif, Jamal M.

doi:10.1016/j.chemosphere.2010.12.074

Cited by 1 publication

(1 citation statement)

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“…These cell lines have been extensively utilized in toxicity studies. [16][17][18][19] To explore the underlying molecular mechanisms of apoptosis induced by ZnO NPs, we have further utilized the human liver cancer HepG2 cells. Quantitative real-time polymerase chain reaction (PCR) and Western blotting techniques were used to determine both the mRNA and protein levels of p53, bax, bcl-2, and caspase-3 genes involved in apoptotic pathways.…”

Section: Introductionmentioning

confidence: 99%

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

Akhtar¹,

Ahamed²,

Kumar³

et al. 2012

IJN

275

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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Section: Introductionmentioning

confidence: 99%