ZnO Particulate Matter Requires Cell Contact for Toxicity in Human Colon Cancer Cells

Moos, Philip J.; Chung, Kevin K.; Woessner, David W.; Honeggar, Matthew; Cutler, N. Shane; Veranth, John M.

doi:10.1021/tx900203v

Cited by 196 publications

(127 citation statements)

References 40 publications

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“…Similarly, three types of cancer cells HepG2, A549 and BEAS-2B were suppressed by the effect of ZnO nanoparticles, while normal rat astrocytes and hepatocytes were not affected [40]. The nano-sized ZnO was found more cytotoxic than the micrometer-sized ZnO with LC 50 values of 15 ± 1 and 29 ± 4 lg, respectively [41]. Prolonged exposure to ZnO nanoparticles at 10 lg ml results in decreased mitochondrial activity, loss of normal cell morphology, and disturbances in cell cycle distribution [42].…”

Section: Discussionmentioning

confidence: 99%

Toxicity on Dengue Mosquito Vectors Through Myristica fragrans-Synthesized Zinc Oxide Nanorods, and Their Cytotoxic Effects on Liver Cancer Cells (HepG2)

et al. 2016

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Dengue is an arbovirus mainly vectored by Aedes mosquitoes. Its prevention and control depends to effective vector control measures. Cancer causes millions of death every year. Most of the anticancer drugs have high toxicity and low specificity of action, leading to systemic toxicity and severe side effects. Thus, the development of effective tools is a priority. We fabricated zinc oxide nanoparticles using the Myristica fragrans extract as a reducing and stabilizing agent. Nanoparticles were studied using UV-vis spectrophotometry, Fourier transform infrared spectroscopy, X-ray diffraction, zeta potential, dynamic light scattering, energy dispersive X-ray analysis, field emission scanning electron microscopy and transmission electron microscopy. ZnO nanorods were highly effective against A. aegypti young instars, with LC 50 ranging from 3.44 (larva I) to 14.63 ppm (pupa). Nanorods showed adult LC 50 of 15.004 ppm. ZnO nanorods exhibited dose-dependent cytotoxicity against human hepato-cancer cells (HepG2). After 48 and 24 h of incubation, the IC 50 were 20 and 22 lg/ml, respectively. Nanorods triggered the induction of apoptosis. Overall, this study highlights that the possibility to employ M. fragrans-synthesized ZnO nanorods in mosquito control, as well as in the development of novel chemotherapeutic agents with reduced systemic toxicity.

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Section: Discussionmentioning

confidence: 99%

Toxicity on Dengue Mosquito Vectors Through Myristica fragrans-Synthesized Zinc Oxide Nanorods, and Their Cytotoxic Effects on Liver Cancer Cells (HepG2)

et al. 2016

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“…Several recent studies, along with our previous publication, showed that ZnO NPs liberate Zn 2+ in an aqueous state, but the levels of Zn 2+ released were insufficient to promote toxicity to cells unless the particulate matter is in contact with the cells. 18,52,53 Moreover, in a recent investigation, Kilari et al 54 showed the protective effect of Zn 2+ in colon cancer (Caco-2) cells.…”

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

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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“…17 Indeed, recent studies have been focused on the relationship between the size of ZnO nanoparticles and their toxicological effects. 9,12,13,[18][19][20] However, most studies have focused on comparing the toxic effects of nanosized particles with those of micron-sized ones, providing less information about toxicity per se, particularly for nanoparticles below 100 nm. Moreover, many researchers have published toxicity data only from in vitro studies, so the impact of particle size on systemic toxicity in vivo remains to be clarified.…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetics, tissue distribution, and excretion of zinc oxide nanoparticles

Baek¹,

Chung²,

Jin³

et al. 2012

IJN

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Background: This study explored the pharmacokinetics, tissue distribution, and excretion profile of zinc oxide (ZnO) nanoparticles with respect to their particle size in rats. Methods: Two ZnO nanoparticles of different size (20 nm and 70 nm) were orally administered to male and female rats, respectively. The area under the plasma concentration-time curve, tissue distribution, excretion, and the fate of the nanoparticles in organs were analyzed. Results: The plasma zinc concentration of both sizes of ZnO nanoparticles increased during the 24 hours after administration in a dose-dependent manner. They were mainly distributed to organs such as the liver, lung, and kidney within 72 hours without any significant difference being found according to particle size or rat gender. Elimination kinetics showed that a small amount of ZnO nanoparticles was excreted via the urine, while most of nanoparticles were excreted via the feces. Transmission electron microscopy and x-ray absorption spectroscopy studies in the tissues showed no noticeable ZnO nanoparticles, while new Zn-S bonds were observed in tissues. Conclusion: ZnO nanoparticles of different size were not easily absorbed into the bloodstream via the gastrointestinal tract after a single oral dose. The liver, lung, and kidney could be possible target organs for accumulation and toxicity of ZnO nanoparticles was independent of particle size or gender. ZnO nanoparticles appear to be absorbed in the organs in an ionic form rather than in a particulate form due to newly formed Zn-S bonds. The nanoparticles were mainly excreted via the feces, and smaller particles were cleared more rapidly than the larger ones. ZnO nanoparticles at a concentration below 300 mg/kg were distributed in tissues and excreted within 24 hours. These findings provide crucial information on possible acute and chronic toxicity of ZnO nanoparticles in potential target organs.

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ZnO Particulate Matter Requires Cell Contact for Toxicity in Human Colon Cancer Cells

Cited by 196 publications

References 40 publications

Toxicity on Dengue Mosquito Vectors Through Myristica fragrans-Synthesized Zinc Oxide Nanorods, and Their Cytotoxic Effects on Liver Cancer Cells (HepG2)

Toxicity on Dengue Mosquito Vectors Through Myristica fragrans-Synthesized Zinc Oxide Nanorods, and Their Cytotoxic Effects on Liver Cancer Cells (HepG2)

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

Pharmacokinetics, tissue distribution, and excretion of zinc oxide nanoparticles

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