Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.

Copper oxide nanoparticles (CuO NPs) are heavily utilized in semiconductor devices, gas sensor, batteries, solar energy converter, microelectronics and heat transfer fluids. It has been reported that liver is one of the target organs for nanoparticles after they gain entry into the body through any...

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Autores principales: Maqsood A Siddiqui, Hisham A Alhadlaq, Javed Ahmad, Abdulaziz A Al-Khedhairy, Javed Musarrat, Maqusood Ahamed
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/bffb2059fa164819a063ceabeb924ed7
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spelling oai:doaj.org-article:bffb2059fa164819a063ceabeb924ed72021-11-18T09:01:26ZCopper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.1932-620310.1371/journal.pone.0069534https://doaj.org/article/bffb2059fa164819a063ceabeb924ed72013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23940521/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Copper oxide nanoparticles (CuO NPs) are heavily utilized in semiconductor devices, gas sensor, batteries, solar energy converter, microelectronics and heat transfer fluids. It has been reported that liver is one of the target organs for nanoparticles after they gain entry into the body through any of the possible routes. Recent studies have shown cytotoxic response of CuO NPs in liver cells. However, the underlying mechanism of apoptosis in liver cells due to CuO NPs exposure is largely lacking. We explored the possible mechanisms of apoptosis induced by CuO NPs in human hepatocellular carcinoma HepG2 cells. Prepared CuO NPs were spherical in shape with a smooth surface and had an average diameter of 22 nm. CuO NPs (concentration range 2-50 µg/ml) were found to induce cytotoxicity in HepG2 cells in dose-dependent manner, which was likely to be mediated through reactive oxygen species generation and oxidative stress. Tumor suppressor gene p53 and apoptotic gene caspase-3 were up-regulated due to CuO NPs exposure. Decrease in mitochondrial membrane potential with a concomitant increase in the gene expression of bax/bcl2 ratio suggested that mitochondria mediated pathway involved in CuO NPs induced apoptosis. This study has provided valuable insights into the possible mechanism of apoptosis caused by CuO NPs at in vitro level. Underlying mechanism(s) of apoptosis due to CuO NPs exposure should be further invested at in vivo level.Maqsood A SiddiquiHisham A AlhadlaqJaved AhmadAbdulaziz A Al-KhedhairyJaved MusarratMaqusood AhamedPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e69534 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Maqsood A Siddiqui
Hisham A Alhadlaq
Javed Ahmad
Abdulaziz A Al-Khedhairy
Javed Musarrat
Maqusood Ahamed
Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
description Copper oxide nanoparticles (CuO NPs) are heavily utilized in semiconductor devices, gas sensor, batteries, solar energy converter, microelectronics and heat transfer fluids. It has been reported that liver is one of the target organs for nanoparticles after they gain entry into the body through any of the possible routes. Recent studies have shown cytotoxic response of CuO NPs in liver cells. However, the underlying mechanism of apoptosis in liver cells due to CuO NPs exposure is largely lacking. We explored the possible mechanisms of apoptosis induced by CuO NPs in human hepatocellular carcinoma HepG2 cells. Prepared CuO NPs were spherical in shape with a smooth surface and had an average diameter of 22 nm. CuO NPs (concentration range 2-50 µg/ml) were found to induce cytotoxicity in HepG2 cells in dose-dependent manner, which was likely to be mediated through reactive oxygen species generation and oxidative stress. Tumor suppressor gene p53 and apoptotic gene caspase-3 were up-regulated due to CuO NPs exposure. Decrease in mitochondrial membrane potential with a concomitant increase in the gene expression of bax/bcl2 ratio suggested that mitochondria mediated pathway involved in CuO NPs induced apoptosis. This study has provided valuable insights into the possible mechanism of apoptosis caused by CuO NPs at in vitro level. Underlying mechanism(s) of apoptosis due to CuO NPs exposure should be further invested at in vivo level.
format article
author Maqsood A Siddiqui
Hisham A Alhadlaq
Javed Ahmad
Abdulaziz A Al-Khedhairy
Javed Musarrat
Maqusood Ahamed
author_facet Maqsood A Siddiqui
Hisham A Alhadlaq
Javed Ahmad
Abdulaziz A Al-Khedhairy
Javed Musarrat
Maqusood Ahamed
author_sort Maqsood A Siddiqui
title Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
title_short Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
title_full Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
title_fullStr Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
title_full_unstemmed Copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
title_sort copper oxide nanoparticles induced mitochondria mediated apoptosis in human hepatocarcinoma cells.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/bffb2059fa164819a063ceabeb924ed7
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AT hishamaalhadlaq copperoxidenanoparticlesinducedmitochondriamediatedapoptosisinhumanhepatocarcinomacells
AT javedahmad copperoxidenanoparticlesinducedmitochondriamediatedapoptosisinhumanhepatocarcinomacells
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