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Aluminum doping tunes band gap energy level as well as oxidative stress-mediated cytotoxicity of ZnO nanoparticles in MCF-7 cells.

Akhtar MJ, Alhadlaq HA, Alshamsan A, Majeed Khan MA, Ahamed M - Sci Rep (2015)

Bottom Line: Characterization study confirmed the formation of single phase of Al(x)Zn(1-x)O nanocrystals with the size range of 33-55 nm.The IC50 for undoped ZnO nanoparticles was 44 μg/ml while for the Al-doped ZnO counterparts was 31 μg/ml.Up-regulation of apoptotic genes (e.g. p53, bax/bcl2 ratio, caspase-3 &caspase-9) along with loss of mitochondrial membrane potential suggested that Al-doped ZnO nanoparticles induced apoptosis in MCF-7 cells through mitochondrial pathway.

View Article: PubMed Central - PubMed

Affiliation: King Abdullah Institute for Nanotechnology, King Saud University, Riyadh 11451, Saudi Arabia.

ABSTRACT
We investigated whether Aluminum (Al) doping tunes band gap energy level as well as selective cytotoxicity of ZnO nanoparticles in human breast cancer cells (MCF-7). Pure and Al-doped ZnO nanoparticles were prepared by a simple sol-gel method. Characterization study confirmed the formation of single phase of Al(x)Zn(1-x)O nanocrystals with the size range of 33-55 nm. Al-doping increased the band gap energy of ZnO nanoparticles (from 3.51 eV for pure to 3.87 eV for Al-doped ZnO). Al-doping also enhanced the cytotoxicity and oxidative stress response of ZnO nanoparticles in MCF-7 cells. The IC50 for undoped ZnO nanoparticles was 44 μg/ml while for the Al-doped ZnO counterparts was 31 μg/ml. Up-regulation of apoptotic genes (e.g. p53, bax/bcl2 ratio, caspase-3 &caspase-9) along with loss of mitochondrial membrane potential suggested that Al-doped ZnO nanoparticles induced apoptosis in MCF-7 cells through mitochondrial pathway. Importantly, Al-doping did not change the benign nature of ZnO nanoparticles towards normal cells suggesting that Al-doping improves the selective cytotoxicity of ZnO nanoparticles toward MCF-7 cells without affecting the normal cells. Our results indicated a novel approach through which the inherent selective cytotoxicity of ZnO nanoparticles against cancer cells can be further improved.

No MeSH data available.


Related in: MedlinePlus

NAC prevented oxidative stress and preserved cell viability reduction caused by pure and Al-doped ZnO nanoparticles.(A) ROS, (B) GSH, (C) TSH and (D) cell viability. Data represented are mean ± SD of three identical experiments made in triplicate. *Statistically significant difference as compared to controls (p < 0.05). #Significant inhibitory effect of NAC on oxidative stress and cytotoxicity (p < 0.05).
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f6: NAC prevented oxidative stress and preserved cell viability reduction caused by pure and Al-doped ZnO nanoparticles.(A) ROS, (B) GSH, (C) TSH and (D) cell viability. Data represented are mean ± SD of three identical experiments made in triplicate. *Statistically significant difference as compared to controls (p < 0.05). #Significant inhibitory effect of NAC on oxidative stress and cytotoxicity (p < 0.05).

Mentions: ROS generation and oxidative stress has been suggested as an explanation behind the cytotoxicity of nanoparticles2829. In order to explore whether oxidative stress could play a key role in cytotoxicity, MCF-7 cells were exposed to both pure and Al-doped ZnO nanoparticles in the presence or absence of N-acetyl-cysteine (NAC). Results showed that NAC significantly prevented generation of ROS and depletion of antioxidants (GSH & TSH) caused by pure and Al-doped ZnO nanoparticles exposure (Fig. 6A–C). We further noticed that co-exposure of NAC, abolished almost fully the cell viability reduction caused by pure and Al-doped ZnO nanoparticles exposure (Fig. 6D). These results suggested that cytotoxicity caused by both pure and Al-doped ZnO nanoparticles was mediated through oxidative stress.


Aluminum doping tunes band gap energy level as well as oxidative stress-mediated cytotoxicity of ZnO nanoparticles in MCF-7 cells.

Akhtar MJ, Alhadlaq HA, Alshamsan A, Majeed Khan MA, Ahamed M - Sci Rep (2015)

NAC prevented oxidative stress and preserved cell viability reduction caused by pure and Al-doped ZnO nanoparticles.(A) ROS, (B) GSH, (C) TSH and (D) cell viability. Data represented are mean ± SD of three identical experiments made in triplicate. *Statistically significant difference as compared to controls (p < 0.05). #Significant inhibitory effect of NAC on oxidative stress and cytotoxicity (p < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4561961&req=5

f6: NAC prevented oxidative stress and preserved cell viability reduction caused by pure and Al-doped ZnO nanoparticles.(A) ROS, (B) GSH, (C) TSH and (D) cell viability. Data represented are mean ± SD of three identical experiments made in triplicate. *Statistically significant difference as compared to controls (p < 0.05). #Significant inhibitory effect of NAC on oxidative stress and cytotoxicity (p < 0.05).
Mentions: ROS generation and oxidative stress has been suggested as an explanation behind the cytotoxicity of nanoparticles2829. In order to explore whether oxidative stress could play a key role in cytotoxicity, MCF-7 cells were exposed to both pure and Al-doped ZnO nanoparticles in the presence or absence of N-acetyl-cysteine (NAC). Results showed that NAC significantly prevented generation of ROS and depletion of antioxidants (GSH & TSH) caused by pure and Al-doped ZnO nanoparticles exposure (Fig. 6A–C). We further noticed that co-exposure of NAC, abolished almost fully the cell viability reduction caused by pure and Al-doped ZnO nanoparticles exposure (Fig. 6D). These results suggested that cytotoxicity caused by both pure and Al-doped ZnO nanoparticles was mediated through oxidative stress.

Bottom Line: Characterization study confirmed the formation of single phase of Al(x)Zn(1-x)O nanocrystals with the size range of 33-55 nm.The IC50 for undoped ZnO nanoparticles was 44 μg/ml while for the Al-doped ZnO counterparts was 31 μg/ml.Up-regulation of apoptotic genes (e.g. p53, bax/bcl2 ratio, caspase-3 &caspase-9) along with loss of mitochondrial membrane potential suggested that Al-doped ZnO nanoparticles induced apoptosis in MCF-7 cells through mitochondrial pathway.

View Article: PubMed Central - PubMed

Affiliation: King Abdullah Institute for Nanotechnology, King Saud University, Riyadh 11451, Saudi Arabia.

ABSTRACT
We investigated whether Aluminum (Al) doping tunes band gap energy level as well as selective cytotoxicity of ZnO nanoparticles in human breast cancer cells (MCF-7). Pure and Al-doped ZnO nanoparticles were prepared by a simple sol-gel method. Characterization study confirmed the formation of single phase of Al(x)Zn(1-x)O nanocrystals with the size range of 33-55 nm. Al-doping increased the band gap energy of ZnO nanoparticles (from 3.51 eV for pure to 3.87 eV for Al-doped ZnO). Al-doping also enhanced the cytotoxicity and oxidative stress response of ZnO nanoparticles in MCF-7 cells. The IC50 for undoped ZnO nanoparticles was 44 μg/ml while for the Al-doped ZnO counterparts was 31 μg/ml. Up-regulation of apoptotic genes (e.g. p53, bax/bcl2 ratio, caspase-3 &caspase-9) along with loss of mitochondrial membrane potential suggested that Al-doped ZnO nanoparticles induced apoptosis in MCF-7 cells through mitochondrial pathway. Importantly, Al-doping did not change the benign nature of ZnO nanoparticles towards normal cells suggesting that Al-doping improves the selective cytotoxicity of ZnO nanoparticles toward MCF-7 cells without affecting the normal cells. Our results indicated a novel approach through which the inherent selective cytotoxicity of ZnO nanoparticles against cancer cells can be further improved.

No MeSH data available.


Related in: MedlinePlus