Induction of apoptosis and autophagy by sodium selenite in A549 human lung carcinoma cells through generation of reactive oxygen species

Park, Shin‐Hyung; Kim, Jeong‐Hwan; Yong, Gyoo; Kim, Gi‐Young; Chang, Young‐Chae; Moon, Sung‐Kwon; Nam, Soo-Wan; Kim, Wun-Jae; Yoo, Young Hyun; Choi, Yung Hyun

doi:10.1016/j.toxlet.2012.06.007

Cited by 119 publications

(94 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results for Na 2 SeO 3 were consistent with previous findings in which 6×10 −6 mol/L Na 2 SeO 3 for 1 d suppressed the growth of A549 cells that was attributed to the increase in the sub-G 1 phase and the induction of apoptosis. 20) Previous studies examined the cell cycle arrest and induction of apoptosis by MSA in other cancer cell lines, but not the A549 cell line. Sinha et al reported that MSA at a low concentration (5×10 −6 mol/L) inhibited the growth of the mouse mammary epithelial tumor cell line, TM6 at the G 1 phase, whereas a high concentration (5×10 −5 mol/L) could induce apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Glutathione-Dependent Cell Cycle G<sub>1</sub> Arrest and Apoptosis Induction in Human Lung Cancer A549 Cells Caused by Methylseleninic Acid: Comparison with Sodium Selenite

Okuno

Honda

Arakawa

et al. 2014

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The aim of the present study was to clarify the mechanism underlying the inhibition of cell proliferation in human lung cancer A549 cells by selenium (Se) compounds. Methylseleninic acid (CH 3 SeO 2 H, abbreviated as MSA), a synthetic Se compound, is a direct precursor of active methylselenol (CH 3 SeH) and is considered to be one of beneficial agents for cancer prevention and therapy. Sodium selenite (Na 2 SeO 3 ), an inorganic Se form, is utilized in clinical Se supplementation. MSA markedly inhibited the growth of A549 cells at a concentration of 2.5 10 6 mol/L for 1 d. On Day 1, Na 2 SeO 3 also inhibited A549 cell growth at the concentration of 7.5 10 6 mol/L. These compounds induced cell cycle arrest at the G 1 phase and apoptosis under the inhibitory condition. Reduced glutathione (GSH) is critical to MSA or Na 2 SeO 3 metabolism. The depletion of intracellular GSH suppressed Na 2 SeO 3 -induced G 1 arrest, but promoted Na 2 SeO 3 -induced apoptosis. Therefore, Na 2 SeO 3 appears to have directly induced apoptosis. In contrast, the MSA-induced G 1 arrest was ameliorated by a marked decrease in GSH content. Additionally, the depletion of GSH slightly suppressed MSA-induced apoptosis. The difference in inhibitory effects between MSA and Na 2 SeO 3 may be due to this variation in GSH-related metabolism. After exposure of A549 cells to MSA, the GSH content was significantly decreased. These results indicate that because MSA-induced G 1 arrest and apoptosis induction are enhanced by GSH, the maintenance of GSH is essential for the effective anticancer action of MSA in A549 cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Glutathione-Dependent Cell Cycle G<sub>1</sub> Arrest and Apoptosis Induction in Human Lung Cancer A549 Cells Caused by Methylseleninic Acid: Comparison with Sodium Selenite

Okuno

Honda

Arakawa

et al. 2014

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…Preventing this cascade of events would require providing the necessary reducing equivalents for the surge in ROS. Park et al [22] showed that exogenous NAC supplied these reducing equivalents; however, we found that supplying the cells with Glu restored proliferation as well. This suggests that impaired glutaminolysis via decreased GAC expression is one of the primary sources for escalating ROS production and selenite mediated cell death.…”

Section: Glu Rescue Experimentscontrasting

confidence: 55%

“…Recently, selenite was shown to cause ROS mediated autophagy in A549 cells by Park et al [22]. Fan et al has demonstrated the use of stable isotoperesolved metabolomics (SIRM) combined with transcriptomics for probing metabolic alterations caused by selenite [23] Despite these findings, however, the mechanism behind selenite toxicity is only partially understood.…”

Section: Selenium Compounds Possess Anti-cancer Activitymentioning

confidence: 99%

See 1 more Smart Citation

Probing the anti-cancer mechanism of selenite : a metabolic approach.

Belshoff¹

View full text Add to dashboard Cite

“…27 Second, incubation of A549 cells with MICDH for 24 hours caused an obvious increase in the proportion of apoptotic cells compared with incubation with free DFM. 28 The increased induction of apoptosis by MICDH in human lung adenocarcinoma A549 cells, compared with that by free DFM, may be due to the increases of ROS 29 and intracellular Ca 2+ concentration 30 and the decrease of mitochondrial membrane potential. 31 A previous study has shown that DFM can inhibit tumor cell growth via different mechanisms other than those mentioned here.…”

Section: -22mentioning

confidence: 99%

An optimized molecular inclusion complex of diferuloylmethane: enhanced physical properties and biological activity

Tan¹,

Li²,

Wu³

et al. 2012

IJN

View full text Add to dashboard Cite

Objective: The purpose of this study was to explore and evaluate the enhanced physical properties and biological activity of a molecular inclusion complex (MICDH) comprising diferuloylmethane (DFM) and hydroxypropyl-β-cyclodextrin. Methods: The preparation conditions of MICDH were optimized using an orthogonal experimental design. The solubility, in vitro release and model fitting, microscopic morphology, molecular structure simulation, anti-lung cancer activity, and action mechanism of MICDH were evaluated. Results: The solubility of DFM was improved 4400-fold upon complexation with hydroxypropyl-β-cyclodextrin. The release rate of DFM was significantly higher from MICDH than from free DFM. MICDH exhibited higher antitumor activity against human lung adenocarcinoma A549 cells than free DFM. More cells were arrested in the S/G2 phase of the cell cycle or were induced to undergo apoptosis when treated with MICDH than when treated with free DFM. Furthermore, increased reactive oxygen species and intracellular calcium ion levels and decreased mitochondrial membrane potential were observed in cells treated with MICDH. Conclusion: MICDH markedly improved the physical properties and antitumor activity of DFM. MICDH may prove to be a preferred alternative to free DFM as a formulation for DFM delivery in lung cancer treatment.

show abstract

Induction of apoptosis and autophagy by sodium selenite in A549 human lung carcinoma cells through generation of reactive oxygen species

Cited by 119 publications

References 59 publications

Glutathione-Dependent Cell Cycle G<sub>1</sub> Arrest and Apoptosis Induction in Human Lung Cancer A549 Cells Caused by Methylseleninic Acid: Comparison with Sodium Selenite

Glutathione-Dependent Cell Cycle G<sub>1</sub> Arrest and Apoptosis Induction in Human Lung Cancer A549 Cells Caused by Methylseleninic Acid: Comparison with Sodium Selenite

Probing the anti-cancer mechanism of selenite : a metabolic approach.

An optimized molecular inclusion complex of diferuloylmethane: enhanced physical properties and biological activity

Contact Info

Product

Resources

About