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Ellagic acid, a polyphenolic compound, selectively induces ROS-mediated apoptosis in cancerous B-lymphocytes of CLL patients by directly targeting mitochondria.

Salimi A, Roudkenar MH, Sadeghi L, Mohseni A, Seydi E, Pirahmadi N, Pourahmad J - Redox Biol (2015)

Bottom Line: Based on our results EA decreased the percentage of viable cells and induced apoptosis.EA increased ROS formation, mitochondria swelling, MMP decrease and cytochrome c release in mitochondria isolated from CLL BUT NOT healthy B-lymphocytes while pre-treatment with cyclosporine A and Butylated hydroxyl toluene (BHT) prevented these effects.Our results suggest that EA can act as an anti cancer candidate by directly and selectively targeting mitochondria could induce apoptosis through mitochondria pathway with increasing ROS production which finally ends in cytochrome c release, caspase 3 activation and apoptosis in cancerous B-lymphocytes isolated from CLL patients.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

No MeSH data available.


Related in: MedlinePlus

The effect of EA on ΔΨm decreasing. Freshly isolated purified mitochondria from healthy and CLL B-lymphocytes were treated as indicated above. ΔΨm was measured by rhodamine 123 staining with spectrofluorescence method. The presented data revealed that EA-induced a decrease in ΔΨm in CLL mitochondria obtained from CLL patients (graph B) BUT NOT in healthy mitochondria obtained from healthy donors (graph A). Data presented as fluorescence intensity. n=5. *The minimum significant level was p<0.05.
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f0040: The effect of EA on ΔΨm decreasing. Freshly isolated purified mitochondria from healthy and CLL B-lymphocytes were treated as indicated above. ΔΨm was measured by rhodamine 123 staining with spectrofluorescence method. The presented data revealed that EA-induced a decrease in ΔΨm in CLL mitochondria obtained from CLL patients (graph B) BUT NOT in healthy mitochondria obtained from healthy donors (graph A). Data presented as fluorescence intensity. n=5. *The minimum significant level was p<0.05.

Mentions: To search for the identification of mechanisms involved in apoptosis, we examined the effects of EA on membrane permeability of mitochondria (ΔΨm) in isolated mitochondria from both groups. Treatment with different concentrations of EA (5, 10 and 20 µM for 1 h) induced significant decrease in ΔΨm only in mitochondria obtained from CLL patient lymphocytes in comparison to the their untreated control (Fig. 8, graph B). Treatment with EA (5, 10 and 20 µM for 1 h) did not induce ΔΨm collapse in mitochondria obtained from normal lymphocytes in comparison to their untreated control (Fig. 8, graph A). Furthermore, 5 µM cyclosporine A (an MPT blocker) strongly inhibited the decline of ΔΨm induced by 10 μM of EA in CLL B-lymphocyte mitochondria (p<0.05). An MPT inducer, CaCl2 (50 µM) was also used as a positive control in ΔΨm assay (Fig. 8).


Ellagic acid, a polyphenolic compound, selectively induces ROS-mediated apoptosis in cancerous B-lymphocytes of CLL patients by directly targeting mitochondria.

Salimi A, Roudkenar MH, Sadeghi L, Mohseni A, Seydi E, Pirahmadi N, Pourahmad J - Redox Biol (2015)

The effect of EA on ΔΨm decreasing. Freshly isolated purified mitochondria from healthy and CLL B-lymphocytes were treated as indicated above. ΔΨm was measured by rhodamine 123 staining with spectrofluorescence method. The presented data revealed that EA-induced a decrease in ΔΨm in CLL mitochondria obtained from CLL patients (graph B) BUT NOT in healthy mitochondria obtained from healthy donors (graph A). Data presented as fluorescence intensity. n=5. *The minimum significant level was p<0.05.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588415&req=5

f0040: The effect of EA on ΔΨm decreasing. Freshly isolated purified mitochondria from healthy and CLL B-lymphocytes were treated as indicated above. ΔΨm was measured by rhodamine 123 staining with spectrofluorescence method. The presented data revealed that EA-induced a decrease in ΔΨm in CLL mitochondria obtained from CLL patients (graph B) BUT NOT in healthy mitochondria obtained from healthy donors (graph A). Data presented as fluorescence intensity. n=5. *The minimum significant level was p<0.05.
Mentions: To search for the identification of mechanisms involved in apoptosis, we examined the effects of EA on membrane permeability of mitochondria (ΔΨm) in isolated mitochondria from both groups. Treatment with different concentrations of EA (5, 10 and 20 µM for 1 h) induced significant decrease in ΔΨm only in mitochondria obtained from CLL patient lymphocytes in comparison to the their untreated control (Fig. 8, graph B). Treatment with EA (5, 10 and 20 µM for 1 h) did not induce ΔΨm collapse in mitochondria obtained from normal lymphocytes in comparison to their untreated control (Fig. 8, graph A). Furthermore, 5 µM cyclosporine A (an MPT blocker) strongly inhibited the decline of ΔΨm induced by 10 μM of EA in CLL B-lymphocyte mitochondria (p<0.05). An MPT inducer, CaCl2 (50 µM) was also used as a positive control in ΔΨm assay (Fig. 8).

Bottom Line: Based on our results EA decreased the percentage of viable cells and induced apoptosis.EA increased ROS formation, mitochondria swelling, MMP decrease and cytochrome c release in mitochondria isolated from CLL BUT NOT healthy B-lymphocytes while pre-treatment with cyclosporine A and Butylated hydroxyl toluene (BHT) prevented these effects.Our results suggest that EA can act as an anti cancer candidate by directly and selectively targeting mitochondria could induce apoptosis through mitochondria pathway with increasing ROS production which finally ends in cytochrome c release, caspase 3 activation and apoptosis in cancerous B-lymphocytes isolated from CLL patients.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

No MeSH data available.


Related in: MedlinePlus