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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

Succinate dehydrogenase activity. The effect of EA on succinate dehydrogenase activity in both healthy and CLL mitochondria obtained from human lymphocytes were evaluated by MTT assay following 1 h of treatment. Values are mean±SD of three determinations (graph A and B).
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f0030: Succinate dehydrogenase activity. The effect of EA on succinate dehydrogenase activity in both healthy and CLL mitochondria obtained from human lymphocytes were evaluated by MTT assay following 1 h of treatment. Values are mean±SD of three determinations (graph A and B).

Mentions: Evaluations of EA for potential activity on mitochondria obtained from both CLL and healthy B-lymphocytes were carried out by studying the inhibitory effects of the compound on succinate dehydrogenase activity using the MTT assay. EA (10, 50 µM) strongly inhibited succinate dehydrogenase activity in only CLL BUT NOT healthy B-lymphocyte mitochondria(Fig. 6, graph B). In healthy B-lymphocytes the inhibitory effect was shown only at the highestconcentrations 100 and 200 µM (Fig. 6, graph A).


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)

Succinate dehydrogenase activity. The effect of EA on succinate dehydrogenase activity in both healthy and CLL mitochondria obtained from human lymphocytes were evaluated by MTT assay following 1 h of treatment. Values are mean±SD of three determinations (graph A and B).
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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

f0030: Succinate dehydrogenase activity. The effect of EA on succinate dehydrogenase activity in both healthy and CLL mitochondria obtained from human lymphocytes were evaluated by MTT assay following 1 h of treatment. Values are mean±SD of three determinations (graph A and B).
Mentions: Evaluations of EA for potential activity on mitochondria obtained from both CLL and healthy B-lymphocytes were carried out by studying the inhibitory effects of the compound on succinate dehydrogenase activity using the MTT assay. EA (10, 50 µM) strongly inhibited succinate dehydrogenase activity in only CLL BUT NOT healthy B-lymphocyte mitochondria(Fig. 6, graph B). In healthy B-lymphocytes the inhibitory effect was shown only at the highestconcentrations 100 and 200 µM (Fig. 6, graph A).

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