Abstract
Background: Cellfood™ (CF) is a nutritional supplement containing deuterium sulphate, minerals, amino acids, and enzymes, with well documented antioxidant properties. Its organic and inorganic components are extracted from the red algae Lithothamnion calcareum, whose mineral extract has shown growth-inhibitory effect both on in vitro and in vivo models. The purpose of this study was to evaluate the antiproliferative effects of CF on leukemic cells. In fact, according to its capacity to modulate O§ssub§2§ esub§ availability and to improve mitochondrial respiratory metabolism, we wondered if CF could affect cancer cell metabolism making cells susceptible to apoptosis. Methods. Three leukemic cell lines, Jurkat, U937, and K562, were treated with CF 5 μl/ml up to 72 hours. Cell viability, apoptosis (i.e. caspase-3 activity and DNA fragmentation), hypoxia inducible factor 1 alpha (HIF-1α) concentration, glucose transporter 1 (GLUT-1) expression, lactate dehydrogenase (LDH) activity and lactate release in the culture medium were detected and compared with untreated cells. Results: CF significantly inhibited leukemic cell viability by promoting cell apoptosis, as revealed by caspase-3 activation and DNA laddering. In particular, CF treated cells showed lower HIF-1α levels and lower GLUT-1 expression as compared to untreated cells. At the same time, CF was able to reduce LDH activity and, consequently, the amount of lactate released in the extracellular environment. Conclusions: We supplied evidence for an antiproliferative effect of CF on leukemia cell lines by inducing cell death through an apoptotic mechanism and by altering cancer cell metabolism through HIF-1α and GLUT-1 regulation. Thanks to its antioxidative and proapoptotic properties, CF might be a good candidate for cancer prevention.
| Original language | English |
|---|---|
| Article number | 63 |
| Journal | Journal of Experimental and Clinical Cancer Research |
| Volume | 32 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2013 |
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Keywords
- Apoptosis
- Cellfood™
- Glucose transporter 1
- Hypoxia inducible factor 1 alpha
- Lactate dehydrogenase
- Leukemic cells
- Tumor metabolism
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Metabolism modifications and apoptosis induction after Cellfood™ administration to leukemia cell lines. / Catalani, Simona; Carbonaro, Valentina; Palma, Francesco; Arshakyan, Marselina; Galati, Rossella; Nuvoli, Barbara; Battistelli, Serafina; Canestrari, Franco; Benedetti, Serena.
In: Journal of Experimental and Clinical Cancer Research, Vol. 32, No. 1, 63, 2013.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Metabolism modifications and apoptosis induction after Cellfood™ administration to leukemia cell lines
AU - Catalani, Simona
AU - Carbonaro, Valentina
AU - Palma, Francesco
AU - Arshakyan, Marselina
AU - Galati, Rossella
AU - Nuvoli, Barbara
AU - Battistelli, Serafina
AU - Canestrari, Franco
AU - Benedetti, Serena
PY - 2013
Y1 - 2013
N2 - Background: Cellfood™ (CF) is a nutritional supplement containing deuterium sulphate, minerals, amino acids, and enzymes, with well documented antioxidant properties. Its organic and inorganic components are extracted from the red algae Lithothamnion calcareum, whose mineral extract has shown growth-inhibitory effect both on in vitro and in vivo models. The purpose of this study was to evaluate the antiproliferative effects of CF on leukemic cells. In fact, according to its capacity to modulate O§ssub§2§ esub§ availability and to improve mitochondrial respiratory metabolism, we wondered if CF could affect cancer cell metabolism making cells susceptible to apoptosis. Methods. Three leukemic cell lines, Jurkat, U937, and K562, were treated with CF 5 μl/ml up to 72 hours. Cell viability, apoptosis (i.e. caspase-3 activity and DNA fragmentation), hypoxia inducible factor 1 alpha (HIF-1α) concentration, glucose transporter 1 (GLUT-1) expression, lactate dehydrogenase (LDH) activity and lactate release in the culture medium were detected and compared with untreated cells. Results: CF significantly inhibited leukemic cell viability by promoting cell apoptosis, as revealed by caspase-3 activation and DNA laddering. In particular, CF treated cells showed lower HIF-1α levels and lower GLUT-1 expression as compared to untreated cells. At the same time, CF was able to reduce LDH activity and, consequently, the amount of lactate released in the extracellular environment. Conclusions: We supplied evidence for an antiproliferative effect of CF on leukemia cell lines by inducing cell death through an apoptotic mechanism and by altering cancer cell metabolism through HIF-1α and GLUT-1 regulation. Thanks to its antioxidative and proapoptotic properties, CF might be a good candidate for cancer prevention.
AB - Background: Cellfood™ (CF) is a nutritional supplement containing deuterium sulphate, minerals, amino acids, and enzymes, with well documented antioxidant properties. Its organic and inorganic components are extracted from the red algae Lithothamnion calcareum, whose mineral extract has shown growth-inhibitory effect both on in vitro and in vivo models. The purpose of this study was to evaluate the antiproliferative effects of CF on leukemic cells. In fact, according to its capacity to modulate O§ssub§2§ esub§ availability and to improve mitochondrial respiratory metabolism, we wondered if CF could affect cancer cell metabolism making cells susceptible to apoptosis. Methods. Three leukemic cell lines, Jurkat, U937, and K562, were treated with CF 5 μl/ml up to 72 hours. Cell viability, apoptosis (i.e. caspase-3 activity and DNA fragmentation), hypoxia inducible factor 1 alpha (HIF-1α) concentration, glucose transporter 1 (GLUT-1) expression, lactate dehydrogenase (LDH) activity and lactate release in the culture medium were detected and compared with untreated cells. Results: CF significantly inhibited leukemic cell viability by promoting cell apoptosis, as revealed by caspase-3 activation and DNA laddering. In particular, CF treated cells showed lower HIF-1α levels and lower GLUT-1 expression as compared to untreated cells. At the same time, CF was able to reduce LDH activity and, consequently, the amount of lactate released in the extracellular environment. Conclusions: We supplied evidence for an antiproliferative effect of CF on leukemia cell lines by inducing cell death through an apoptotic mechanism and by altering cancer cell metabolism through HIF-1α and GLUT-1 regulation. Thanks to its antioxidative and proapoptotic properties, CF might be a good candidate for cancer prevention.
KW - Apoptosis
KW - Cellfood™
KW - Glucose transporter 1
KW - Hypoxia inducible factor 1 alpha
KW - Lactate dehydrogenase
KW - Leukemic cells
KW - Tumor metabolism
UR - http://www.scopus.com/inward/record.url?scp=84883688502&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84883688502&partnerID=8YFLogxK
U2 - 10.1186/1756-9966-32-63
DO - 10.1186/1756-9966-32-63
M3 - Article
VL - 32
JO - Journal of Experimental and Clinical Cancer Research
JF - Journal of Experimental and Clinical Cancer Research
SN - 0392-9078
IS - 1
M1 - 63
ER -