Abstract
The effect of Ionidamine (LND) on the mitochondrial membrane potential, in situ, of Ehrlich ascites tumour cells was investigated by using the safranine method. LND, because of its ability to inhibit electron transport from endogenous substrates to respiratory carriers, induced a de-energization of mitochondria. Addition of glucose to rotenone-treated cells induced mitochondrial membrane potential as shown by the spectral shift similar to that which occurred upon energization of mitochondria. The build-up of membrane potential in rotenone-treated cells was due to glycolytically-generated ATP because the response to glucose was abolished by LND which inhibited the glycolysis of neoplastic cells by affecting the mitochondria bound hexokinase.
| Original language | English |
|---|---|
| Pages (from-to) | 419-424 |
| Number of pages | 6 |
| Journal | Anticancer Research |
| Volume | 16 |
| Issue number | 1 |
| Publication status | Published - Jan 1996 |
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Keywords
- Ehrlish ascites tumor cells
- Glycolysis
- Lonidamine
- Mitochondrial membrane
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Effect of lonidamine on the mitochondrial potential in situ in ehrlich ascites tumor cells. / Pulselli, Rossana; Amadio, Lorena; Fanciulli, Maurizio; Floridi, Aristide.
In: Anticancer Research, Vol. 16, No. 1, 01.1996, p. 419-424.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of lonidamine on the mitochondrial potential in situ in ehrlich ascites tumor cells
AU - Pulselli, Rossana
AU - Amadio, Lorena
AU - Fanciulli, Maurizio
AU - Floridi, Aristide
PY - 1996/1
Y1 - 1996/1
N2 - The effect of Ionidamine (LND) on the mitochondrial membrane potential, in situ, of Ehrlich ascites tumour cells was investigated by using the safranine method. LND, because of its ability to inhibit electron transport from endogenous substrates to respiratory carriers, induced a de-energization of mitochondria. Addition of glucose to rotenone-treated cells induced mitochondrial membrane potential as shown by the spectral shift similar to that which occurred upon energization of mitochondria. The build-up of membrane potential in rotenone-treated cells was due to glycolytically-generated ATP because the response to glucose was abolished by LND which inhibited the glycolysis of neoplastic cells by affecting the mitochondria bound hexokinase.
AB - The effect of Ionidamine (LND) on the mitochondrial membrane potential, in situ, of Ehrlich ascites tumour cells was investigated by using the safranine method. LND, because of its ability to inhibit electron transport from endogenous substrates to respiratory carriers, induced a de-energization of mitochondria. Addition of glucose to rotenone-treated cells induced mitochondrial membrane potential as shown by the spectral shift similar to that which occurred upon energization of mitochondria. The build-up of membrane potential in rotenone-treated cells was due to glycolytically-generated ATP because the response to glucose was abolished by LND which inhibited the glycolysis of neoplastic cells by affecting the mitochondria bound hexokinase.
KW - Ehrlish ascites tumor cells
KW - Glycolysis
KW - Lonidamine
KW - Mitochondrial membrane
UR - http://www.scopus.com/inward/record.url?scp=0029968371&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029968371&partnerID=8YFLogxK
M3 - Article
C2 - 8615647
AN - SCOPUS:0029968371
VL - 16
SP - 419
EP - 424
JO - Anticancer Research
JF - Anticancer Research
SN - 0250-7005
IS - 1
ER -