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 |
Keywords
- Ehrlish ascites tumor cells
- Glycolysis
- Lonidamine
- Mitochondrial membrane
ASJC Scopus subject areas
- Cancer Research
- Oncology