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Copper(II) diacetyl-di(N4-methylthiosemicarbazone).

Authors

The MICAD Research Team.

Source

Molecular Imaging and Contrast Agent Database (MICAD) [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2004-2013.
2004 Nov 10 [updated 2005 Jul 31].

Excerpt

Hypoxia in malignant tumors can affect the outcome of anticancer treatments. Malignant tumors are relatively resistant to chemotherapy and irradiative therapy because of their lack of oxygen, which is a potent radiosensitizer. There is great interest in copper nuclides in nuclear medicine, which include isotopes with both diagnostic (60,61,62,64Cu) and therapeutic (64,67Cu) potential. Cu-ATSM has significant selectivity for hypoxic tissues in vivo and in vitro because of a reduction-oxidation (redox) trapping mechanism (1). Cu-ATSM accumulates avidly in hypoxic cells and delineates hypoxic areas within tumors, whereas it washes out in normoxic cells and in tissues where Cu-ATSM is not reduced and retained to the same extent (2-4). The mechanism of retention of Cu-ATSM (with a redox potential of -297 mV) is a reduction of Cu(II) to Cu(I), followed by a loss of the radiometal from the complex. This reductive mechanism requires an intact enzymatic system of sequential electron transport chains (1, 5), which shows that the cells have an intact mitochondrial or microsomal electron transport system. Cu-ATSM accumulates mainly in the outer rims of tumor masses, which contain active tumor cells with high viability and high resistance to radiation therapy and to some chemotherapy treatments (6). For this reason, Cu-ATSM is regarded as a useful tool in positron emission tomography (PET) oncology.

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