1 phy for doxorubicin and the major metabolite doxorubicinol.

2 lating levels of the cardiotoxic metabolite, doxorubicinol, after administration.

3 vidence that doxorubicin and its metabolite, doxorubicinol, bind to the cardiac ryanodine receptor (R

4 ticulum vesicles by SERCA2A was inhibited by doxorubicinol, but not doxorubicin.

5 te constants associated with doxorubicin and doxorubicinol canalicular egress were decreased, and oth

6 canalicular egress were decreased, and other doxorubicinol disposition pathways were increased slight

7 ages of doxorubicin (dox) and its metabolite doxorubicinol (dox'ol) in single living cells.

8 he chemotherapeutic anthracycline metabolite doxorubicinol (doxOL) has been shown to interact with an

9               Due to comigration of DOX with doxorubicinol (DOXone), the presence of DOXone had to be

10                                              Doxorubicinol (dxol) is the major metabolite formed in t

11 he rate-limiting process for doxorubicin and doxorubicinol elimination was biliary excretion.

12        Unexpectedly, in the presence of DTT, doxorubicinol enhanced the rate of Ca(2+) uptake by SERC

13  decrease in doxorubicin canalicular egress, doxorubicinol formation, and other doxorubicinol pathway

14  describe the disposition of doxorubicin and doxorubicinol in the isolated perfused rat liver.

15 nce provided here shows that doxorubicin and doxorubicinol interact with RyR2 and SERCA2A in similar

16 f doxorubicin were not altered by quinidine; doxorubicinol liver concentrations were increased.

17  perfusate concentrations or doxorubicin and doxorubicinol liver concentrations.

18 r egress, doxorubicinol formation, and other doxorubicinol pathways.

19 orubicin was reduced significantly; however, doxorubicinol recovery in bile was not altered.

20                              Doxorubicin and doxorubicinol reduced the abundance of thiol groups on R

21 18, the biliary excretion of doxorubicin and doxorubicinol was decreased significantly without altera