Supportive Evidence | Disproving Evidence | |
---|---|---|
Free radical formation | Free radical formation in rat glioblastoma cells exposed to DOX | Supraclinical concentrations of DOX |
H2O2 formation in human colon adenocarcinoma cells | 16-h lag prior to H2O2 detection (delayed rather than primary metabolic perturbation?) | |
Generation of H2O2 in MCF-7 cells exposed to 0.1 μM DOX | H2O2 detected 9 days after DOX (delayed rather than primary metabolic perturbation?) | |
DNA damage | Production of non-protein-associated strand breaks in L1210 leukemic cells exposed to DOX | Supraclinical concentrations of anthracyclines |
Nonprotein associated DNA strand cleavage in MCF-7 breast tumor cells at > 5 μM DOX | Protein-associated strand breaks at <5 μM DOX | |
Lipid peroxidation | Lipid peroxidation in mouse lymphocytic leukemia cells, but not in kidney tubular epithelial cells, exposed to 1 μM DOXa | |
No enhanced lipid peroxidation after injection of DOX into a subcutaneously growing rat mammary carcinoma. | ||
Lipid peroxidation in rat glioblastoma and MCF-7 breast tumor cells treated with low to supraclinical concentrations of DOX | Lack of dose dependence | |
bEnhanced cytotoxicity but not lipid peroxidation in glioblastoma and bronchial carcinoma cells exposed to DOX and docosahexaenoic acid |
Based on Gewirtz (1999), except a(Kiyomiya et al., 2001a) and b(Rudra and Krokan 2001).