Table I.
Anti-cancer agents associated with increased levels of glutathione-S-transferase (GST) and resistance (adapted from Tewi[2] and Fan and Chambers[4])
| Agent | |
|---|---|
| Substrates of GST and thereby inactivated via GSH-conjugation | Chlorambucil |
| Acrolein | |
| Hydroxyalkenals | |
| Carmustine | |
| Nitrogen mustard | |
| Melphalan | |
| Ethacrynic acid | |
| Corticosteroids | |
| Phosphoramide mustard | |
| Non-substrates | Bleomycin |
| Hepsulfam | |
| Carboplatin | |
| Non-substrates but require JNK activation to elicit cytotoxicity | Antimetabolites |
| Antimicrotubule drugs | |
| Topoisomerase I and II inhibitors | |
| Mitomycin C | |
| Adriamycin | |
| Cisplatin |
GSH = glutathione; JNK = c-Jun N-terminal kinase.