摘要: Dose-limiting toxicity secondary to antineoplastic chemotherapy is due the inability of cytotoxic drugs differentiate between normal and malignant cells. The consequences this may include impairment patient quality life, because toxicity, reduced tumour control deliver adequate dose-intensive therapy against cancer. Specific examples tissues cisplatin-related neurotoxicity nephrotoxicity, myelotoxicity treatment with alkylating agents carboplatin, oxazaphosphorine-induced haemorrhagic cystitis, cumulative dose-related cardiac anthracycline treatment. Chemoprotectants have been developed as a means ameliorating associated by providing site-specific protection for tissues, without compromising antitumour efficacy. Clinical trials protectors must sufficient dose-limiting events study, assessment both (allowing measurement efficacy protection) effect. Several chemoprotective compounds now extensively investigated, including dexrazoxane, amifostine, glutathione, mesna ORG 2766. Dexrazoxane appears complex metal co-factors iron, reduce incidence anthracycline-induced cardiotoxicity, allowing delivery higher doses anthracyclines expected consequence cardiomyopathy. Numerous studies demonstrated that sulfur-containing nucleophiles, can specifically bind cisplatin- or agent-generated free radicals agent metabolites cisplatin-associated agent-associated myelosuppression urothelial toxicity. These studies, in majority instances, not revealed any evidence reduction Further randomised are required identify optimal role chemoprotectants when used alone combination other modifiers haemopoietic growth factors.