Cisplatm (cis-diamminedichloroplatinum), an inorganic platinum coordination complex, has been assessed clinically against a variety of tumours (1) because of its solid antineoplastic activity against testicular (2) and ovarian (3) cancers. However, renal and gastrointestinal toxicities originally limited its clinical development (1). Cisplatin became a major chemotherapeutic agent when Hayes and associates demonstrated that patient hydration can significantly reduce cisplatin-induced nephrotoxicity (4) while increasing the therapeutic index of cisplatin threefold. This development was a major factor in the cisplatin approval decision, although the incidence of adverse effects, such as renal dysfunction, neurotoxicity, and nausea and vomiting, remained high. Since the time of its approval, cisplatin has been widely used, either alone or, more often, in combination with other antineoplastics (1). The therapeutic activity of cisplatin appears to be proportional to the intensity of the individual dose and to the cumulative treatment dose (5-7). However, the exploitation of its full therapeutic potential has been limited by dose-dependent nephrological and neurological toxicities (8-11). Since the development of hydration, additional efforts have been made to reduce cisplatin-induced toxicity. Effective antiemetic regimens have been developed, and potential cytoprotective agents have