Antitumor activity of platinum complexes.
Contemporary ideas about the mechanism of antitumor activity of platinum complexes are reviewed and discussed. The induction of SOS functions in bacteria is emphasized and an analogous mechanism in animal cells is suggested. The fate of the leaving ligand in the body is not known. Therefore the complex which reaches the target DNA may be very different from the applied compound. Even the amino ligand may be detached in the body, probably as part of the detoxication by binding to proteins. In the case of fast or medium-speed reactive complexes most of the platinum is inactivated by binding to proteins, whereas slow-reacting drugs are mostly excreted unchanged in the urine. Thus, the quantity of the complex which reaches the target is also difficult to assess. Due to peculiar pharmacokinetics, the results obtained with poorly soluble compounds administered in the solid form cannot be compared with those obtained in true solutions. There are many reasons for believing that the study of a coordination anticancer drug may contribute to our understanding of cancer growth and its reversal.
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D002945:Cisplatin / Q000494:pharmacology; D004247:DNA / Q000378:metabolism; D004261:DNA Replication / Q000187:drug effects; D006801:Humans; D007700:Kinetics; D009369:Neoplasms / Q000188:drug therapy*; D010984:Platinum / Q000494:pharmacology*; D013329:Structure-Activity Relationship
D000970:Antineoplastic Agents; D010984:Platinum; D004247:DNA; D002945:Cisplatin