[Problems of antineoplastic effects by PLDR (potential lethal damage repair) inhibitor--pharmacokinetics].
PLDR is one known cause of tumor cell radioresistance. Drugs like ara-A have been reported to inhibit PLDR, thus increasing antineoplastic effects. In this research, ara-A concentration was measured by high-pressure liquid chromatography (HPLC) to investigate its metabolism. Ara-A deaminases in vitro in about 30 minutes, but by using a deaminase inhibitor such as 2'-deoxycoformycin, a fixed level of ara-A can be maintained. Furthermore, the new derivative, ara-AMP, does not deaminase. It is hoped that antineoplastic effects can be effectively increased by maintaining the ara-A concentration through the combined use of deaminase inhibitors and through new derivatives.
D000230:Adenocarcinoma / Q000097:blood / Q000532:radiotherapy; D000368:Aged; D000818:Animals; D002851:Chromatography, High Pressure Liquid; D003070:Coformycin / Q000031:analogs & derivatives / Q000494:pharmacology*; D003131:Combined Modality Therapy; D004357:Drug Synergism; D005260:Female; D006801:Humans; D007700:Kinetics; D008175:Lung Neoplasms / Q000097:blood / Q000532:radiotherapy; D051379:Mice; D008807:Mice, Inbred BALB C; D015649:Pentostatin; D011817:Rabbits; D051381:Rats; D011916:Rats, Inbred F344; D012263:Ribonucleosides / Q000494:pharmacology*; D014740:Vidarabine / Q000097:blood* / Q000378:metabolism / Q000494:pharmacology
D012263:Ribonucleosides; D003070:Coformycin; D015649:Pentostatin; D014740:Vidarabine