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调节剂一般本身无毒性,可调整药物的生化药理过程,提高治疗指数。细胞膜氮芥和苯丙氨酸氮芥经膜转运入细胞。耐药株转运下降,胆碱和苯丙氨酸分别与两药竞争转运,减少细胞毒,研究中,未显示对治疗有益的临床前证据。谷胱苷肽(GSH) 在转移酶(GST)催化下结合烷化剂自由基,中和药物活性。Buthionine sulfoximine(BSO)抑制GSH 合成,逆转耐药,与烷化剂合用有效,正用于Ⅱ期临床试验.谷胱苷肽转移酶(GSTs) 为同功酶系统,耐药株中活性增高,利尿酸或Piriprost 抑制GSTs 活性,逆转耐药性。
Regulators are generally non-toxic in nature and can adjust the biochemical and pharmacological processes of drugs to increase the therapeutic index. Membranous nitrogen mustard and phenylalanine mustard were transported through the membrane into cells. The translocation of drug-resistant strains decreased, and choline and phenylalanine competed with the two drugs respectively for transport, reducing cytotoxicity. In the study, no preclinical evidence of therapeutic benefit was shown. Glutathione (GSH) binds alkylating agent free radicals under the catalysis of transferase (GST) to neutralize drug activity. Buthionine sulfoximine (BSO) inhibits GSH synthesis, reverses drug resistance, and is effective in combination with alkylating agents. It is being used in Phase II clinical trials. GSTs are isoenzymes and their activity is increased in resistant strains. Uric acid or Piriprost inhibits GSTs activity and reverses drug resistance.