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Possible Tumor‐initiating and ‐promoting Activity of p‐Methylcatechol and Methylhydroquinone in the Pyloric Mucosa of Rat Stomach

机译:对甲基邻苯二酚和甲基对苯二酚在大鼠胃幽门粘膜中可能的促肿瘤和促癌活性

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摘要

The possible tumor‐promoting and tumor‐initiating activities of p‐methylcatechol and methylhydroquinone in the pyloric mucosa of male F344 rats were studied. Ornithine decarboxylase (ODC) and replicative DNA synthesis (RDS) were used as markers of tumor promotion and DNA single strand scission and unscheduled DNA synthesis (UDS) as markers of tumor initiation. The compounds were administered by gastric intubation and results were compared with those after administration of catechol. p‐Methylcatechol at doses of 60 to 180 mg/kg body weight dose‐dependently induced up to 20‐fold increase in ODC activity and 9‐fold increase in RDS with maxima 24 h after its administration, but it did not induce significant DNA single strand scission or UDS. Methylhydroquinone at a dose of 200 mg/kg body weight induced up to 6‐fold increase in ODC activity 24 h, and 5‐fold increase in RDS 16 h after its administration, but the induction was not dose‐dependent. At a dose of 200 mg/kg body weight it induced DNA single strand scission, but not UDS. These results and previous findings show that the possible tumor‐promoting activities of catechol are several times higher than those of p‐methylcatechol and 10 times higher than those of methylhydroquinone.
机译:研究了雄性F344大鼠幽门粘膜中对甲基邻苯二酚和甲基对苯二酚可能的促肿瘤和促肿瘤活性。鸟氨酸脱羧酶(ODC)和复制性DNA合成(RDS)用作肿瘤促进的标志物,DNA单链断裂和计划外DNA合成(UDS)用作肿瘤起始的标志物。通过胃插管给药该化合物,并将结果与​​儿茶酚给药后的结果进行比较。对甲基儿茶酚的剂量在60到180 mg / kg体重时最大剂量可在24小时内最大程度地导致ODC活性增加20倍,RDS引起9倍增加,但不会诱导显着的DNA单个断链或UDS。给予200 mg / kg体重的甲基氢醌后24小时,ODC活性最多可增加6倍,RDS最多可增加5倍,但该诱导作用与剂量无关。在200 mg / kg体重的剂量下,它诱导DNA单链断裂,而不诱导UDS。这些结果和以前的发现表明,儿茶酚可能的促肿瘤活性是对甲基儿茶酚的几倍,是甲基氢醌的十倍。

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