对吖啶可能致癌性的生物测定。

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引用次数: 0

摘要

以Fischer 344大鼠和B6C3F1小鼠为实验对象,进行了对哌替啶可能致癌性的生物测定。在饲料中以两种浓度中的任意一种给药,每组50只雄性和50只雌性动物。低剂量和高剂量大鼠慢性生物测定中使用的膳食浓度分别为0.5%和1.0%。低剂量雄鼠、低剂量雌鼠、高剂量雄鼠、高剂量雌鼠的时间加权平均浓度分别为0.22、0.22。分别为0.46%和0.44%。除高剂量雄性小鼠外,所有给药的动物都在饮食中给予对克参啶104周,并观察长达2周的额外时间。所有高剂量雄性小鼠在第92周结束时死亡。对每个物种,雌雄各50只作为对照,只饲喂基础实验室饲料。两种动物的两性死亡率均与剂量有关。某些肿瘤在低剂量组的发生率高于高剂量组,这可能是由于高剂量组的死亡率加快。在给药的雌雄大鼠中,膀胱癌(乳头状癌、鳞状细胞癌、移行细胞乳头状瘤、移行细胞癌和未分化癌的合并发病率)和嗅觉神经母细胞瘤的发病率均有统计学意义。在低剂量雄性大鼠中,肝脏肿瘤结节、肝细胞癌或肝/胆管混合癌的合并发病率也很显著。在雄性和雌性给药小鼠中,膀胱癌(NOS癌、鳞状细胞癌和移行性癌的联合发病率)的发生率均显著。在给药的雌性小鼠中,肝细胞癌的发生率也很高。在本生物试验条件下,对克雷辛对Fischer 344大鼠具有致癌性,导致两性大鼠的癌和膀胱乳头状瘤的发病率增加,两性大鼠的嗅觉神经母细胞瘤的发病率增加,雄性大鼠的肝脏肿瘤发病率增加。对cresidine在B6C3F1小鼠中也具有致癌性,可导致两性膀胱癌和雌性肝细胞癌。
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Bioassay of p-cresidine for possible carcinogenicity.

A bioassay of p-cresidine for possible carcinogenicity was conducted using Fischer 344 rats and B6C3F1 mice. p-Cresidine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. The dietary concentrations used in the chronic bioassay for low and high dose rats were 0.5 and 1.0 percent, respectively. The time-weighted average concentrations fed to low dose male, low dose female, high dose male and high dose female mice were 0.22, 0.22. 0.46, and 0.44 percent, respectively. All dosed animals, except for high dose male mice, were administered p-cresidine in the diet for 104 weeks and observed for an additional period of up to 2 weeks. All high dose male mice were dead by the end of week 92. For each species, 50 animals of each sex were placed on test as controls and fed only the basal laboratory diet. Mortality rates were dose-related for both sexes of both species. That incidences of certain tumors were higher in low dose than in high dose groups was probably due to accelerated mortality in the high dose group. In dosed rats of both sexes, statistically significant incidences of bladder carcinomas (combined incidences of papillary carcinomas, squamous-cell carcinomas, transitional-cell papillomas, transitional-cell carcinomas, and undifferentiated carcinomas) and olfactory neuroblastomas were observed. The combined incidence of neoplastic nodules of the liver, hepatocelular carcinomas, or mixed hepato/cholangio carcinomas was also significant in low dose male rats. In both male and female dosed mice, the incidence of bladder carcinomas (combined incidence of carcinomas NOS, squamous-cell carcinomas, and transitional carcinomas) was significant. The incidence of hepatocellular carcinomas was also significant in dosed female mice. Under the conditions of this bioassay, p-cresidine was carcinogenic to Fischer 344 rats, causing increased incidences of carcinomas and of papillomas of the urinary bladder in both sexes, increased incidences of olfactory neuroblastomas in both sexes, and of liver tumors in males. p-Cresidine was also carcinogenic in B6C3F1 mice, causing carcinomas of the urinary bladders in both sexes and hepatocellular carcinomas in females.

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