首页> 外文OA文献 >Modulatory effects of neonatal exposure to TCDD, or a mixture of PCBs, p,p'-DDT, and p-p'-DDE, on methylnitrosourea-induced mammary tumor development in the rat.
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Modulatory effects of neonatal exposure to TCDD, or a mixture of PCBs, p,p'-DDT, and p-p'-DDE, on methylnitrosourea-induced mammary tumor development in the rat.

机译:新生儿接触TCDD或多氯联苯,p,p'-DDT和p-p'-DDE的混合物对甲基亚硝基脲诱导的大鼠乳腺肿瘤形成的调节作用。

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摘要

The role of organochlorine (OC) exposure in the etiology of breast cancer remains controversial. Thus, our objective was to determine whether the most abundant and toxic OCs found in human milk could, when ingested during the neonatal period, modulate the development of mammary tumors in the rat. We prepared a mixture composed of p,p'-dichlorodiphenyltrichloroethane (DDT), its major metabolite, p,p'-dichlorodiphenyldichloroethene (DDE), and 19 polychlorinated biphenyls (PCB) based on their concentrations found in the milk of Canadian women. Neonate rats at 1, 5, 10, 15, and 20 days of age were gavaged with this mixture, at 10, 100, and 1,000 times the amount that a human baby would consume. An additional group received 2.5 microg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg body weight (bw) by gavage at 18 days of age, instead of the mixture. On day 21, all treatment groups, except for a control group and a 1,000-mix group, received a single intraperitoneal injection of methylnitrosourea (MNU, 30 mg/kg bw), the initiator of the carcinogenic process. The average number of rats per treatment group was 33. Rats were sacrificed when their tumors reached 1 cm in size, or at 308 days of age. We prepared mammary tumors and mammary gland whole mounts for histologic analysis. There were no significant effects when only the malignant or only the benign tumors were considered. After all benign and malignant lesions were pooled, the number of mammary tumors differed among all MNU-treated groups (p = 0.02) with more lesions developing in the MNU-1,000[times] (median = 4.5; p = 0.05) and MNU-TCDD (median = 5.5; p = 0.07) compared to the MNU-0 rats (median = 2). Compared to the MNU-0 group, the percentage of rats that developed palpable tumors (benign plus malignant) was slightly higher (p = 0.06) in the MNU-TCDD group, but not in the MNU-1,000[times] group. The percentage of palpable tumors that were malignant was higher (p = 0.02) in the MNU-100[times] group (15/16, 94%) than in the MNU-0 group (10/18, 56%). The highest dose of the mixture delayed (p = 0.03) the development of tumors, but this was not observed with the MNU-TCDD treatment. These results suggest that neonatal exposure to high doses of organochlorines could favor the development of MNU-induced mammary lesions, but also delays the development of palpable tumors in the rat.
机译:有机氯(OC)暴露在乳腺癌病因中的作用仍存在争议。因此,我们的目标是确定在新生儿期间摄入人乳中发现的最丰富和最有毒的OC是否可以调节大鼠乳腺肿瘤的发展。根据加拿大妇女牛奶中的浓度,我们制备了一种混合物,该混合物由对位,对位-二氯二苯基三氯乙烷(DDT),其主要代谢产物,对位对位-二氯二苯基二氯乙烯(DDE)和19种多氯联苯(PCB)组成。用1、5、10、15和20天龄的新生鼠喂食这种混合物,其量是人类婴儿消耗量的10、100和1,000倍。另一组在18日龄时通过管饲法接受了2.5微克2,3,7,8-四氯二苯并-对-二恶英(TCDD)/ kg体重(bw),而不是混合物。在第21天,除对照组和1000混合组外,所有治疗组均接受腹膜内注射甲基亚硝基脲(MNU,30 mg / kg bw),这是致癌过程的发起者。每个治疗组的平均大鼠数为33。当肿瘤尺寸达到1厘米或308天时,处死大鼠。我们准备了乳腺肿瘤和乳腺整块进行组织学分析。当仅考虑恶性肿瘤或仅考虑良性肿瘤时,没有显着影响。合并所有良性和恶性病变后,所有MNU治疗组之间的乳腺肿瘤数目均不同(p = 0.02),在MNU-1,000 [倍](中位数= 4.5; p = 0.05)和MNU-与MNU-0大鼠(中位数= 2)相比,TCDD(中位数= 5.5; p = 0.07)。与MNU-0组相比,MNU-TCDD组中出现明显肿瘤(良性和恶性)的大鼠百分比略高(p = 0.06),而在MNU-1,000 [times]组中则没有。 MNU-100×组(15 / 16,94%)比MNU-0组(10 / 18,56%)高出明显的恶性肿瘤百分比(p = 0.02)。混合物的最高剂量延迟(p = 0.03)肿瘤的发展,但是用MNU-TCDD治疗未观察到。这些结果表明,新生儿暴露于高剂量的有机氯可能有利于MNU诱导的乳腺病变的发展,但也延迟了大鼠可触及的肿瘤的发展。

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