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雄性Wistar [Crl:(WI)BR]大鼠的镉致癌作用:前列腺、睾丸及注射部位肿瘤诱导的剂量反应分析

Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of tumor induction in the prostate and testes and at the injection site.

作者信息

Waalkes M P, Rehm S, Riggs C W, Bare R M, Devor D E, Poirier L A, Wenk M L, Henneman J R, Balaschak M S

机构信息

Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701.

出版信息

Cancer Res. 1988 Aug 15;48(16):4656-63.

PMID:3396014
Abstract

Carcinogenic dose-response effects of CdCl2 in male Wistar [Crl:(WI)BR] rats were studied over a 2-year period. Groups of rats received a single s.c. injection of CdCl2 at doses of 0, 1.0, 2.5, 5.0, 10.0, 20.0, or 40.0 mumol/kg in the dorsal thoracic midline. Other groups received either four separate s.c. doses of 5 mumol Cd/kg each (at 0, 48, 96, and 168 h), or low dose cadmium (5.0 mumol/kg, s.c., at 0 h) followed by a higher dose (10.0 or 20.0 mumol/kg, s.c., at 48 h). The cadmium treatments resulted in appearance of tumors at the injection site, in the testes, and in the ventral prostate. Injection site tumors (mostly sarcomas) appeared to be strictly related to accumulated dose of cadmium and approached a 45% incidence at the highest cadmium dose (40 mumol/kg). Testicular tumors (mostly Leydig cell adenomas) were found to be highly dependent on testicular degeneration caused by cadmium. The highest Leydig cell tumor incidence occurred in the 40 mumol/kg (83%) and 20 mumol/kg (72%) dosage groups. Low dose pretreatment (5.0 mumol/kg) reduced or prevented the testicular degeneration and tumor formation that would otherwise result from a subsequent higher dose of CdCl2 (20 mumol/kg). Prostatic tumors (mostly adenomas of the ventral lobe) were also found to be associated with cadmium treatment, but in a non-dose related fashion. Prostatic tumor incidence was significantly elevated at the 2.5 mumol/kg dose of CdCl2 (eight tumors/26 rats; 31%) and showed a strong positive correlation between 0.0 and 2.5 mumol/kg in both tumor incidence and multiplicity. At higher doses, including those that caused marked testicular degeneration and induced prostatic atrophy, an elevated incidence of tumors did not occur. The occurrence of hyperplastic foci of the prostate, however, showed a strong positive correlation with increasing dose after single injections of cadmium up to and including 20.0 mumol/kg. Results indicate that CdCl2 can induce preneoplastic lesions of the prostate that appear to develop into tumors only at doses well below those causing marked degeneration of the testes and atrophy of the prostate.

摘要

在为期2年的时间里,研究了氯化镉对雄性Wistar [Crl:(WI)BR]大鼠的致癌剂量反应效应。将大鼠分组,在胸背中线处单次皮下注射剂量为0、1.0、2.5、5.0、10.0、20.0或40.0 μmol/kg的氯化镉。其他组分别接受4次皮下注射,每次剂量为5 μmol Cd/kg(分别在0、48、96和168小时),或者先低剂量皮下注射镉(5.0 μmol/kg,在0小时),然后在48小时皮下注射更高剂量(10.0或20.0 μmol/kg)。镉处理导致在注射部位、睾丸和腹侧前列腺出现肿瘤。注射部位肿瘤(大多为肉瘤)似乎与镉的累积剂量密切相关,在最高镉剂量(40 μmol/kg)时发病率接近45%。发现睾丸肿瘤(大多为睾丸间质细胞瘤)高度依赖于镉引起的睾丸变性。睾丸间质细胞瘤的最高发病率出现在40 μmol/kg(83%)和20 μmol/kg(72%)剂量组。低剂量预处理(5.0 μmol/kg)可减少或预防随后更高剂量氯化镉(20 μmol/kg)导致的睾丸变性和肿瘤形成。前列腺肿瘤(大多为腹叶腺瘤)也被发现与镉处理有关,但与剂量无关。在2.5 μmol/kg的氯化镉剂量下,前列腺肿瘤发病率显著升高(8只肿瘤/26只大鼠;31%),并且在0.0至2.5 μmol/kg之间,肿瘤发病率和肿瘤数量均呈现出强正相关。在更高剂量下,包括那些导致明显睾丸变性和前列腺萎缩的剂量,肿瘤发病率并未升高。然而,单次注射镉直至20.0 μmol/kg,前列腺增生灶的出现与剂量增加呈现出强正相关。结果表明,氯化镉可诱导前列腺的癌前病变,这些病变似乎仅在远低于导致睾丸明显变性和前列腺萎缩的剂量下才发展为肿瘤。

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