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锌对镉诱导的雌性大鼠不育的保护作用。锌和镉对培养的颗粒细胞孕酮分泌的影响。

Zinc protection against cadmium-induced infertility in female rats. Effect of zinc and cadmium on the progesterone production of cultured granulosa cells.

作者信息

Paksy K, Varga B, Lázár P

机构信息

National Institute of Occupational Health, Budapest, Hungary.

出版信息

Biometals. 1997 Jan;10(1):27-35. doi: 10.1023/a:1018362603065.

DOI:10.1023/a:1018362603065
PMID:9002180
Abstract

Adult female rats were treated subcutaneously (s.c.) with zinc chloride (ZnCl2, 10 or 20 mg kg-1 body weight, bw) four times during two ovarian cycles. The third injection was accompanied by cadmium chloride (CdCl2) administration sc (2.5, 5 and 10 mg kg-1 bw). The fourth zinc (Zn) treatment was followed by mating. ZnCl2 (20 mg kg-1) itself impaired fertility by 20%, while CdCl2 dose-dependently blocked the receptivity of female rats. In combination with 2.5 and 5 mg kg-1 CdCl2 the metal salts decreased fertility in an additive fashion, whereas at the highest CdCl2 dose (10 mg kg-1) a marked ameliorating effect of ZnCl2 (10 and 20 mg kg-1) on cadmium (Cd)-caused sterility was observed. In the pregnant animals apart from the higher Cd-induced blood progesterone levels and reduced body weight gain of dams, no significant treatment-related maternal and fetal effects could be observed. ZnCl2 (10 to 80 microM) and CdCl2 (10 to 80 microM) were added to the culture medium of ovarian granulosa cells. CdCl2 suppressed follicle-stimulating-hormone- (FSH-) and cAMP-stimulated progesterone accumulation. No protective effect of Zn against Cd-induced drop in progesterone production could be seen, while Zn by itself induced a significant increase in FSH-supported progesterone synthesis. In conclusion, while Zn protected against Cd-induced sterility in vivo, it failed to counteract the direct effect of Cd on steroid biosynthesis. The data indicate that Zn protection does not take place at the level of ovary. Moreover, Zn and Cd seem to affect FSH-stimulated progesterone production by different mechanisms.

摘要

成年雌性大鼠在两个卵巢周期内接受了4次皮下注射(s.c.)氯化锌(ZnCl2,10或20 mg kg-1体重,bw)。第三次注射时同时皮下注射氯化镉(CdCl2,2.5、5和10 mg kg-1 bw)。第四次锌(Zn)处理后进行交配。ZnCl2(20 mg kg-1)自身使生育力降低了20%,而CdCl2呈剂量依赖性地阻断雌性大鼠的受孕能力。与2.5和5 mg kg-1 CdCl2联合使用时,金属盐以相加的方式降低生育力,而在最高CdCl2剂量(10 mg kg-1)时,观察到ZnCl2(10和20 mg kg-1)对镉(Cd)所致不育有明显的改善作用。在怀孕动物中,除了镉诱导的较高血孕酮水平和母鼠体重增加减少外,未观察到与处理相关的明显母体和胎儿效应。将ZnCl2(10至80 microM)和CdCl2(10至80 microM)添加到卵巢颗粒细胞的培养基中。CdCl2抑制促卵泡激素(FSH)和cAMP刺激的孕酮积累。未观察到锌对镉诱导的孕酮生成下降有保护作用,而锌自身可使FSH支持的孕酮合成显著增加。总之,虽然锌在体内可防止镉诱导的不育,但它未能抵消镉对类固醇生物合成的直接作用。数据表明锌的保护作用并非在卵巢水平发生。此外,锌和镉似乎通过不同机制影响FSH刺激的孕酮生成。

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