Effects of continuous and intermittent exposure of lactating mothers to Aroclor 1242 on testicular steroidogenic function in the adult male offspring
Effects of continuous and intermittent exposure of lactating mothers to Aroclor 1242 on testicular steroidogenic function in the adult male offspring
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DOI：
10.1054/tice.2000.0168
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发表时间：
2001-04-01
期刊：
影响因子：
2.6
通讯作者：
Mendis-Handagama, SMLC
中科院分区：
文献类型：
--
作者：
Kim, IS;Ariyaratne, HBS;Mendis-Handagama, SMLC
多氯联苯（PCBs）是一种世界性的污染物，对包括人类在内的许多动物物种造成了危害。在母乳中检测到多氯联苯，因此，如果母乳喂养，新生儿接触多氯联苯是不可避免的。我们提出了我们的研究结果进行两个实验，以测试间歇性和连续暴露的哺乳期大鼠两种不同剂量（80杯和8杯）的Aroclor 1242（PCB同源物）对睾丸类固醇功能的成年雄性后代的影响。在实验I中，三组哺乳期母鼠分别每日皮下（SC）注射玉米油、80 μ g Aroclor 1242和8 μ g Aroclor 1242玉米油溶液。在实验II中，三组泌乳母鼠每周分别接受两次玉米油或Aroclor 1242（80 μ g和8 μ g）玉米油SC注射。所有组中的幼仔（每组n=8）在第21天断奶，并以正常饮食饲养，直至第90天处死。实验一：与玉米油对照组相比，多氯联苯暴露组大鼠每个睾丸的间质细胞数量显著增加（P <0.05），间质细胞的平均体积显著减少（P < 0.05）。与玉米油处理的对照组相比，两种剂量的多氯联苯均导致血清睾酮水平降低（P < 0.05）。LH刺激的睾丸激素的生产，每个睾丸间质细胞是较低的多氯联苯暴露大鼠相比，对照组。实验二：睾丸间质细胞的大小和数量在三组间无明显变化。Aroclor处理的子代大鼠的血清LH、睾酮和LH刺激的睾丸睾酮产生与玉米油处理的子代大鼠无显著差异（P > 0.05）。然而，这些参数在用Aroclor 80 μ g处理的母鼠的后代中的值较低，与其他两组相比，LH刺激的睾丸激素分泌能力/Leydig细胞在用Aroclor处理的母鼠的后代中显著低于对照组。在两个实验中，多氯联苯暴露组和对照组大鼠的血清T-4和T-3水平无显著差异。这些结果表明，哺乳期母亲连续暴露于8和80 μ g Aroclor 1242会导致成年雄性后代的Leydig细胞萎缩和功能障碍，从而导致雄激素不足状态。
Polychlorinated biphenyls (PCBs) are worldwide pollutants and have caused hazardous effects on many animal species including humans. They have been detected in human milk and therefore exposure of newborns to PCBs is unavoidable if they are breast-fed. We present our findings on two experiments performed to test the effects of intermittent and continuous exposure of lactating rats to two different doses (80 mug and 8 mug) of Aroclor 1242 (a PCB congener) on testicular steroidogenic function of their adult male offspring. In experiment I, three groups of lactating dams received daily subcutaneous (SC) injections of either corn oil, 80 mug of Aroclor 1242 and 8 mug of Aroclor 1242 in corn oil, respectively. In experiment II, three groups of lactating dams received two SC injections per week of either corn oil or Aroclor 1242 (80 mug and 8 mug) in corn oil, respectively. Pups in all groups (n=8 per group) were weaned at day 21 and were raised on a normal diet until sacrificed at 90 days. Experiment I: Leydig cell number per testis was significantly (P < 0.05) increased and the average volume of a Leydig cell was significantly (P < 0.05) reduced in both groups of Aroclor-exposed rats compared to corn oil controls. Both doses of Aroclor resulted in reduced (P < 0.05) serum testosterone levels compared to corn oil-treated controls. LH-stimulated testosterone production per testis and per Leydig cell was lower in Aroclor-exposed rats compared to controls. Experiment II: No changes were observed in Leydig cell size and number per testis among the three groups. Serum LH, testosterone and LH-stimulated testicular testosterone production in offspring rats of Aroclor-treated darns were not significantly different (P > .05) from the offspring of corn oil-treated dams. However, these parameters were lower in value in the offspring of dams treated with Aroclor 80 mug compared to the other two groups, LH-stimulated testosterone secretory capacity per Leydig cell was significantly lower in off spring of darns treated with Aroclor compared to controls. Serum T-4 and T-3 levels were not significantly different among the Aroclor-exposed and control rats in both experiments. These results demonstrate that continuous exposure of lactating mothers to 8 and 80 mug of Aroclor 1242 causes hypotrophy and malfunctioning of Leydig cells in the adult male offspring resulting in a hypoandrogenic status.