鎘對小白鼠母體、胎盤及胎兒之影響

Abstract

本實驗研究目的乃欲探討氯化鎘對懷孕小白鼠母體、胎盤及胎兒間的影響。方法為將ICR種系之未懷孕與懷孕小白鼠，分別於飼養期間或懷孕第7、10、13天，給予五種不同濃度(0,20,40,60,80μg/30g體重)的氯化鎘，各施以皮下注射一次，並於第18天時將小白鼠犧牲。實驗結果顯示，懷孕小白鼠肝、腎臟中鹼性磷酸酯解?之活性皆較未懷孕小白鼠為高。而懷孕小白鼠血清中鹼性磷酸酯解?之活性則降低。在低劑量處理組中(20,40 μg)，母體肝、腎臟中的鹼性磷酸酯解?和胎盤及胎兒肝臟中鹼性磷酸酯解?之活性皆受鎘影響而降低。而在高劑量處理下(60, 80μg)不僅也有此現象，更導致母體體重減輕，胎兒體重及胎盤相對重量的增加。血球比容比(Hct)受鎘抑制，且懷孕小白鼠之Hct較未懷孕小白鼠為低。鎘在母體肝和腎臟及胎盤中的積存量，隨著處理劑量的增高而直線增加。且未懷孕小白鼠肝、腎臟中的積存量較懷孕的高。而胎兒肝臟中並無鎘的積存。鎘積存在胎盤中造成胎盤組織病變和功能受損（因位於胎盤滋胚層中的鹼性磷酸酯解?受抑制）。並且導致胎兒畸形。實驗結果證實，鎘並無法經由胎盤積存在胎兒體內，直接影響胎兒，而是積存在母體肝、腎臟和胎盤中，致使其正常功能受阻，胎兒無法獲得足夠之營養物質，導致胎兒不正常發育、畸形等。嚴重危害下一代。

Cadmium in the cigarette has been proved to be deleterious to the pregnant female and affect the fetal development and viability. The purpose of the present investigation was to find out the effects of cadmium chloride on the non-pregnant and pregnant ICR strain mice, their placentae and fetuses. The pregnant mice were injected subcutaneously with either one of the different doses of CdCl2 (20, 40, 60, 80μg/ 30 g body wt.) on the gestational days 7,10 and 13. The non-pregnant mice were injected at the same time. The mice were sacrificed on day 18 of pregnancy. The results indicated that the activities of the ALP of the pregnant maternal liver and kidney were higher when compared with the non-pregnant ones. However serum level was lower. In the low dosage CdCl2 groups ( 20, 40 μg), the activities of ALP of maternal liver and kidney as well as placenta and fetal liver were inhibited when compared with the control. In the groups which were injected with 60 or 80 μg CdCl2 not only the activity of the ALP but also the maternal body weight was decreased when compared with the control. Coincidentally, the relative fetal body and placental weights were increased. Significant reductions of hematocrit values were found in the pregnant Cd-exposed mice and those values were also lower than those of the Cd-injected non-pregnant ones. The augmentations of the concentration of cadmium in the maternal liver, kidney and placenta were dose-dependent. The contents of cadmium in the non-pregnant liver and kidney were higher than those in the pregnant ones. However, cadmium was not detectable in the fetal liver. The high concentrations of cadmium in the placentae might have resulted in damage to the trophoblastic tissues or impairmant of their functions. From the results it seems that cadmium could not cross the placenta to cause fetal toxicity directly. Instead, it was accumulated in the maternal liver, kidney and placenta, damaging their physiological functions, impairing the fetal nutrition, and resulting in reduction of ALP activity, fetal lethality and malformations.