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Full length article| Volume 34, ISSUE 6, P625-637, December 01, 1986

Disruption of pregnancy in mouse by Aristolic acid: I. Plausible explanation in relation to early pregnancy events

DOI:https://doi.org/10.1016/S0010-7824(86)80018-X
Disruption of pregnancy in mouse by Aristolic acid: I. Plausible explanation in relation to early pregnancy events
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      Abstract

      Aristolic acid (AA), obtained from Aristolochia indica Linn, disrupted nidation in mice when administered on Day 1 of pregnancy. The implantation inhibiting effect of the compound was assessed with respect to certain paramenters which are characteristics of early pregnancy, such as tubal transport of ova into the uterus, hyperpermeability of the endometrial capillaries, increase in uterine weight and total protein content, endometrial bed preparation and changes in uterine phosphatase enzymes during Days 4–6 of pregnancy. The compound did not affect tubal transport of eggs, but the uterine blue reaction, caused by extravasation of the dye, pontamine blue, at future implanation sites was inhibited significantly in treated mice. Histological picture of the uterus revealed AA-induced impairment of development (i.e. decidualization) and reconciled with decreases found in uterine weight and its total protein contents in treated animals. In control untreated mice, specific uterine alkaline phosphatase (ALP) activity increased significantly from Days 4 through 6 of pregnancy, but this was prevented in treated mice. On the other hand, specific uterine acid phosphatase (AP) activity was high on Day 5, while in treated mice uterine AP activity remained low during Days 4 and 5 and increased significantly thereafter.
      It was inferred that AA interferes with steroidal conditioning of the uterus and renders it hostile to ovum implantation.
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      Article Info

      Publication History

      Accepted: December 1, 1986
      Received: November 6, 1986

      Identification

      DOI: https://doi.org/10.1016/S0010-7824(86)80018-X

      Copyright

      © 1987 Geron-X, Inc. Published by Elsevier Inc. All rights reserved.

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