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Estradiol dominance induces hemodilution and mild hematological alterations in mifepristone-treated rats. | LitMetric

Estradiol dominance induces hemodilution and mild hematological alterations in mifepristone-treated rats.

J Toxicol Sci

Safety Research Department, R&D, Kissei Pharmaceuticals Co., Ltd.

Published: July 2022

AI Article Synopsis

  • The study investigated how an excess of estradiol compared to progesterone affects blood parameters through a process called hemodilution, which is influenced by plasma volume increase.
  • Researchers conducted a repeated oral dose study with mifepristone on female rats, measuring various blood components and hormone levels over 2 and 3 weeks.
  • Results showed that mifepristone treatment increased plasma volume and estradiol levels while decreasing red blood cell counts, hemoglobin, and hematocrit, highlighting estradiol's role in mifepristone-related blood changes.

Article Abstract

We examined that an estradiol-dominant state against progesterone could affect hematological parameters through hemodilution because estradiol is known to increase plasma volume via oncotic pressure. We performed a 2- and 3-week repeated oral dose study with mifepristone, a progesterone receptor antagonist, in female rats and examined erythrocyte counts, hemoglobin, hematocrit, plasma volume, levels of estradiol and progesterone, water intake, and water loss. Mifepristone treatment decreased some hematological parameters mildly and increased plasma volume. There were no remarkable changes in the balance of water intake and water loss through urination. Both estradiol and progesterone levels and the ratio of estradiol to progesterone increased. Therefore, our findings indicate that repeated mifepristone treatment increases estradiol levels and plasma volume, resulting in lower erythrocyte counts, hemoglobin, and hematocrit. The present study proved the possible contribution of estradiol to understanding the toxicological significance of mifepristone-induced hemodilution.

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Source
http://dx.doi.org/10.2131/jts.47.301DOI Listing

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