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FS Arendrup, S Mazaud-Guittot, B Jégou and DM Kristensen
Abstract
Concern has been raised over chemical induced disruption of ovarigenesis during fetal life resulting in long-lasting consequences only manifesting themselves much later during adulthood. A growing body of evidence suggest that prenatal exposure to the mild analgesic acetaminophen/paracetamol can cause such a scenario. In this Review, we therefore discuss three recent reports that collectively indicating that prenatal exposure in a window around 13.5 days post coitum in both rats and mouse can result in reduced female reproductive health. The combined data show that the exposure results in reduction in primordial follicles, irregular cycling, premature absence of corpus luteum, as well as reduced fertility, resembling premature ovarian insufficiency syndrome in humans that is linked to premature menopause. This could be problematic in the Western world where the age at childbirth is continuously being delayed and because acetaminophen is recommended during pregnancy for pain, fever. We therefore highlight an urgent need for more studies to verify these data including both experimental and epidemiological approaches.
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Concepts
Fetus, Corpus luteum, Reproduction, Reproductive system, Uterus, Menstrual cycle, Fertility, Pregnancy
MeSH headings
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