Iron overload compromises preimplantation mouse embryo development

Xiaopan Chen, Yier Zhou, Dandan Wu, Chongyi Shu, Ruifang Wu, Shishi Li, Qiongxiao Huang, Jing Shu
Reproductive toxicology (Elmsford, N.Y.) · 2021 · vol. 105 , pp. 156–165 · doi:10.1016/j.reprotox.2021.08.010 · PMID:34481919 · W3197116508
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Iron overload impairs mouse preimplantation embryo development by disrupting mitochondrial function and increasing apoptosis and ferroptosis, which can be partially restored by iron chelation.

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Abstract

We and others have previously shown that abnormal pelvic environment plays an important role in the unexplained infertility of endometriosis. However, whether iron overload caused by ectopic periodic bleeding found in patients with endometriosis participates in endometriosis-associated reproductive failure is unknown. This study aimed to investigate effects of iron at level relevant to pelvic iron overload on the development of preimplantation mouse embryo. Two-cell embryos were collected, and cultured to blastocysts in G1/G2 medium supplemented with iron alone or in combination with iron chelator. The development rates, ATP level, mitochondrial membrane potential (MMP), reactive oxygen species level (ROS), and apoptotic and ferroptotic indices were compared between control and iron treatments across each specific developmental stage. Prolonged exposure to iron remarkably impaired early embryo development in vitro by hampering blastocyst formation (P < 0.001), which could be partly restored by iron chelator (P < 0.001). The arrest of embryo development was linked with iron-initiated mitochondrial dysfunction with reduction of ATP generation and MMP (P < 0.05 and P < 0.001, respectively). Impaired mitochondria altered ROS accumulation post-iron exposure at morula stage and blastocyst stage (P < 0.05). Moreover, Iron-exposed blastocyst stage embryos showed higher apoptotic and ferroptotic rates (P < 0.001 and P < 0.05, respectively). Our results highlight that pathologically relevant level of iron compromises preimplantation mouse embryo development by disrupting mitochondrial function and triggering both apoptosis and ferroptosis, which implicates that excess iron found in peritoneal fluid of women with endometriosis likely participates in endometriosis-associated reproductive failure.

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Condition tags

endometriosisinfertility

MeSH descriptors

Embryonic Development Iron Overload Iron Overload Adenosine Triphosphate Adenosine Triphosphate Animals Apoptosis Embryo, Mammalian Female Ferroptosis Membrane Potential, Mitochondrial Mice Mice, Inbred C57BL Mitochondria Mitochondria Oxidative Stress Reactive Oxygen Species

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