Biomarkers of oxidative stress and reproductive complications

Marı́n, Reinaldo; Abad, Cilia; Rojas, Deliana; Chiarello, Delia I.; Teppa-Garrán, Alejandro

doi:10.1016/bs.acc.2022.11.004

Cited by 12 publications

(2 citation statements)

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“…Acute prepubertal hyperglycemia is known to delay meiotic progression and increase spindle defects in oocytes [ 23 ]. On the other hand, when prepubertal mouse ovaries were exposed to prolonged hyperglycemia, germinal vesicle (GV) stage oocytes experienced a significant reduction in the germinal vesicle breakdown (GVBD) process, an increased frequency of meiotic spindle defects, and chromosome misalignment after in vitro maturation (IVM) [ 15 ]. In the present study, surprisingly, when ovulated oocytes from hyperglycemic mice were assessed for maturity and spindle structure, only a moderate but non-significant increase in the spindle defects was observed.…”

Section: Discussionmentioning

confidence: 99%

“…Eventually, the oxidative stress induced by ROS can affect the embryonic epigenome [ 12 , 13 ], disrupt transcriptional regulation, and impair embryonic development [ 14 ]. Oxidative stress is a major mechanism by which diabetes may impair embryonic development [ 15 ]. Importantly, ART laboratories do not follow individualized protocols for patient-specific health conditions due to a lack of scientific research.…”

Section: Introductionmentioning

confidence: 99%

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Embryos from Prepubertal Hyperglycemic Female Mice Respond Differentially to Oxygen Tension In Vitro

Predheepan,

Salian,

Uppangala

et al. 2024

Cells

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Reduced oxygen during embryo culture in human ART prevents embryo oxidative stress. Oxidative stress is also the major mechanism by which maternal diabetes impairs embryonic development. This study employed induced hyperglycemia prepubertal mice to mimic childhood diabetes to understand the effects of varying oxygen tension during in vitro embryonic development. The oocytes were fertilized and cultured at low (≈5%) oxygen (LOT) or atmospheric (≈20%) oxygen tension (HOT) for up to 96 h. Embryo development, apoptosis in blastocysts, inner cell mass (ICM) outgrowth proliferation, and Hif1α expression were assessed. Though the oocyte quality and meiotic spindle were not affected, the fertilization rate (94.86 ± 1.18 vs. 85.17 ± 2.81), blastocyst rate (80.92 ± 2.92 vs. 69.32 ± 2.54), and ICM proliferation ability (51.04 ± 9.22 vs. 17.08 ± 3.05) of the hyperglycemic embryos were significantly higher in the LOT compared to the HOT group. On the other hand, blastocysts from the hyperglycemic group, cultured at HOT, had a 1.5-fold increase in apoptotic cells compared to the control and lower Hif1α transcripts in ICM outgrowths compared to the LOT. Increased susceptibility of embryos from hyperglycemic mice to higher oxygen tension warrants the need to individualize the conditions for embryo culture systems in ART clinics, particularly when an endogenous maternal pathology affects the ovarian environment.

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Section: Discussionmentioning

confidence: 99%