ArticleToxics2025
Acrylamide and Its Metabolite Glycidamide Induce Reproductive Toxicity During In Vitro Maturation of Bovine Oocytes.
Article in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Toxicological effects of acrylamide on oocyte maturation and subsequent embryonic development in a porcine model.Biology direct · 2026Article
- Acrylamide disrupts meiotic G2/M transition and SAC activity during oocyte maturation.Biology direct · 2026Article
- Review
- Autophagy in ovary: protective roles, pathological consequences, and unresolved issues.Journal of ovarian research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Acrylamide (ACR) and its metabolite glycidamide (GLY) are contaminants with known toxic effects, especially in reproductive systems. However, the mechanisms underlying their embryotoxic effects remain inadequately understood. In the current study, we investigated the effects of ACR and GLY exposure on oocyte and embryo developmental competence, focusing on DNA damage, apoptosis, autophagy, and epigenetic regulation. Oocytes were exposed to varying concentrations of ACR and GLY during in vitro maturation. The results demonstrated that both ACR and GLY significantly reduced cleavage and blastocyst developmental rates in a dose-dependent manner. Consequently, treated oocytes exhibited actin organization disruption, increased DNA damage, and heightened apoptosis compared to the control. Autophagy-related markers, including LC3A, LC3B, and ATG7, were significantly elevated in the treatment groups. Moreover, both ACR and GLY compounds altered the expression of the epigenetic and MAPK signaling pathway regulators, such as DPPA3, EZH1, EZH2, EED, DUSP1, and ASK1. These disruptions collectively impaired embryonic development. This study underscores the adverse effects of ACR and GLY on reproductive health, driven by oxidative stress, genotoxicity, dysregulated autophagy, and epigenetic alterations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.