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Published on: November 30, 2022
Gut microbiota modulation by L-Fucose as a strategy to alleviate Ochratoxin A toxicity on primordial follicle
Ruiting Wang1, Jie Song1, Muyu Cai1
1College of Life Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, Qingdao Agricultural University, Qingdao 266109, China.
Abstract:
In this study, we investigated the potential benefits of L-Fucose administration to pregnant mice exposed to Ochratoxin A (OTA), a widespread mycotoxin, producing ovarian damage in offspring. The results showed that administration of 3.5 μg/d OTA induced alterations in intestinal tissues and gut microbiota of pregnant mice, leading to heightened local and systemic inflammation. This inflammatory affected the ovaries of their 3 dpp offspring, in which elevated levels of LPS and ROS were found associated to significant decreased oocyte count and impaired primordial follicle assembly. Moreover, mRNA-Seq analysis showed significant changes in ovarian transcriptomes linked to various GO terms and KEGG pathways, notably ferroptosis, a recognized form of cell death observed. Interestingly, administration of 0.3 g/kg b. w. L-Fucose following OTA exposure mitigated these effects on intestinal tissues and gut microbiota in mothers and on the offspring's ovaries. Similar benefits were obtained by gut microbiota transplantation from L-Fucose-treated pregnant females into OTA-exposed mothers. These findings suggest that inflammatory impact of OTA on maternal intestine/gut can pass to the fetus causing offspring ovary defects and support the use of L-Fucose as adjuvant to counteract the adverse effects of mycotoxins on the gut microbiota, particularly reference to those affecting reproductive organs.
Insights
L-Fucose administration counteracts Ochratoxin A (OTA) induced ovarian damage in offspring by mitigating maternal gut inflammation and restoring gut microbiota balance. This suggests L-Fucose as a potential adjuvant therapy against mycotoxin reproductive toxicity.
Area of Science:
- Reproductive Toxicology
- Microbiome Research
- Immunology
Background:
- Ochratoxin A (OTA) is a prevalent mycotoxin causing ovarian damage in offspring.
- OTA exposure in pregnant mice leads to maternal intestinal inflammation and gut dysbiosis.
- This inflammation negatively impacts fetal ovarian development, causing reduced oocyte count and impaired follicle assembly.
Purpose of the Study:
- To investigate the protective effects of L-Fucose against OTA-induced reproductive toxicity in offspring.
- To explore the role of maternal gut microbiota and inflammation in OTA's teratogenic effects.
- To assess L-Fucose's potential as an adjuvant therapy for mycotoxin-induced reproductive harm.
Main Methods:
- Pregnant mice were exposed to OTA, with some receiving L-Fucose treatment.
- Gut microbiota and intestinal tissues of dams were analyzed.
- Ovarian tissues, oocyte counts, and primordial follicle assembly in offspring were assessed.
- mRNA-Seq analysis was performed on ovarian tissues to identify molecular pathways affected.
- Gut microbiota transplantation experiments were conducted.
Main Results:
- OTA exposure caused intestinal alterations, inflammation, and gut microbiota changes in pregnant mice.
- Offspring exhibited ovarian damage, including decreased oocyte count and impaired follicle assembly, linked to LPS and ROS.
- mRNA-Seq revealed significant changes in ovarian transcriptomes, including ferroptosis pathways.
- L-Fucose administration mitigated OTA's adverse effects on maternal gut and offspring ovaries.
- Gut microbiota transplantation from L-Fucose-treated mice conferred similar protective benefits.
Conclusions:
- OTA-induced maternal gut inflammation and dysbiosis contribute to offspring ovarian defects.
- L-Fucose effectively counteracts OTA's detrimental effects on the maternal gut-fetal-ovarian axis.
- L-Fucose shows promise as an adjuvant therapy to protect reproductive health from mycotoxin exposure.
- Targeting the gut microbiota is a viable strategy to mitigate mycotoxin-induced reproductive toxicity.
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