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Restoring mitochondrial function and normalizing ROS-JNK/MAPK pathway exert key roles in glutamine ameliorating
Abstract:
Bisphenol A (BPA) is toxic to the reproductive and nervous system, even carcinogenetic in humans and animals. However, few studies focused on effects of BPA on the intestinal tract. Here, we detected BPA-induced injuries on intestinal mucosa and explored a reliable approach to counteract BPA effects. C57BL/6J mice were gavage BPA or BPA accompanied with ingestion of 4% (w/w) of glutamine for 4-wks. In vitro, IEC-6 cells were treated with 0.4 mmol/L BPA for 6 hours mimicking acute injury and 0.2 mmol/L BPA for 12 hours followed with or without the inclusion of 4 mmol/L glutamine for 12 hours to determine cell renewal, mitochondrial function and ROS-JNK/MAPK pathway upon moderate BPA exposure. As results, BPA exposure caused severe intestinal injury, and disturbed intestinal epithelial cell proliferation and apoptosis, accompanied with mitochondrial malfunction and activated JNK/MAPK pathway as well. Notably, glutathione metabolism was implicated in BPA-induce injury. Glutamine could well rescue cell renewal and mitochondrial function from BPA exposure-induced injuries. In conclusion, we demonstrated impaired effect of BPA exposure on intestinal functions, which could be well counteracted by glutamine partly via restoring mitochondrial function and normalizing ROS-JNK/MAPK pathway. Thereby, we provided a novel application of glutamine to rescue intestinal injury.
Insights
Bisphenol A (BPA) causes intestinal injury by disrupting cell function and pathways. Glutamine supplementation effectively counteracts these harmful effects, offering a potential therapeutic strategy.
Area of Science:
- Toxicology
- Gastroenterology
- Cell Biology
Background:
- Bisphenol A (BPA) is a known endocrine disruptor with established toxicity to reproductive and nervous systems.
- Limited research has investigated the specific impacts of BPA on the intestinal tract.
- Understanding BPA's effects on intestinal mucosa is crucial for public health.
Purpose of the Study:
- To investigate BPA-induced injuries in the intestinal mucosa.
- To explore glutamine as a potential counteracting agent against BPA toxicity in the gut.
- To elucidate the mechanisms underlying BPA's intestinal damage and glutamine's protective effects.
Main Methods:
- In vivo study using C57BL/6J mice gavaged with BPA or BPA plus glutamine for 4 weeks.
- In vitro study using IEC-6 cells treated with BPA to mimic acute and moderate injury.
- Assessment of cell renewal, apoptosis, mitochondrial function, ROS levels, and the JNK/MAPK pathway.
Main Results:
- BPA exposure induced significant intestinal injury, affecting epithelial cell proliferation and apoptosis.
- Mitochondrial dysfunction and activation of the ROS-JNK/MAPK pathway were observed following BPA exposure.
- Glutamine administration effectively rescued cell renewal and mitochondrial function, mitigating BPA-induced damage.
- Glutathione metabolism was identified as a key pathway involved in BPA-induced injury.
Conclusions:
- BPA exposure impairs intestinal function through mechanisms involving mitochondrial damage and oxidative stress.
- Glutamine demonstrates a protective effect against BPA-induced intestinal injury, partly by restoring mitochondrial function and normalizing the ROS-JNK/MAPK pathway.
- Glutamine represents a promising therapeutic approach for counteracting BPA-related intestinal damage.
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