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Published on: July 29, 2019
A Review: Epigenetic Mechanism in Ochratoxin A Toxicity Studies
Liye Zhu1,2, Boyang Zhang3,4, Yaqi Dai5
1Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China. zlyhome@163.com.
Abstract:
Ochratoxin A (OTA) is a natural contaminant that has displayed nephrotoxicity and hepatotoxicity in mammals. It contaminates a great variety of foodstuffs and threatens people's lives. The molecular mechanism of OTA-induced toxicity has been studied since 1965. Moreover, epigenetic mechanisms are also studied in OTA-induced toxicity. Additionally, the mode of OTA epigenetic research has been advanced in research hotspots. However, there is still no epigenetic study of OTA-induced toxicity. In this review, we discuss the relationship between these epigenetic mechanisms and OTA-induced toxicity. We found that studies on the epigenetic mechanisms of OTA-induced toxicity all chose the whole kidney or liver as the model, which cannot reveal the real change in DNA methylation or miRNAs or histone in the target sites of OTA. Our recommendations are as follows: (1) the specific target site of OTA should be detected by advanced technologies; and (2) competing endogenous RNAs (ceRNA) should be explored with OTA.
Insights
Ochratoxin A (OTA) contamination poses health risks due to kidney and liver toxicity. Current epigenetic studies lack specificity, hindering understanding of OTA
Area of Science:
- Toxicology
- Epigenetics
- Molecular Biology
Background:
- Ochratoxin A (OTA) is a widespread food contaminant.
- OTA exhibits nephrotoxicity and hepatotoxicity in mammals.
- Epigenetic mechanisms are implicated in OTA toxicity, but research is limited.
Purpose of the Study:
- To review the relationship between epigenetic mechanisms and OTA-induced toxicity.
- To identify gaps in current epigenetic research on OTA toxicity.
- To propose future research directions for understanding OTA's epigenetic effects.
Main Methods:
- Literature review of epigenetic studies on OTA toxicity.
- Analysis of research methodologies and findings.
- Identification of limitations in current approaches.
Main Results:
- Existing epigenetic studies on OTA toxicity use whole organs (kidney/liver), masking specific molecular changes.
- Current methods fail to pinpoint changes in DNA methylation, miRNAs, or histone modifications at OTA's target sites.
- There is a lack of studies specifically investigating epigenetic alterations in OTA-induced toxicity.
Conclusions:
- Advanced technologies are needed to identify OTA's specific molecular targets.
- Exploring competing endogenous RNA (ceRNA) networks is crucial for understanding OTA's epigenetic impact.
- Future research should focus on site-specific epigenetic changes and ceRNA interactions to elucidate OTA toxicity mechanisms.
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