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A review on fumonisin B1-induced mitochondrial dysfunction and its impact on mitophagy and DNA methylation
Anthia C Govender1, Anil A Chuturgoon1, Terisha Ghazi1
1Discipline of Medical Biochemistry, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, 4041, South Africa.
Abstract:
Fumonisin B1 (FB1) is a food-borne mycotoxin synthesized by Fusarium verticillioides and has been identified as a group 2B carcinogen. Recent research shows that the mitochondria and DNA in cells are targets of FB1. Mitophagy is a form of autophagy that functions to break down impaired mitochondria to preserve the overall functionality of the cell. DNA methylation is an epigenetic process that involves the enzymatic transfer of methyl groups from S-adenosylmethionine (SAM) to the C-5 region of the DNA cytosine ring by DNA methyltransferases (DNMTs). DNA methylation plays a key role in maintaining DNA integrity and FB1 disrupts DNA methylation via FB1-induced folate deficiency. However, there is limited research available on the impact of FB1 on mitophagy as well as FB1-induced oxidative stress and its influence on DNA methylation regulation. In this review, we aim to combine and summarize the current information on FB1-induced mitochondrial dysfunction, its impact on mitophagy as well as its DNA methylation effects.
Insights
Fumonisin B1 (FB1), a food toxin, damages cells by impairing mitochondria and disrupting DNA methylation. This review explores FB1
Area of Science:
- Toxicology
- Cell Biology
- Epigenetics
Background:
- Fumonisin B1 (FB1) is a food-borne mycotoxin classified as a group 2B carcinogen.
- FB1 targets cellular mitochondria and DNA, impacting cell function and integrity.
- Mitophagy, the degradation of damaged mitochondria, and DNA methylation, an epigenetic process crucial for DNA integrity, are cellular mechanisms affected by FB1.
Purpose of the Study:
- To review and synthesize current knowledge on FB1-induced mitochondrial dysfunction.
- To examine the impact of FB1 on mitophagy, a key cellular quality control process.
- To summarize the effects of FB1 on DNA methylation regulation, including oxidative stress mechanisms.
Main Methods:
- Literature review and synthesis of existing research on Fumonisin B1.
- Analysis of studies investigating FB1's effects on mitochondrial function and mitophagy.
- Examination of research on FB1's influence on DNA methylation and related epigenetic processes.
Main Results:
- FB1 induces mitochondrial dysfunction, a critical cellular target.
- FB1 exposure impacts mitophagy, potentially compromising cellular health.
- FB1 disrupts DNA methylation through mechanisms including folate deficiency and oxidative stress.
Conclusions:
- FB1 poses a significant threat to cellular health through mitochondrial damage and epigenetic disruption.
- Further research is needed to fully elucidate the mechanisms linking FB1, mitophagy, and DNA methylation.
- Understanding these pathways is crucial for assessing the health risks associated with FB1 exposure.
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