Impact of mycotoxins on placental function: Focus on cyclopiazonic acid, deoxynivalenol, patulin, and zearalenone's metabolites
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View abstract on PubMed
Summary
This summary is machine-generated.Certain mycotoxins inhibit human placental 3β-hydroxysteroid dehydrogenase 1 (h3β-HSD1), impacting progesterone production. This study reveals their inhibitory mechanisms and structure-activity relationships for potential health risk assessment.
Area Of Science
- Biochemistry
- Toxicology
- Endocrinology
Background
- Mycotoxins, fungal secondary metabolites, pose risks to human and animal health.
- Human placental 3β-hydroxysteroid dehydrogenase 1 (h3β-HSD1) is crucial for converting pregnenolone to progesterone.
Purpose Of The Study
- To evaluate the inhibitory effects of seven mycotoxins on h3β-HSD1 and rat homolog r3β-HSD4.
- To analyze the impact of these mycotoxins on progesterone production in human JAr cells.
- To investigate the mechanism of inhibition and structure-activity relationships.
Main Methods
- Enzyme inhibition assays for h3β-HSD1 and r3β-HSD4.
- Progesterone output measurement in JAr cells.
- Molecular docking and 3D-QSAR analyses.
Main Results
- Cyclopiazonic acid, deoxynivalenol, patulin, α-zearalenol, β-zearalenol, and β-zearalanol inhibited h3β-HSD1 and r3β-HSD4.
- Mycotoxins reduced progesterone output in JAr cells.
- Inhibitors acted as mixed inhibitors, with IC50 values ranging from 8.25–42.83 μM.
- Docking revealed interactions with the NAD+ binding site; structure-activity relationships were established.
Conclusions
- Several mycotoxins interfere with key steroidogenic enzymes, potentially disrupting hormonal balance.
- Understanding these interactions is vital for assessing mycotoxin-related health risks.
- Structure-activity relationship analysis provides a basis for predicting and designing less toxic compounds.
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