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Published on: March 6, 2018
Bisphenol F exposure induced vascular toxicity through intestinal microbiota imbalance
Jianlong Yan1, Yanbin Pan2, Huadong Liu1
1Department of Cardiology, Shenzhen Cardiovascular Minimally Invasive Medical Engineering Technology Research and Development Center, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, Guangdong, China.
Introduction:
Bisphenol F (BPF), a common substitute for bisphenol A (BPA), has documented toxicity in multiple organs, but its vascular effects remain unclear. This study investigated BPF's role in vascular calcification (VC) and underlying mechanisms.
Methods:
Differences in the intestinal microbiota were analyzed by 16S ribosomal RNA gene sequencing. Metabolites were analyzed using liquid chromatography-mass spectrometry. Faecal microbiota transplantation and antibiotic treatment experiments were performed to evaluate the functions of the intestinal microbiota in VC.
Results:
We enrolled consecutively 57 patients. Patients were assigned to a calcification group (30 patients) and a non-calcification group (27 patients) based on the presence or absence of calcification in the thoracic aorta wall. The results showed that patients with vascular calcification (VC) had higher levels of bisphenol F (BPF), bisphenol S (BPS) and bisphenol A (BPA) in the fecal samples than patients without VC. The thoracic aortic calcification score was significantly positively correlated with the BPF (Spearman r = 0.4935, p < 0.001), BPA (Spearman r = 0.2860, p < 0.05) and BPS (Spearman r = 0.2650, p < 0.05). We then explored the effects of BPF exposure on normal and vitamin D3 + nicotine (VDN)-treated rats. BPF exposure induced mild VC in normal rats and aggravated VC in VDN-treated rats. BPF exposure disturbed the gut microbiota and promoted inflammatory responses.
Conclusion:
The results here elucidate the mechanism underlying BPF-triggered or BPF-aggravated VC through the gut-vascular axis and provide a theoretical basis for cardiovascular disease risk assessment in humans.
Insights
Bisphenol F (BPF) exposure is linked to vascular calcification (VC) by disrupting the gut microbiota. This study reveals BPF
Area of Science:
- Environmental Health
- Cardiovascular Research
- Microbiome Studies
Background:
- Bisphenol F (BPF), a substitute for Bisphenol A (BPA), has known organ toxicity, but its impact on vascular health is not well understood.
- Vascular calcification (VC) is a significant risk factor for cardiovascular diseases.
Purpose of the Study:
- To investigate the role of Bisphenol F (BPF) in the development and progression of vascular calcification (VC).
- To elucidate the underlying mechanisms, particularly the involvement of the gut microbiota and the gut-vascular axis.
Main Methods:
- Analysis of fecal samples from 57 patients (30 with VC, 27 without) for bisphenol levels (BPF, BPA, BPS) and correlation with thoracic aortic calcification scores.
- 16S ribosomal RNA gene sequencing and liquid chromatography-mass spectrometry to analyze gut microbiota and metabolites.
- Faecal microbiota transplantation and antibiotic treatment experiments in rats to assess the functional role of the gut microbiota in BPF-induced VC.
- Animal studies involving BPF exposure in normal and VDN-treated rats to evaluate its effects on VC, gut microbiota, and inflammation.
Main Results:
- Patients with VC exhibited significantly higher fecal levels of BPF, BPS, and BPA compared to controls.
- Thoracic aortic calcification scores positively correlated with fecal BPF, BPA, and BPS levels.
- BPF exposure induced mild VC in normal rats and exacerbated VC in rats treated with vitamin D3 + nicotine (VDN).
- BPF exposure was found to disrupt the gut microbiota composition and promote inflammatory responses.
Conclusions:
- Bisphenol F (BPF) plays a role in triggering or aggravating vascular calcification (VC) through the gut-vascular axis.
- Disturbance of the gut microbiota and promotion of inflammation are key mechanisms involved in BPF-induced VC.
- These findings provide a basis for assessing cardiovascular disease risk associated with BPF exposure.
