Ractopamine at legal residue dosage accelerates atherosclerosis by inducing endothelial dysfunction and promoting macrophage foam cell formation

Chen, Chia‐Hui; Guo, Bei-Chia; Hu, Po-An; Lee, Hsueh-Te; Hu, Hsuan-Yun; Hsu, Man-Chen; Chen, Wenhua; Lee, Tzong‐Shyuan

doi:10.1016/j.envpol.2022.120080

Cited by 2 publications

(2 citation statements)

References 48 publications

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“…Thus, HUA triggers apoptosis as a booster, rather than a starting factor. Furthermore, blood lipids play an important role in the development of atherosclerosis 31,32) . In this experiment, there was no significant change in blood lipid; thus, UA may have contributed directly to the progression of atherosclerosis rather than by affecting lipids.…”

Section: Conflicts Of Interestmentioning

confidence: 99%

High Uric Acid Promotes Atherosclerotic Plaque Instability by Apoptosis Targeted Autophagy

Liu

Xie

et al. 2023

JAT

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Aims: Acute rupture or erosion of unstable atherosclerotic plaques is a major cause of adverse consequences of atherosclerotic cardiovascular disease, often leading to myocardial infarction or stroke. High uric acid (HUA) is associated with the increasing risk of cardiovascular events and death. However, the mechanism by which HUA promotes atherosclerosis and whether HUA affects plaque stability are still unclear. Methods: We constructed an atherosclerotic Apoe−/− mouse model with HUA. The progression of atherosclerosis and plaques was determined by Oil Red O staining, hematoxylin and eosin (H&E) staining, and Masson staining. TdT-mediated dUTP nick-end labeling assay and immunohistochemistry were used to observe the changes of apoptosis and autophagy in plaques, respectively. Then, we validated the in vivo results with RAW 264.7 cell line. Results: HUA promoted atherosclerosis and exacerbated plaque vulnerability, including significantly increased macrophage infiltration, lipid accumulation, enlarged necrotic cores, and decreased collagen fibers. HUA increased cell apoptosis and inhibited autophagy in plaques. In vitro results showed that HUA decreased cell viability and increased cell apoptosis in foam cells macrophages treated with oxidized low-density lipoprotein. An activator of autophagy, rapamycin, can partially reverse the increasing apoptosis. Conclusion: HUA promoted atherosclerosis and exacerbated plaque vulnerability, and HUA facilitates foam cell apoptosis by inhibiting autophagy.

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Section: Conflicts Of Interestmentioning

confidence: 99%

High Uric Acid Promotes Atherosclerotic Plaque Instability by Apoptosis Targeted Autophagy

Liu

Xie

et al. 2023

JAT

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“…In contrast, ingestion of dietary food with an excessive β‐agonist residues will result in nausea, dizziness, muscle trembling, and heart palpitation [12]. Ractopamine at a legal residue dosage could accelerate the progression of atherosclerosis by inducing endothelial cell dysfunction and deregulating the cholesterol metabolism of macrophages [13]. Clenbuterol administration enlarged the stroke volume in a middle cerebral artery occlusion stroke model in mice [14].…”

Section: Introductionmentioning

confidence: 99%

Transfer of β‐agonists from animal feed into Tricholoma gambosum through manure

Han,

Zhan,

Zhang

et al. 2023

Animal Research and One Health

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Fungi are dependent on animal manure as a cultivation medium and may be vulnerable to feed‐derived β‐agonist contamination. To test whether β‐agonists incorporated in animal feed can transport into fungi through manure, a greenhouse study was conducted with Tricholoma gambosum grown in a culture medium amended with medicated cattle manure. Cattle were orally administrated with a single (ractopamine, 670.0 μg/kg BW/day) or a mixture of β‐agonists (clenbuterol, ractopamine, and salbutamol at the doses of 5.3, 223.3, and 50.0 μg/kg BW/day, respectively) for 28 days. Three batches of T. gambosum were harvested. A liquid chromatography tandem mass spectrometry‐based method was developed to quantify the number of β‐agonists taken up by T. gambosum from animal manure. The analytical recoveries for β‐agonists were between 66.61% and 91.78% with relative standard deviations between 1.70% and 12.18%, and the limit of quantification (LOQ) was 0.3 ng/g. The ractopamine residues in T. gambosum from batch 1 were 1.3 ng/g and were below the LOQ in batches 2 and 3 in the single treatment group. In the mixed treatment group, ractopamine concentrations were 0.42 and 0.50 ng/g in batches 1 and 2, respectively, and the salbutamol concentration was 1.94 ng/g in batch 1, while clenbuterol was undetectable in all three batches. These results indicated that the β‐agonists transferred to T. gambosum in trace amounts and presented a limited risk to consumers.

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Ractopamine at legal residue dosage accelerates atherosclerosis by inducing endothelial dysfunction and promoting macrophage foam cell formation

Cited by 2 publications

References 48 publications

High Uric Acid Promotes Atherosclerotic Plaque Instability by Apoptosis Targeted Autophagy

High Uric Acid Promotes Atherosclerotic Plaque Instability by Apoptosis Targeted Autophagy

Transfer of β‐agonists from animal feed into Tricholoma gambosum through manure

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