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49. Degradation of citrinin by different types of light and hydrogen peroxide.

Author

Zhang, Xiaowei, Wang, Penghui, Li, Jing, Shu, Qi, Lu, Qian, Wang, Fenghe, Zhao, Yixin, Niu, Huanhuan, and Chen, Ting

Subjects
ELECTRON paramagnetic resonance, MONASCUS purpureus, LIGHT sources, DENSITY functional theory, CITRININ
Abstract

Citrinin (CIT), a mycotoxin produced by Monascus, Penicillium, and other fungies, can contaminate red yeast rice and other foods, thus constraining their application and development. Exploring efficient degradation methods of citrinin is becoming as one of the hot research topics. In this study, the degradation of citrinin, irradiated by visible (Vis) light, ultraviolet (UV) light, and simulated sunlight alone, as well as in combination with hydrogen peroxide (light/H2O2), was investigated. The research demonstrates UV, Vis, and simulated sunlight all have a degree of degradation on citrinin, and the degradation efficiency correlates with light source and light intensity. Interestingly, when combined with 100 W Vis and 0.01 M H2O2, the citrinin degradation rate increases to 32%, compared to 1% and 5% achieved by Vis and H2O2 alone. Hydroxyl radicals, arising from the uniform cracking of H2O2 under Vis, were experimentally validated by electron spin resonance measurement and could accelerate the dissociation of citrinin by nucleophilic attacking. Employing the density functional theory, we deduced nucleophilic •OH mainly attack onto C8 and C5 site by comparing the electrophilic Parr functions (Pk+) value of main C atom of citrinin. This research presents a rapid and efficient degradation of citrinin by combining visible light with H2O2. Practical Application: This research presents a rapid and efficient method for the degradation of citrnin in red yeast rice and other citrnin containing products by combining visible light with H2O2. [ABSTRACT FROM AUTHOR]

Published
2024
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50. Inhibitory effect of flavonoids on multidrug and toxin extrusion protein 1 function: Implications for food/herb–drug interaction and drug‐induced kidney injury.

Author

Duan, Xiaoyan, Bai, Wanting, Hu, Jiahuan, Wu, Jinjin, Tan, Huixin, Wang, Fenghe, Lang, Xuli, Wang, Baolian, and Hu, Jinping

Subjects
BLOOD urea nitrogen, KIDNEY tubules, CYTOTOXINS, KIDNEY injuries, SILYMARIN
Abstract

Multidrug and toxin extrusion protein 1 (MATE1), an efflux transporter mainly expressed in renal proximal tubules, mediates the renal secretion of organic cationic drugs. The inhibition of MATE1 will impair the excretion of drugs into the tubular lumen, leading to the accumulation of nephrotoxic drugs in the kidney and consequently potentiating nephrotoxicity. Screening and identifying potent MATE1 inhibitors can predict or minimize the risk of drug‐induced kidney injury. Flavonoids, a group of polyphenols commonly found in foodstuffs and herbal products, have been reported to cause transporter‐mediated food/herb–drug interactions. Our objective was to investigate the inhibitory effects of flavonoids on MATE1 in vitro and in vivo and to assess the effects of flavonoids on cisplatin‐induced kidney injury. Thirteen flavonoids exhibited significant transport activity inhibition (>50%) on MATE1 in MATE1‐MDCK cells. Among them, the six strongest flavonoid inhibitors, including irisflorentin, silymarin, isosilybin, sinensetin, tangeretin, and nobiletin, markedly increased cisplatin cytotoxicity in these cells. In cisplatin‐induced in vivo renal injury models, irisflorentin, isosilybin, and sinensetin also increased serum creatinine and blood urea nitrogen levels to different degrees, especially irisflorentin, which exhibited the most potent nephrotoxicity with cisplatin. The pharmacophore model indicated that the hydrogen bond acceptors at the 3, 5, and 7 positions may play a critical role in the inhibitory effect of flavonoids on MATE1. Our findings provide helpful information for predicting the potential risks of flavonoid‐containing food/herb–drug interactions and avoiding the exacerbation of drug‐induced kidney injury via MATE1 mediation. Our research indicates flavonoids exhibited significant inhibition of MATE1, blocking the renal secretion of cationic drugs and heightening nephrotoxicity risks, especially when combined with cisplatin. Six potent flavonoid MATE1 inhibitors, especially irisflorentin, exacerbated cisplatin cytotoxicity and renal injury to different degrees. The pharmacophore model clarified that hydrogen bond acceptors in the 3, 5, and 7 positions play a critical role for flavonoids in inhibiting MATE1. Our findings help predict the potential risk of FDI and avoid MATE1‐mediated DIKI in clinical practice. [ABSTRACT FROM AUTHOR]

Published
2024
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