Lycopene alleviates multiple-mycotoxin-induced toxicity by inhibiting mitochondrial damage and ferroptosis in the mouse jejunum

Lin, Jianhua; Zuo, Cuige; Liang, Tianzeng; Huang, Yang; Kang, Ping; Xiao, Kan; Liu, Yulan

doi:10.1039/d2fo02994d

Cited by 22 publications

(12 citation statements)

References 46 publications

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“…Ferroptosis is a form of non-apoptotic regulatory cell death caused by the Fenton reaction, which is driven by LPO and iron accumulation . Several studies have demonstrated that ferroptosis is directly associated with mitochondrial oxidative stress and that ferroptosis can inhibit GPX4 expression while raising LPO generation. , Co-exposure to zearalenone, DON, and aflatoxin B1 has been proven in recent research to produce jejunal injury in mice, in addition to the mechanism involved in ferroptosis . In this investigation, we discovered that DON exposure can alter ferroptosis-related indices and parameters, as evidenced by an increase in iron concentration, TfR protein expression, and the lipid peroxide products MDA and 4HNE.…”

Section: Discussionmentioning

confidence: 99%

“…38,39 Co-exposure to zearalenone, DON, and aflatoxin B1 has been proven in recent research to produce jejunal injury in mice, in addition the mechanism involved in ferroptosis. 40 In this investigation, we discovered that DON exposure can alter ferroptosis-related indices and parameters, as evidenced by an increase in iron concentration, TfR protein expression, and the lipid peroxide products MDA and 4HNE. Moreover, genes associated with ferroptosis (PTGS2, ACSL4, and HAMP1) were elevated, whereas FTH1, SLC7A11, GPX4, FPN1, and FSP1 were downregulated.…”

Section: ■ Discussionmentioning

confidence: 99%

“…In addition, recent studies have shown that concomitant exposure to various mycotoxins, including DON, could induce jejunal injury in mice, which was associated with ferroptosis and oxidative stress. 40 Many studies have shown that ferroptosis stimulates an inflammatory response via TLR4 signaling. 44,45 In relation to our findings, we speculate that DON may lead to intestinal injury in mice by activating the TLR4/NF-κB signaling pathway through ferroptosis.…”

Section: ■ Discussionmentioning

confidence: 99%

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Quercetin Alleviates Deoxynivalenol-Induced Intestinal Damage by Suppressing Inflammation and Ferroptosis in Mice

Jiang

Hong

et al. 2023

J. Agric. Food Chem.

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Deoxynivalenol (DON), one of the most prevalent mycotoxins found in food and feed, can cause gastrointestinal inflammation and systemic immunosuppression, presenting a serious hazard to human and animal health. Quercetin (QUE) is a plant polyphenol with anti-inflammatory and antioxidant properties. In this research, we investigated the potential function of QUE as a treatment for DON-induced intestinal damage. Thirty male specific-pathogen-free BALB/c mice were randomly allocated to treatment with QUE (50 mg/kg) and/or DON (0, 0.5, 1, and 2 mg/kg). We found that QUE attenuated DON-induced intestinal damage in mice by improving jejunal structural injury and changing tight junction proteins (claudin-1, claudin-3, ZO-1, and occludin) levels. QUE also suppressed DON-triggered intestinal inflammation by inhibiting the TLR4/NF-κB signaling pathway. Meanwhile, QUE decreased the oxidative stress caused by DON by enhancing the concentrations of SOD and GSH, while diminishing the contents of MDA. In particular, QUE reduced DON-induced intestinal ferroptosis. DON-induced intestinal damage elevated TfR and 4HNE levels, along with transcription levels of ferroptosis-related genes (PTGS2, ACSL4, and HAMP1) while diminishing mRNA levels of FTH1, SLC7A11, GPX4, FPN1, and FSP1, all of which were reversed by QUE treatment. Our findings imply that QUE alleviates DON-induced intestinal injury in mice by inhibiting the TLR4/NF-κB signaling pathway and ferroptosis. In this study, we elucidate the toxicological mechanism of DON, provide a basic foundation or theory for future DON prevention and treatment, and explore strategies to prevent and alleviate DON's hazardous effects.

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Section: Discussionmentioning

confidence: 99%

Section: ■ Discussionmentioning

confidence: 99%

Section: ■ Discussionmentioning

confidence: 99%

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Quercetin Alleviates Deoxynivalenol-Induced Intestinal Damage by Suppressing Inflammation and Ferroptosis in Mice

Jiang

Hong

et al. 2023

J. Agric. Food Chem.

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“…All the mice were given at least 1 week to adjust to the experimental environment. Forty mice were divided into four groups, each containing ten mice: control (corn oil daily by oral gavage with sterile water, Ctrl group); corn oil daily by oral gavage with 1.5% DSS in sterile water (DSS group); lycopene (12 mg/kg BW) daily by oral gavage with sterile water (LY group), the dose was determined according to previous studies; , and lycopene (12 mg/kg BW) daily by oral gavage with 1.5% DSS in sterile water (LYD group). Mice in the LY and LYD groups were given lycopene orally by gavage for 12 weeks, and after 3 weeks of lycopene gavage, the LYD mice were exposed to 1.5% DSS.…”

Section: Methodsmentioning

confidence: 99%

Lycopene Ameliorated DSS-Induced Colitis by Improving Epithelial Barrier Functions and Inhibiting the Escherichia coli Adhesion in Mice

Yue,

Shi,

Song

et al. 2024

J. Agric. Food Chem.

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Adherent-invasive Escherichia coli plays an important role in the pathogenesis of inflammatory bowel disease. Blocking the adhesion of E. coli to intestinal epithelial cells appears to be useful for attenuating inflammatory bowel disease. Lycopene has been reported to have anti-inflammatory and antimicrobial activities. The aim of this study was to test the intervention effect of lycopene on colitis in mice and to investigate the possible mechanism through which lycopene affects the adhesion of E. coli to intestinal epithelial cells. Lycopene (12 mg/kg BW) attenuated dextran sulfate sodium (DSS)-induced colitis, decreased the proportion of E. coli, and activated the NLR family pyrin domain containing 12 and inactivated nuclear factor kappa B pathways. Furthermore, lycopene inhibited the adhesion of E. coli O157:H7 to Caco-2 cells by blocking the interaction between E. coli O157:H7 and integrin β1. Lycopene ameliorated DSS-induced colitis by improving epithelial barrier functions and inhibiting E. coli adhesion. Overall, these results show that lycopene may be a promising component for the prevention and treatment of colitis.

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“…A recent study has shown that administering oral lycopene supplements at a dosage of 10 mg/kg body weight per day significantly reduced oxidative stress, mitochondrial dysfunction, and ferroptotic cell death caused by a combination of mycotoxins in the jejunum tissue of mice. These mycotoxins included ZEN at 10 mg/kg body weight, DOX at 1 mg/kg body weight, and AFB1 at 0.5 mg/kg body weight [87]. The study found that lycopene's ability to activate the body's antioxidant system played a crucial role in protecting against the toxic effects triggered by AFB1.…”

Section: Inhibition Of Oxidative Stressmentioning

confidence: 95%

Lycopene as a Therapeutic Agent against Aflatoxin B1-Related Toxicity: Mechanistic Insights and Future Directions

Li,

Tang,

Peng

et al. 2024

Antioxidants

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Aflatoxin (AFT) contamination poses a significant global public health and safety concern, prompting widespread apprehension. Of the various AFTs, aflatoxin B1 (AFB1) stands out for its pronounced toxicity and its association with a spectrum of chronic ailments, including cardiovascular disease, neurodegenerative disorders, and cancer. Lycopene, a lipid-soluble natural carotenoid, has emerged as a potential mitigator of the deleterious effects induced by AFB1 exposure, spanning cardiac injury, hepatotoxicity, nephrotoxicity, intestinal damage, and reproductive impairment. This protective mechanism operates by reducing oxidative stress, inflammation, and lipid peroxidation, and activating the mitochondrial apoptotic pathway, facilitating the activation of mitochondrial biogenesis, the endogenous antioxidant system, and the nuclear factor erythroid 2-related factor 2 (Nrf2)/kelch-like ECH-associated protein 1 (KEAP1) and peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1) pathways, as well as regulating the activities of cytochrome P450 (CYP450) enzymes. This review provides an overview of the protective effects of lycopene against AFB1 exposure-induced toxicity and the underlying molecular mechanisms. Furthermore, it explores the safety profile and potential clinical applications of lycopene. The present review underscores lycopene’s potential as a promising detoxification agent against AFB1 exposure, with the intent to stimulate further research and practical utilization in this domain.

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Lycopene alleviates multiple-mycotoxin-induced toxicity by inhibiting mitochondrial damage and ferroptosis in the mouse jejunum

Abstract: The contamination of foods and feeds with multiple mycotoxins threatens human and animal health after they accumulate in the food chain, producing various toxic effects. Feeds are almost universally contaminated...

Cited by 22 publications

References 46 publications

Quercetin Alleviates Deoxynivalenol-Induced Intestinal Damage by Suppressing Inflammation and Ferroptosis in Mice

Quercetin Alleviates Deoxynivalenol-Induced Intestinal Damage by Suppressing Inflammation and Ferroptosis in Mice

Lycopene Ameliorated DSS-Induced Colitis by Improving Epithelial Barrier Functions and Inhibiting the Escherichia coli Adhesion in Mice

Lycopene as a Therapeutic Agent against Aflatoxin B1-Related Toxicity: Mechanistic Insights and Future Directions

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