FOOD RESEARCH INTERNATIONAL
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2026
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IF 8.8
Qiqi Sun,Zhanrui Huang,Wanying He,Lianhua Hu,Yuebo Li,Xiaohu Zhou,Hao Chen,Sen Tao
Dual inhibition of fungal growth and toxin production in marinated food systems. • Linalool-surfactin completely inhibits A. parasiticus growth and AFB 1 synthesis. • The synergy disrupts fungal cell membrane integrity and inhibits ATP synthesis. • Metabolomics reveals disruptions in cell cycle, energy, and amino acid metabolism. • Provides a theoretical basis for green control of AFB 1 in food processing/storage. This study aimed to control mycotoxigenic fungi in repeatedly used marinades and marinated foods and to elucidate the cooperative mechanism of linalool and surfactin against Aspergillus parasiticus growth and aflatoxin B 1 (AFB 1 ) synthesis by analyzing the changes in mycelial growth, AFB 1 content, ATP synthesis, and metabolites. Results showed that linalool inhibited A. parasiticus growth more effectively than surfactin, while their combination exhibited a strong cooperative effect, completely suppressing mycelial growth and AFB 1 synthesis at high doses. The linalool-surfactin combination effectively disrupted cell membrane integrity, reduced ATP synthesis, increased malondialdehyde content to 18.86 nmol/g, and decreased ATPase activity by 80.64%. Metabolomic analysis showed that the linalool-surfactin combination disrupted glucose metabolism and the tricarboxylic acid cycle, leading to the abnormal accumulation of metabolites such as glucose-6-phosphate and malic acid. Moreover, the combination induced abnormal expression of key metabolites such as L-glutamic acid, 3-sulfinylpyruvic acid, and cyclic adenosine monophosphate, disrupting pathways including amino acid metabolism, oxidative phosphorylation, and the cell cycle, thereby inhibiting the growth and toxin synthesis of A. parasiticus at multiple levels. This multi-level inhibition via membrane damage, energy disruption, and metabolic dysregulation provides a mechanistic basis for natural preservation strategies to control AFB 1 in marinade-based systems and marinated products. Download: Download high-res image (254KB) Download: Download full-size image
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2022
·Vol. 23
·期 19
·11086
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IF 6.208
Xiaoyu Chen,Hongyuan Zhao,Yajun Lu,Huawei Liu,Fanqiang Meng,Zhaoxin Lu,Yingjian Lu
Surfactin fromBacillus amyloliquefaciensfmb50 was utilized to treat mice with type 2 diabetes (T2DM) induced by a high-fat diet/streptozotocin (HFD/STZ). Our group’s earlier research indicated that surfactin could lower blood glucose and mitigate liver dysfunction to further improve HFD/STZ-induced T2DM through modulating intestinal microbiota. Thus, we further investigated the effects of surfactin on the pancreas and colon in mice with T2DM to elucidate the detailed mechanism. In the present study, mice with HFD/STZ-induced T2DM had their pancreatic and colon inflammation, oxidative stress, and endoplasmic reticulum stress (ERS) reduced when given oral surfactin at a dose of 80 mg/kg body weight. According to further research, surfactin also improved glucose metabolism by activating the phosphatidylinositol kinase (PI3K)/protein kinase B (Akt) signaling pathway, further protecting islets β-cell, promoting insulin secretion, inhibiting glucagon release and mitigating pancreas dysfunction. Additionally, after surfactin treatment, the colon levels of the tight junction proteins Occludin and Claudin-1 of T2DM mice were considerably increased by 130.64% and by 36.40%, respectively. These findings revealed that surfactin not only ameliorated HFD/STZ-induced pancreas inflammation and dysfunction and preserved intestinal barrier dysfunction and gut microbiota homeostasis but also enhanced insulin sensitivity and glucose homeostasis in T2DM mice. Finally, in the further experiment, we were able to demonstrate that early surfactin intervention might delay the development of T2DM caused by HFD/STZ, according to critical biochemical parameters in serum.Keywords:surfactin;pancreas;inflammation;gut-barrier
研究领域:
药理学
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内分泌学
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免疫学
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胃肠病学
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糖尿病研究
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DOI
PubMed
高影响因子
Journal of Fungi
·
2026
·Vol. 12
·期 8
·576
·
IF 4.3
Dan-Na Ma,Yihan Niu,Mengli Chen,Jun-Nan Yao,Huiming Wu,Taiying Li
Fusarium wilt, caused by the soil-borne fungusFusarium oxysporumf. sp.lycopersici(Fol), is a devastating disease that severely constrains tomato production worldwide. In this study, an endophytic bacterium, designated ZN-S18, was isolated from healthy tomato stems and identified asBacillus amyloliquefaciensbased on phylogenetic analyses of the 16S rRNA andrpoBgenes. Dual culture assays demonstrated that ZN-S18 exhibited strong antagonistic activity against Fol and significantly inhibited fungal mycelial growth. The cell-free culture filtrate of ZN-S18 markedly suppressed Fol spore germination and mycelial growth, and the inhibitory effect on spore germination was irreversible. LC-MS analyses confirmed that ZN-S18 produces the cyclic lipopeptides surfactin and iturin A. In planta assays further demonstrated that pretreatment with ZN-S18, its culture filtrate, or the combination of surfactin and iturin A significantly reduced Fusarium wilt in tomato seedlings. Moreover, the culture filtrate disrupted fungal cell wall integrity, as indicated by the increased sensitivity of Fol to Congo red stress. Notably, the combined application of surfactin and iturin A exhibited significantly stronger antifungal activity than either compound alone under Congo red-containing conditions, suggesting a synergistic effect on fungal cell wall integrity. Collectively, these findings indicate that the endophytic strainB. amyloliquefaciensZN-S18 is a promising biocontrol agent against tomato Fusarium wilt, primarily through the synergistic action of surfactin and iturin A. This study provides an environmentally friendly alternative to chemical fungicides and establishes a foundation for future investigations into the molecular mechanisms underlying lipopeptide-mediated antagonism.
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DOI
高影响因子
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