Linalool-surfactin combination completely suppresses Aspergillus parasiticus growth and aflatoxin B1 synthesis in marinades

The presence of aflatoxin B1 (AFB1), a potent carcinogenic mycotoxin produced by fungi like Aspergillus parasiticus, poses a significant threat to food safety, particularly in repeatedly used marinades and marinated products. Current methods for controlling mycotoxigenic fungi often involve synthetic chemicals, raising concerns about residues and consumer health. There is a critical need for effective, natural preservation strategies that can not only inhibit fungal growth but also prevent toxin synthesis. This study explores the cooperative antifungal and anti-mycotoxin potential of natural compounds, linalool and surfactin, to address this gap.

Researchers investigated the cooperative antifungal mechanism of linalool and surfactin against Aspergillus parasiticus growth and AFB1 synthesis. They treated fungal cultures with individual compounds and their combination, analyzing changes in mycelial growth, AFB1 content, ATP synthesis, malondialdehyde content, and ATPase activity. A comprehensive metabolomic analysis was performed to elucidate the underlying metabolic disruptions. The study aimed to identify specific pathways and metabolites affected by the combined treatment, providing a mechanistic basis for their observed cooperative effect.

The study revealed that linalool was more effective than surfactin at inhibiting A. parasiticus growth individually. However, their combination demonstrated a potent cooperative effect, achieving complete suppression of mycelial growth and AFB1 synthesis at high doses. This synergistic action was attributed to multi-level inhibition mechanisms. The linalool-surfactin combination effectively disrupted fungal cell membrane integrity, significantly reduced ATP synthesis, and increased malondialdehyde content to 18.86 nmol/g. Furthermore, it decreased ATPase activity by 80.64%. > Metabolomic analysis showed the combination severely disrupted glucose metabolism and the tricarboxylic acid cycle, leading to abnormal accumulation of metabolites like glucose-6-phosphate and malic acid. The combination also induced abnormal expression of key metabolites such as L-glutamic acid, 3-sulfinylpyruvic acid, and cyclic adenosine monophosphate, thereby disrupting pathways including amino acid metabolism, oxidative phosphorylation, and the cell cycle, ultimately inhibiting fungal growth and toxin synthesis at multiple levels.