文献类型：期刊文献

英文题名：Antifungal properties and mode of action of natamycin against Monilinia fructicola causing brown rot in Shengzhou nane fruit

作者：Mo, Yiwei[1]; Zeng, Qing[1]; Ye, Jianping[1]; Jin, Wenlong[1]; Guo, Tianrong[1]

机构：[1] School of Life and Environmental Sciences, Shaoxing University, Shaoxing, 312000, China

年份：2025

卷号：233

外文期刊名：LWT

收录：EI(收录号：20253719157457)、Scopus(收录号：2-s2.0-105015564468)

语种：英文

外文关键词：Adenosinetriphosphate - Antibiotics - Cell membranes - Cultivation - Cytology - Enzyme activity - Fungi - Gene expression - Value engineering

外文摘要：Brown rot caused by Monilinia fructicola (M. fructicola) severely affects Shengzhou nane (Prunus salicina var. taoxingli). Natamycin (NAT), a natural antimicrobial preservative, has demonstrated good efficacy in mitigating post-harvest decay and maintaining fruit quality. This study investigated antifungal efficacy and underlying mechanism of NAT against M. fructicola in vitro and in vivo settings. In vitro assay demonstrated that NAT exhibited potent antifungal activity against mycelial growth and spore germination of M. fructicola, with efficacy increasing in correlation with higher concentrations of NAT. Specifically, 20.0 mg L?1 NAT induced notable mycelial and spore deformation, characterized by twisting and breakage, while 25.0 mg L?1 NAT completely inhibited mycelial growth and spore germination. NAT exposure suppressed antioxidative enzyme activity, for example, 20 mg L?1 NAT decreased SOD activity by 61.49 % of the control at 24 h, and downregulated related gene expression, leading to intracellular accumulation of ROS and oxidative stress. Furthermore, NAT disrupted the integrity of cellular membrane, resulting in leakage of intracellular contents. For instance, DNA leakage increased by 3.2-fold after 24 h. NAT exposure damaged mitochondrial structural and impaired its function, as indicated by the decreased adenosine triphosphate content, by 58.54 % of the control, lower energy charge levels, and the reduced activities of malate dehydrogenase, succinate dehydrogenase, Ca2+/Mg2+-ATPase, and Na+/K+-ATPase by 79.67 %, 77.57 %, 81.34 %, and 89.79 % of the control, respectively, following a 24 h exposure. In vivo experiments indicated that NAT treatment resulted in 93.30 % reduction in disease incidence at concentration of 200 mg L?1, as well as a decrease in lesion diameter in Shenzhou nane fruit. Additionally, NAT enhanced the activities of antioxidative enzymes, including superoxide dismutase, catalase, and peroxidase a significant reduction in malondiadehyde levels. NAT also promoted the activity of phenylalanine ammonia-lyase, chitinase, β-1, 3-glucanase, and polyphenol oxidase. The alleviation of oxidative stress and enhancement of defense enzyme activity together increased fruit resistance to M. fructicola. Consequently, higher fruit quality was achieved during storage, thus, 200 mg L?1 NAT increased total soluble solids by 2.42 folds of the control. In conclusion, our findings demonstrated that NAT exhibited a dual-action effect against antibacterial M. fructicola, acting both as a direct antifungal agent and an inducer of host fruit's innate defense mechanism. These findings highlight the potential of NAT treatment as an effective strategy for controlling brown rot caused by M. fructicola in Shengzhou nane fruit. ? 2025 The Authors