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作 者:幸红霞 姚倩[2] 张雨铖 廖俊米 董娟 余沁 郭晓强[2] Xing Hongxia;Yao Qian;Zhang Yucheng;Liao Junmi;Dong Juan;Yu Qin;Guo Xiaoqiang(School of Food and Biological Engineering,Chengdu University,Chengdu 610106;School of Pharmacy,Chengdu University,Chengdu 610106;Sichuan Shuangjinduotai Biotechnology Co.,LTD,Chengdu 610100)
机构地区:[1]成都大学食品与生物工程学院,成都610106 [2]成都大学药学院,成都610106 [3]四川双金多肽生物技术有限责任公司,成都610100
出 处:《中国抗生素杂志》2023年第8期894-899,共6页Chinese Journal of Antibiotics
基 金:四川省重点研发项目(No.2022YFS0435);成都市重点研发支撑计划(No.2022-YF05-00447-SN)。
摘 要:目的考察二氧化氯对桃褐腐病主要致病菌褐腐菌(Monilinia fructicola)、酵母菌(Kazachstania exigua)以及大肠埃希菌(Escherichia coli)的抑制效果。方法以褐腐菌、酵母菌、大肠埃希菌为实验对象,采用固体培养法测定菌斑直径和细菌存活率;测定胞外培养液电导率,蛋白质和DNA含量,检测胞内丙二醛浓度和脱氢酶活性,并采用扫描电镜进行形态学观察。结果随着二氧化氯浓度升高,菌斑直径和细菌存活率逐渐降低,胞外培养液电导率、蛋白质、DNA含量和胞内丙二醛含量增加,脱氢酶活性显著下降;二氧化氯对褐腐菌的抑菌效果显著高于酵母菌和大肠埃希菌(P<0.05)。电镜扫描下可见细菌细胞膜边界模糊,有明显渗出液。结论二氧化氯能有效抑制褐腐菌的生长,其机制与破坏细菌细胞膜,使细菌代谢酶失活有关。Objective To study the inhibitory effect of ClO2 on Monilinia fructicola,the primary pathogen of peaches,as well as yeast(Kazachstania exigua)and Escherichia coli(E.coli).Methods The plaque diameter and bacterial survival rate of Monilinia fructicola,yeast,and E.coli were measured using the solid culture method.The conductivity,protein,and DNA content of the extracellular culture medium,as well as the intracellular malondialdehyde content and dehydrogenase activity,were all tested using the same approach.Finally,scanning electron microscopy was applied to observe the bacterial morphology.Results The plaque diameter and bacterial survival rate gradually reduced as ClO2 concentration increased.However,extracellular conductivity,protein and DNA content as well as intracellular malondialdehyde content increased,while dehydrogenase activity declined dramatically.The inhibitory effect of ClO2 on Monilinia fructicola was notably stronger than that on yeast and E coli(P<0.05).The blurred boundary of bacterial cell membrane with visible intracellular effusion were observed under SEM.Conclusion The antibacterial mechanisms are associated with the impairment of cell membrane and inactivation of bacterial metabolic enzymes.
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