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Journal of Food Quality
Volume 2018, Article ID 9635184, 9 pages
Research Article

Effects of Black Pepper (Piper nigrum L.) Chloroform Extract on the Enzymatic Activity and Metabolism of Escherichia coli and Staphylococcus aureus

1College of Food Science and Technology, Hainan University, Haikou, Hainan 570228, China
2Qianxinan Institution for Food and Drug Inspection Center, Xingyi, Guizhou 562400, China
3College of Material and Chemical Engineering, Hainan University, Haikou, Hainan 570228, China

Correspondence should be addressed to Haiming Chen; moc.621@861nehcmh

Received 30 September 2017; Revised 11 December 2017; Accepted 10 January 2018; Published 5 February 2018

Academic Editor: Frederick Adzitey

Copyright © 2018 Wenxue Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The chemical composition and antimicrobial mechanism of action of black pepper chloroform extract (BPCE) were investigated, as well as the potential antibacterial activities of BPCE against Escherichia coli and Staphylococcus aureus. The results showed that 1H-Cycloprop[e]azulen-7-ol, decahydro-1,1,7-trimethyl-4-methylene-, [1ar-(1aα,4aα,7β,7a,β,7bα.)]- (8.39%) and 2-methylene-4,8,8-trimethyl-4-vinyl-bicyclo[5.2.0]nonane (6.92%) were identified as the two primary components of BPCE. The release of intracellular transaminases from bacteria after being incubated with BPCE revealed that the bacterial cell walls and membranes were degraded and that protein synthesis was inhibited to some extent. The inhibition of bacterial Na+/K+-ATPase activity upon the addition of BPCE also indicated an enhanced permeability of bacterial cell membranes. Moreover, an analysis of hexokinase and pyruvate kinase activities showed that BPCE affected the metabolic rate of glycolysis and disrupted the normal metabolism of bacteria. This phenomenon was supported by an observed accumulation of lactic acid (LA) in the treated bacterial cells. Overall, our results indicated that BPCE damaged bacterial cell walls and membranes, which was followed by a disruption of bacterial cell respiration.