It remains unclear exactly how FFAs exert their antibacterial activities, but the prime target seems to be the bacterial cell membrane and the various essential processes that occur within and at the membrane (Fig. 3). Some of the detrimental effects on bacterial cells can be attributed to the detergent properties of FFAs on account of their amphipathic structure. This allows them to interact with the cell membrane to create transient or permanent pores of variable size. At higher concentrations, detergents, such as FFAs, can solubilise the membrane to such an extent that various membrane proteins or larger sections of the lipid bilayer are released. The key membrane-located process affected by FFAs is the production of energy caused by interference with the electron transport chain and the disruption of oxidative phosphorylation (Sheu and Freese 1972; Galbraith and Miller 1973b; Miller et al. 1977; Boyaval et al. 1995; Wojtczak and Więckowski 1999). Other processes that may contribute to bacterial growth inhibition or death include cell lysis, inhibition of enzyme activity, impairment of nutrient uptake and the generation of toxic peroxidation and auto-oxidation products (Fig. 3). FFAs can kill a bacterium outright (bactericidal action) or inhibit its growth (bacteriostatic action), which is reversible and means that the bacterium remains viable but cannot undergo cell division in the presence of the FFA (Kodicek and Worden 1945; Sheu and Freese 1972). Assays used to investigate the antibacterial activities of FFAs do not always discriminate between bactericidal and bacteriostatic actions, but it is reasonable to assume that growth inhibition cannot continue indefinitely, and eventually, a growth-inhibited bacterium will die. In describing the processes of antibacterial activity below, little distinction is made as to whether the outcome is bactericidal or bacteriostatic.