Membrane eicosapentaenoic acid is involved in the hydrophobicity of bacterial cells and affects the entry of hydrophilic and hydrophobic compounds.

Eicosapentaenoic acid (EPA)-producing Shewanella marinintestina IK-1 (IK-1) and its EPA-deficient mutant IK-1Δ8 (IK-1Δ8) were grown on microtitre plates at 20 °C in a nutrient medium that contained various types of growth inhibitors. The minimal inhibitory concentrations of hydrogen peroxide and tert -butyl hydroxyl peroxide were 100 μM and 1 mM, respectively, for IK-1 and 10 and 100 μM, respectively, for IK-1Δ8. IK-1 was much more resistant than IK-1Δ8 to the four water-soluble antibiotics (ampicillin sodium, kanamycin sulphate, streptomycin sulphate, and tetracycline hydrochloride) tested. In contrast, IK-1 was less resistant than IK-1Δ8 to two hydrophobic uncouplers: carbonyl cyanide m -chloro phenylhydrazone (CCCP) and N,N ′-dicyclohexylcarbodiimide (DCCD). The hydrophobicity of the IK-1 and IK-1Δ8 cells grown at 20 °C was determined using the bacterial adhesion to hydrocarbon method. EPA-containing (∼10% of total fatty acids) IK-1 cells were more hydrophobic than their counterparts with no EPA. These results suggest that the high hydrophobicity of IK-1 cells can be attributed to the presence of membrane EPA, which shields the entry of hydrophilic membrane-diffusible compounds, and that hydrophobic compounds such as CCCP and DCCD diffuse more effectively in the membranes of IK-1, where they can fulfil their inhibitory activities, than in the membranes of IK-1Δ8.