Antimicrobial peptides are produced by nearly all organisms: bacteria, plants, invertebrates, and vertebrates. Certain antimicrobial peptides from multicellular animals also kill a variety of tumour cells at concentrations not affecting normal eukaryotic cells. Recently, it was reported that also Plantaricin A (PlnA), which is a peptide with strain-specific antibacterial activity produced by Lactobacillus plantarum, may kill eukaryotic cells (Sand et al. 2007). It was shown that PlnA permebilizes cancerous rat pituitary cells (GH4 cells), whereas normal rat anterior pituitary cells are resistant to the peptide. In order to examine if the preferential permeabilization of cancerous cells is a general feature of PlnA, we have studied its effect on primary cultures of rat liver cells (hepatocytes and endothelial cells) and two epithelial cell lines of primate kidney origin (Vero cells from green monkey and human Caki-2 cells). The Vero cell line is derived from normal cells, whereas the Caki-2 cell line is derived from a cancerous tumour. The membrane effects were studied by means of patch clamp recordings and microfluorometric (fura-2) monitoring of the cytosolic concentrations of Ca²⁺ ([Ca²⁺]_i) and fluorochrome. In all the tested cell types, exposure to 10–100 mM PlnA induced a nearly instant permeabilization of the membrane, indicated by the following criteria: increased membrane conductance, membrane depolarization, increased [Ca²⁺]_i, and diffusional loss of fluorochrome from the cytosol. At a concentration of 5 mM, PlnA had no effect on any of the cell types. We conclude that the permeabilizing effect of PlnA is not restricted to cancerous cells.

Reference: 

Sand, S.L., Haug, T.M, Nissen-Meyer, J. & Sand, O. 2007. J Membrane Biol 216, 61–71.