Behavior of Antimicrobial Peptide K4 in a Marine Environment.

K4 is a de novo peptide with antibacterial activity on human pathogens. It has a short sequence (14 amino acids), with a cationic N-terminal moiety and an amphipathic ɑ-helix structure. The present paper demonstrates its activity on Vibrio bacteria in a marine environment. It was found non-toxic on marine organisms including Artemia salina, Dicentrarchus labrax, and Magallana gigas at different developmental stages, but influenced the growth of unicellular organisms like microalgae, depending on the algal strain and on K4 concentration. Furthermore, an original approach coupling liquid chromatography (RP-HPLC) and mass spectrometry (MS/MS) allowed us to monitor the degradation time course of the peptide for the first time in conditions close to a hatchery environment, i.e., in the presence of oyster spat. We detected truncated forms over time, and the full K4 was gradually no longer found in these filter-feeder oysters. Finally, using an automated optical density meter, we monitored the growth of several aquatic bacteria identified as pathogenic on animals. K4 had a bactericidal effect on Aeromonas salmonicida and Vibrio splendidus LGP32 at concentrations below 45 µg mL-1. Our results show that K4 could be an environment-friendly alternative to antibiotics, non-toxic to several marine organisms. The use of K4 would be particularly useful to decrease the bacterial load associated with food intake in the early developmental stages of marine animals reared in hatcheries.

Cytochrome P450dbl phenotypes in malignant and benign breast disease.

129 female patients with breast cancer and 79 controls undergoing biopsy for benign breast conditions had debrisoquine hydroxylator phenotype established. 129 female hospital patients with known hydroxylator phenotype were used as another control group. The breast cancer cases differed significantly from the benign controls in their debrisoquine phenotype, with 10% being poor metabolisers compared with none of the controls (P less than 0.01). However, while a comparison of the distributions of metabolic ratio (an inverse measure of debrisoquine metabolism) of breast cancer patients and hospital controls showed a significant difference by rank, there was no significant difference in the proportion of poor metabolisers in these two groups. The cases with benign disease differed from the hospital controls in both metabolic ratio distribution (P less than 0.001) and frequency of poor metabolisers (P less than 0.05). Although there was a shift in metabolic ratio distribution, debrisoquine hydroxylator phenotype was not a genetic marker for breast cancer. Why no patients undergoing biopsies for benign conditions were poor metabolisers is unknown.