Bacterial production of tetrodotoxin in the pufferfish Arothron hispidus.

This study evaluates the presence, location and production source of tetrodotoxin (TTX) in two species of pufferfish, Diodon histrix and Arothron hispidus, common to Hawaiian waters. Organs from each fish were analysed for TTX and used to isolate bacteria for evaluation of possible TTX production. Comparative analyses of extracts of fish and bacterial culture media were performed with liquid chromatography-mass spectrometry (LC-MS) and a sodium channel specific bioassay. Bacterial cultivation experiments were performed in two different growth media and bacteria were identified through sequence homology of the 16S rRNA gene. Forty-two and forty-seven distinct strains were cultivated from D. histrix and A. hispidus, respectively. However, no commonality was found between the populations of bacteria isolated from the two fish. TTX was detected only in A. hispidus and was present in the flesh, pectoral fin and kidneys, as well as the skin slime. Sixteen of the forty-seven bacterial species isolated from A. hispidus were cultivated for further evaluation of TTX production. Among these sixteen bacterial species, Vibrio harveyi strains isolated from the skin slime and kidneys of A. hispidus were found to produce TTX, being the source of TTX produced in the pufferfish.

Angiotensin converting enzyme concentrations in the lung lavage of normal rabbits and rabbits treated with nitrogen mustard exposed to hyperoxia.

Increased concentrations of angiotensin converting enzyme (ACE) were found in lung lavages from rabbits exposed to hyperoxia for 72 h and the concentrations of ACE were correlated with ratios of extravascular lung water to body weight (r = 0.69, p less than 0.05) and albumin concentrations in lung lavages (r = 0.89, p less than 0.01). In parallel studies, rabbits treated with nitrogen mustard in which granulocytopenia was maintained throughout the 72-h hyperoxic exposure period had less evidence of edematous lung injury and lower concentrations of ACE in their lung lavages than similarly treated rabbits in which granulocytopenia was not maintained. The results suggested that granulocytes contribute to acute edematous lung injury from hyperoxia and that ACE concentrations in lung lavages reflect this process.