Biosynthesis of deuteriated amino acids byCandida lipolytica

Summary Biosynthesis of a whole series of deuteriated amino acids has been carried out, by cultivation of the yeastCandida lipolytica in an artificial medium composed of a deuterio-alkane, heavy water, water and some mineral salts.Acknowledgments. This work has been carried out with the aid of grants from The Swedish Medical Research Council. Thanks are due to Mr Nils Engström for his skilful technical assistance during the yeast growth, and to Mrs Monica Olsson for the Moore-Stein analysis.     

Effect of some phosphonic amino acids on the activity of central neurons]

Microiontophoretic applications of DL-2-amino-3-phosphonopropionic, DL-3-amino-4-phosphonobutyric, aminomethylphosphonic, 2-aminoethylphosphonic and 3-aminopropylphosphonic acids in the course of extracellular recordings of central neurons in the Rat resulted in effects which appeared similar to those observed with their carboxylic analogs. The involvement of the same post-synaptic receptors is suggested.     

Zn65 et calcification du squelette

Summary Five days after intravenous administration of Zn⁶⁵ to young monkeys, autoradiograms of compact bone show that radioactivity is exclusively located at the frontier line, where preosseous tissue is becoming mineralized. Since no diffuse reaction can be detected at this stage in the pre-existing calcified bone, it is concluded that Zn⁶⁵ is not exchanged with the constituents of bone tissue, but does indicate accretion of new mineral substance.     

Pfiesteria shumwayae kills fish by micropredation not exotoxin secretion

Pfiesteria piscicida and P. shumwayae reportedly secrete potent exotoxins thought to cause fish lesion events, acute fish kills and human disease in mid-Atlantic USA estuaries. However, Pfiesteria toxins have never been isolated or characterized. We investigated mechanisms by which P. shumwayae kills fish using three different approaches. Here we show that larval fish bioassays conducted in tissue culture plates fitted with polycarbonate membrane inserts exhibited mortality (100%) only in treatments where fish and dinospores were in physical contact. No mortalities occurred in treatments where the membrane prevented contact between dinospores and fish. Using differential centrifugation and filtration of water from a fish-killing culture, we produced 'dinoflagellate', 'bacteria' and 'cell-free' fractions. Larval fish bioassays of these fractions resulted in mortalities (60-100% in less than 24 h) only in fractions containing live dinospores ('whole water', 'dinoflagellate'), with no mortalities in 'cell-free' or 'bacteria'-enriched fractions. Videomicrography and electron microscopy show dinospores swarming toward and attaching to skin, actively feeding, and rapidly denuding fish of epidermis. We show here that our cultures of actively fish-killing P. shumwayae do not secrete potent exotoxins; rather, fish mortality results from micropredatory feeding.     

Targeting NOX enzymes in the central nervous system: therapeutic opportunities

Among the pathogenic mechanisms underlying central nervous system (CNS) diseases, oxidative stress is almost invariably described. For this reason, numerous attempts have been made to decrease reactive oxygen species (ROS) with the administration of antioxidants as potential therapies for CNS disorders. However, such treatments have always failed in clinical trials. Targeting specific sources of reactive oxygen species in the CNS (e.g. NOX enzymes) represents an alternative promising option. Indeed, NOX enzymes are major generators of ROS, which regulate progression of CNS disorders as diverse as amyotrophic lateral sclerosis, schizophrenia, Alzheimer disease, Parkinson disease, and stroke. On the other hand, in autoimmune demyelinating diseases, ROS generated by NOX enzymes are protective, presumably by dampening the specific immune response. In this review, we discuss the possibility of developing therapeutics targeting NADPH oxidase (NOX) enzymes for the treatment of different CNS pathologies. Specific compounds able to modulate the activation of NOX enzymes, and the consequent production of ROS, could fill the need for disease-modifying drugs for many incurable CNS pathologies.