230
Abstracts CHAN, S. L. and Quasre~, J. H. (Neurochemistry Section, Kinsmen Laboratories, University of British Columbia, Vancouver 8, Canada). Tetrodotoxin : Effects on brain metabolism in vitro. Science, N. Y. 156, 1752, 1967 .
A 3-to-molar concentration of tetrodotoxin completely inhibits the stimulation of respiration of rat brain cortex that takes place upon application of electrical impulses . It also inhibits increase in the rate of the respiration that occurs when calcium ions are omitted from the incubation medium. No effxt of tetrodotoxin on brain respiration takes place when stimulation is brought about by the addition of 100m-molar potassium chloride. Tetrodotoxin prevents the fall in the rate of oxidation of cerebral acetate that occurs during electrical stimulation but does not effect the increased rate of the oxidation that occurs in the presence of an increased concentration of potassium chloride. The data indicate that oxidation of cerebral acetate is diminished by influx of sodium ions, which is prevented by tetrodotoxin, and is increased by influx of potassium ions, which is unaffected by tetrodotoxin .
Ynnc, C. C. (Department of Biochemistry, Kaohsiung Medical College, Kaohsiung, Taiwan,
Republic of China) . The disulfide bonds of cobrotoxin and their relationship to lethality. Bia chim. biophys. Acta 133, 346, 1967 .
Tru: roraL wntent of half~ystine plus cysteine of cobrotoxin as measured by the disulfide interchange reaction was 120 moles, while no free sulfhydryl groups were detected by spectrophotometric titration with PCMB after treatment with 8 M urea. These results indicate the presence of 6 disulfide bonds in each molecule of cobrotoxin. In order to correlate the disulfide bonds in cobrotoxin to its lethal toxicity, ß-mercaptcethanol was added to split the disulfide bonds in cobrotoxin dissolved in 8 M urea . Upon addition of ß-mercaptcethanol, the lethal toxicity of cobrotoxin decreased immediately and after 1 hr the toxicity was lost almost completely. The inert, fullyreduced cobrotoxin regained thetoxicity upon oxidation. The rate of oxidation and restoration of the toxicity was dependent upon the pH and the protein concentration. The angtigenicity, i.r spectrum,and levorotation were also restored to the original values upon oxidation of the reduced cobrotoxin. The results reveal the essentiality of the intact disulfide bonds in cobrotoxin for the lethal toxicity. A.O .
BELLAUl3, A. andCARRINGTON, R. The WorldojReptiles,Amste~dam : Elsevier 153 pp .1966. Fsw roxtNOLOCrsrs have access to the more classical works on the biology of the venomous animals. Most of us find ourselves to often dependent on general texts in biology, few of which give consideration to relationships between venomous animals and their toxins. This clear, concise and well-written text by Bellairs and Carrington contains a considerable amount of useful data for the toxinologist, and in spite of its wmpactness gives greater detail on subjects of interest to toxinologists than its size would indicate . The text is divided into chapters on : What is a Reptile? Tortoises and Turtles; Lizards and the Tuatara; Snakes ; and Crocodiles and Their Allies . There is a short appendix on scientific names and nomenclature, and a classification of living reptiles . While the text is written for the general reader, the material is well organized into sections that make the contribution useful to graduate students, biologists and physicians. The photographs and drawings are good and the choice of examples is excellent. The paragraphs dealing with venomous snakes, their venoms and snake venom poisoning are adequate and well put. The book is a refreshing addition to the many recent contributions on reptiles . F.E .R.