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Oxidation reactions of DL-selenomethionine (DL-SeMet) with hydrogen peroxide and ozone were investigated by ¹H and ¹³C NMR spectroscopy. Chemical shifts of the reaction products were measured at different pD values in D2O solutions. In the moderate (4–8) pD range, a pair of singlets of equal intensity appeared at 2·71 and 2·80 ppm, with the disappearance of the DL-SeMet methyl peak at 2·04 ppm. As the pD of the solution decreased, the chemical shifts of both peaks increased relative to 3-trimethylsilylpropionic acid-d4 sodium salt. In strongly acidic solutions (pD<3), the pair collapsed to one singlet at 3·18 ppm. As pD values increased the chemical shifts decreased in numerical value with only a singlet at 2·69 ppm observed in strongly basic solutions (pD>10). These data were assigned to Met selenoxide in basic solution, stabilized by intermolecular hydrogen bonding, and to the hydration of Met selenoxide to Met dihydroxyselenide in acidic solutions. In moderate pD solutions (pD=4–8), both forms of the selenoxide can exist. For the reaction of DL-SeMet with CNBr, two parallel reactions occur, i.e. oxidation and bond cleavage with cyanization: the bond cleavage giving the expected products, i.e. 2-amino-4-butyrolactone and methyl selenocyanate, with an additional singlet observed at 2·54 ppm. © 1988 SCI

Increased pulmonary ventilation in the human individual, whether voluntary or involuntary, is accompanied by a series of biochemical and physiologic changes which are proportional to the intensity and duration of hyperventilation. The resulting symptoms and signs are numerous,1 but certain of these are reasonably characteristic. Dizziness, blurring of vision, and numbness and tingling of the extremities are frequent early symptoms. Excessive pulmonary ventilation, long continued, results usually in spasms of the muscles of the face, hands and feet. In some persons these signs are accompanied or followed by laryngeal stridor, opisthotonos, generalized convulsions and unconsciousness. Physical and nervous fatigue are common sequels to the episode and may persist for several days.The exact biochemical basis for these changes in the irritability of nerve cells has not been clearly established. It is probable that some of the symptoms and signs are initiated by the train of events which follow local

Respiratory paralysis is the usual cause of immediate death from spinal anesthesia. Three mechanisms, or combinations of these, may be involved:Direct action on the medullary respiratory centers by diffusion of the drug to the fourth ventricle in paralytic concentrations. The observations of Koster and Kasman 1 and of Johnston and Henderson,2 who demonstrated experimentally that excessively high concentrations are required to bring about this effect, indicate that this type can probably be excluded from serious consideration.Ascending block of the intercostal and phrenic nerves. This type of paralysis is unquestionably preventable and is secondary either to (a) ignorance of, or inexperience in, the technical aspects of the procedure, or to (b) unsuccessful attempts to produce a selective sensory nerve block of the neck and upper thoracic regions.Insufficient nutrient flow of blood through the central respiratory mechanism secondary to cardiovascular depression. Cardiovascular depression in some degree is attendant on