Acrylonitrile inhalation in rats: II. Excretion of thioethers and thiocyanate in urine

In male Wistar rats, the inhalation exposure to acrylonitrile (AN), 271 mg X m-3, 8 hours a day, 5 days a week, did not affect protein sulfhydryl concentration in liver and blood and decreased glutathione concentration in the liver, but not in the brain at the end of the fifth exposure. The urinary excretion of the main AN metabolites, thioethers (AN-mercapturic acids) and thiocyanate was proportional to the inhaled AN concentration (57, 125, 271 mg X m-3, respectively) in a single exposure for 12 hours, and their mutual ratio was greatly different from that after injection of AN. The results revealed that the urinary excretion of thioethers is a very sensitive and dose-related indicator of exposure to AN and extrapolation of the results indicates that the exposure to AN concentration below 10 mg X m-3 could thus be demonstrated.     

Electron beam relaxation in nonuniform plasma of a steady-state beam-plasma discharge at moderately low gas pressures

Electron beam relaxation in plasma under conditions typical of laboratory plasma devices based on a steady-state beam-plasma discharge was investigated. It is shown that the measured dependences of the beam loss factor in a discharge operating at a moderately low gas pressure disagree with theoretical dependences calculated for a longitudinally uniform plasma. Analytic dependences obtained in the framework of quasilinear theory with allowance for longitudinal plasma inhomogeneity agree with experimental data. Some effects caused by the influence of the main discharge parameters on electron beam relaxation are analyzed.     

Antagonism by an LHRH agonist of the steroidogenic effects of exogenous human chorionic genadotrophin in the rhesus monkey

Fourteen regularly cycling female rhesus monkeys were observed daily for menstruation and bled from the saphenous vein at regular intervals throughout the study. Plasma samples were assayed by RIA for progesterone levels. The animals were divided into 3 subgroups. The first (n=5) received daily subcutaneous injections of 1000 IU hCG from the 18th to 36th day following onset of menstruation. The second (n=7) received the same hCG treatment and was also implanted subcutaneously from the 18th to 40th days with 1.2 mg [Des-gly¹⁰, DTrp⁶, ProNHEt⁹] LHRH contained in cholesterol matrix pellets. The third (n=2) was untreated. Intermenstrual interval was significantly extended by hCG treatment. The extension was partially overcome by the LHRH agonist. The hCG-induced elevation in plasma progesterone to peak values over 17ng/ml was blocked by the LHRH agonist to give mean values not significantly different from control luteal phase levels. Plasma estradiol levels were unaffected by hCG or LHRH agonist.     

Changes in the size of the myocardial damaged area in postischemic reperfusion

The changes in the size of the myocardial injury area during reperfusion after the coronary occlusion-induced ischemia lasting 30 minutes are phasic in nature. Until 3.5 h the injured area increases and after 23.5 h relatively diminishes. After a more prolonged ischemia such manifestations are either unmarked or absent. Ischemia lasting from 30 min to 4 hours followed by reperfusion, as compared with ischemia of the same duration without reperfusion, normally gives rise to the formation of an area of injury, which is less or occasionally equal in size. The data obtained and reported indicate that in the area of coronary occlusion there are groups of cardiomyocytes that differ as regards the resistance to ischemia.     

Induction of electrogenic phosphate transport through the mitochondrial membrane by a thermostable cytoplasmic factor in hyperthyroidism

Addition of a thermostable cytoplasmic fraction leads to the uncoupling of oxidative phosphorylation of the mitochondria. In hyperthyrosis such an effect manifests itself more powerfully than in the control. Addition of the thermostable cytoplasmic fraction induces electrogenic phosphate transport via the mitochondrial membrane. In hyperthyrosis, the activity of the thermostable inducer of phosphate transport in the cytoplasm increases. The functioning of the phosphate cycle may be the cause of the uncoupling of oxidative phosphorylation of the mitochondria during the disease in question.