Effects on fertilization of rabbits of insemination with ejaculates treated with PG-dehydrogenase and antisera to PGE-2 and PGF-2 alpha

PGE-2 and PGF-2 alpha in rabbit semen were selectively inactivated by incubation with antisera, or most of the seminal prostaglandins were transformed into biologically inactive 15-keto-prostaglandins by prostaglandin-15-hydroxydehydrogenase(PG-15-HDH). These treated ejaculates were vaginally inseminated. Compared to the controls (738 eggs of which 94% were fertilized) a dose-dependent reduction of the fertilization rate was observed with the anti-PGF-2 alpha-treated ejaculates. A non-uniformly, but statistically significantly reduced fertility was found in the other 2 treatment groups. After incubation with higher doses of PG-15-HDH, some fertilization was accomplished with ejaculates showing an extremely weak forward progression or immotile spermatozoa. An improvement in sperm motility, however, was observed in ejaculates treated with antiserum to PGF-2 alpha. Seminal prostaglandins may not exclusively affect sperm motility. The observed influences on the fertilization rate after treatment of spermatozoa with antisera to PGE-2 and PGF-2 alpha or PG-15-HDH suggest that these are local effects in the female genital tract.     

Verwertung von Fructose durch Hydrogenomonas H16 (I.)

Zusammenfassung Die Hydrogenomonas-Stämme H 1, H 16 und H 20 nutzen als einziges Kohlenhydrat Fructose; chemolithotroph gewachsene Zellen des Stammes H 16 oxydieren diesen Zucker nach einer lag-Phase von 20 min.Die Fructose wird über den Entner-Doudoroff-Weg umgesetzt; während der Adaptation erhöht sich der Gehalt der Zellen an Phosphoglucose-Isomerase, Glucose-6-phosphat-Dehydrogenase und an den für den Entner-Doudoroff-Weg charakteristischen Enzymen.Die Aktivität der Ribulosediphosphat-Carboxylase geht bei der Adaptation an Fructose innerhalb von 2 Std um 75% zurück, sinkt dann aber während mehrerer Fructose-Passagen nur langsam ab. Folglich kann selbst mit Fructose gewachsener Hydrogenomonas H 16 Kohlendioxyd über den Calvin-Cyclus fixieren.

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Summary The only carbohydrate utilized by Hydrogenomonas strains H 1, H 16 and H 20 is fructose; chemolithotrophically grown cells of strain H 16 oxidize this sugar following a lag-period of 20 min. Fructose is metabolized via the Entner-Doudoroff-pathway. During the adaptation to fructose, the level of the following enzymes increases in the cells: phosphoglucoseisomerase, glucose-6-phosphate-dehydrogenase and the enzymes characteristic of the Entner-Doudoroff-pathway.During the change from chemolithotrophic to organotrophic growth, with fructose serving as a substrate, the activity of ribulose-diphosphate carboxylase is reduced by 75% within 2 hrs. However, following repeated growth in a fructose medium, this enzyme activity decreases only very slowly. Consequently fructose-grown Hydrogenomonas H 16 is capable of fixing carbon dioxide via the Calvin cycle.

     

R-Bodies in newly isolated free-living hydrogen-oxidizing bacteria

R-Bodies have been found in a recently isolated pseudomonas-like free-living hydrogen oxidizing bacterium. Their isolation, fine structure and chemical composition are described and compared with the R-bodies from the kappa particles (Caedobacter), obligate endosymbionts of Paramecium aurelia. The 2K 1 R-bodies exhibited essential characteristics of the kappa R-bodies; however, their size and some other structural aspects proved that they represent a new type of R-bodies. The presence of phage tail-like particles in cells induced with Mitomycin C is in favour of the hypothesis that the R-bodies might be coded by defective prophages, or by extrachromosomal elements.     

Ca2+ accumulation and loss by aberrant endocytic vesicles in sickle erythrocytes.

Sickle cells contain internal vesicles which accumulate Ca2+. As shown here, the membrane enclosing the vesicles contains the plasma membrane Ca(2+)-ATPase, or Ca2+ pump, as judged by staining with an antibody directed against the protein. Moreover, the number of cells containing such vesicles increases upon deoxygenation. These findings argue strongly that the vesicles arise by endocytosis from the plasma membrane, and explain how they accumulate Ca2+. When sickle cells are depleted of ATP, Ca2+ is lost from the vesicles, as judged by the disappearance of staining with the Ca2+/membrane probe chlortetracycline (CTC), without a corresponding loss of antibody staining. This loss of Ca2+ can be inhibited by nitrendipine, a Ca2+ channel blocker. These results suggest that the vesicle membrane allows outward passage of Ca2+ by a nitrendipine-sensitive pathway, which can be overcome by the inward-directed activity of the Ca2+ pump of the vesicle membrane. If so, the Ca2+ which vesicles contain is in dynamic equilibrium with the cytoplasm of the sickle erythrocyte.     

Pharmacokinetics of non-steroidal anti-inflammatory drugs in male rabbits after acute and chronic administration and effect of chronic treatment on seminal prostaglandins, sperm quality and fertility

The pharmacokinetics of various non-steroidal anti-inflammatory drugs were determined to find dosage regimens by which drug concentrations known as active from human anti-inflammatory therapy could be reached and maintained in rabbits during continued administration. Based on the pharmacokinetics and side-effects of the different drugs, phenylbutazone was selected for the fertility experiments. Treatment of male rabbits with phenylbutazone for 9 consecutive days significantly reduced seminal concentrations of PGE-2 and PGF-2 alpha and tended to increase ejaculate volumes, sperm motility, and fertility. These results indicate that, at least in rabbits, inhibition of PG synthesis by prolonged treatment with non-steroidal anti-inflammatory drugs does not impair male fertility. Instead, chronic treatment with the drugs at non-toxic doses may improve sperm quality and fertility.     

Concentrations of prostaglandin E2 and F2 alpha in the cardiovascular system of infants with persisting patent ductus arteriosus

The distribution of prostaglandin E2 and F2 alpha was examined in the peripheral veins and in several positions of the cardiovascular system before and after the blood had passed through the lungs in 37 infants. Prostaglandin E2 varied from 0.25 +/- 0.09 ng/ml to 0.44 +/- 0.09 ng/ml when measured in the pulmonary artery, the ductus arteriosus, the right atrium, the right ventricle, the left atrium, the left ventricle, the inferior vena cava and the descending aorta. Prostaglandin F2 alpha was much higher in these positions of the cardiovascular system. The range was 0.99 +/- 0.36 ng/ml to greater than 2.0 ng/ml. The vascular tissues produced virtually identical high amounts of prostaglandin E2 and F2 alpha, but there were no significant differences in prostaglandin E2 and F2 alpha, concentrations, in venous blood as well as in systemic arterial blood. The results suggest that prostaglandin E2 is not responsible for the persisting patency of the ductus arteriosus in infants. There is no explanation for the increased prostaglandin F2 alpha concentrations in these patients.