A unique pathway for the plasma elimination of alpha 2-antiplasmin-protease complexes in mice

Radiolabeled alpha 2-antiplasmin cleared slowly from the circulation of mice. Complex formation with either plasmin or trypsin resulted in a significant increase in the plasma elimination rate of the protease inhibitor. Approximately 20 min and 14 min were required for 50% of the injected alpha 2-antiplasmin-plasmin and alpha 2-antiplasmin-trypsin to clear from the circulation, respectively. Significant competition was observed when radiolabeled alpha 2-antiplasmin-plasmin was cleared in the presence of a large molar excess of unlabeled alpha 2-antiplasmin-plasmin. alpha 1-Antitrypsin-trypsin failed to complete with radiolabeled alpha 2-antiplasmin-plasmin even when present at 2000 fold molar excess. Organ distribution studies localized the major site of alpha 2-antiplasmin-plasmin clearance in the liver. Microscopic autoradiography data suggested that the cell responsible for the clearance pathway was the hepatocyte.     

Translocation,distribution and metabolism of triforine in plants

After short-term root-treatment of plants with³H-triforine (labelled in the piperazine ring) or¹⁴C-triforine (labelled in the side chain), the label was translocated primarily to the leaves present at the time of treatment, without any redistribution of the label taking place after termination of the treatment. Autoradiography showed the radioactivity to be very evenly distributed over the leaf blades, without any appreciable accumulation in leaf margins. In infected leaves, however, there was a tendency for increased accumulation at the infection sites.In dilute aqueous solution triforine was decomposed rather rapidly, the chemical half-life being three days only. From these solutions several non-fungitoxic degradation products have been isolated and their chemical structures determined. In plants, decomposition of triforine was considerably slower than in aqueous solutions, the half-life of the compound varying depending on plant species. In plants, at least four conversion products could be demonstrated, one of which is piperazine. Whether the other three compounds are identical with or structurally related to the breakdown products found in aqueous solution is not yet known.Its low persistence and low animal toxicity suggest that triforine does not offer serious hazards to the environment.Presented at the Third International Congress of Pesticide Chemistry (IUPAC), Helsinki, Finland, 1974.     

Hormonal changes in buserelin therapy

Buserelin has been applied intranasal in 31 women of the reproductive age for endometriosis that had been diagnosed by laparoscopic and bioptic means. The treatment period was 6 month and hormonal changes were evaluated after 2, 4, 8, 12, 17, 20, and 24 weeks. After 2 weeks we observed a decrease of FSH to the lower normogonadotropic range, and of progesteron to less than 0.5 ng/ml. After 4 weeks LH decreased to the lower normogonadotropic range and E2 was below 55 pg/ml. Prolactin concentrations varied between 6 and 8 ng/ml.     

Mutagenicity studies on urine concentrates from female users of dark hair color products.

Urines from women, collected before and after hair dyeing, were evaluated for mutagenic activity in the Ames Salmonella-Microsome Test. Thirty (30) sets of samples were tested as concentrates following removal of histidine on an XAD-2 resin column. None of the samples taken following the use of various Clairol products containing high levels of dyes gave any indication of increased mutagenic activity when compared to samples taken before hair dyeing. These results indicate that the use of hair dyes does not result in exposure of the urinary system to mutagens detectable in a sensitive microbial system, and thus suggest the absence of significant biological effects among users of hair dyes and persons occupationally exposed.     

Prostaglandins in primary dysmenorrhea: Comparison of prophylactic and nonprophylactic treatment with ibuprofen and use of oral contraceptives

Prostaglandin synthetase inhibitors have been used in clinical trials for the treatment of primary dysmenorrhea on the theory that the disorder may be caused by a high level of prostaglandins. However, a causal role of prostaglandin in dysmenorrhea has not been established, and there is only indirect evidence that the amelioration of dysmenorrhea by prostaglandin synthetase inhibitors is related to their inhibition of prostaglandin synthesis in the uterus. We, therefore, monitored menstrual prostaglandin release in 14 dysmenorrheic patients in a controlled, double-blind, cross-over trial of ibuprofen (Motrin®) and in two dysmenorrheic subjects while they were receiving oral contraceptive therapy and while they were not. A total of 89 menstrual cycles were studied. We found that ibuprofen therapy reduced menstrual prostaglandin release and relieved dysmenorrhea but that placebo therapy did not. Oral contraceptives decreased menstrual flow, reduced prostaglandin release and also alleviated dysmenorrhea. We conclude that primary dysmenorrhea is related to a high level of menstrual prostaglandin release. Ibuprofen inhibits prostaglandin synthesis whereas oral contraceptives inhibit ovulation and cyclic endometrial development. Thus, the two drugs suppress endometrial prostaglandin through different mechanisms. Reduction of menstrual prostaglandin release leads to alleviation of dysmenorrhea.