Effect of prostaglandin E1 on the cyclic adenosine-3',5'--monophosphate system and radiosensitivity of B-82 cells cultured in vitro

The cyclic AMP (cAMP) system of mice fibroblasts L, clone B-82 has been studied. B-82 cells possess receptors to prostaglandin E1 (PGE1) and are deficient in beta-adrenoreceptors. It has been shown that 10 mM NaF, 1.10(-4) M GTP and 1.10(-5) M PGE1 stimulate adenylate cyclase of B-82 cells. PGE1 causes increase in the intracellular content of cAMP and protects B-82 cells against irradiation. Specifict beta-agonist isoproterenol fails to modulate adenylate cyclase activity and does not change cAMP content in B-82 cells. Isoproterenol has no effect on the B-82 cells radiosensitivity, although it is known to be a potent radioprotector. It is presumed that the stimulation of cAMP system by radioprotector is necessary for the performance of radioprotective effect.     

Pythium aphanidermatum May Reduce Cucumber Growth without Affecting Leaf Photosynthesis

Plants respond to many stress factors, including infections caused by root pathogens, with reductions in photosynthesis and growth. We studied the response of mature cucumber plants after a weak inoculation of the roots with Pythium aphanidermatum. The epidemiology of the disease was recorded using an indirect ELISA. Although mycelium was detected in the roots, photosynthesis was not affected over a period of five weeks. Nevertheless, plant growth was significantly reduced by the pathogen. Possible modes of action are discussed.     

Fertility Defects in Mice Expressing the L68Q Variant of Human Cystatin C: A ROLE FOR AMYLOID IN MALE INFERTILITY*

Hereditary cystatin C amyloid angiopathy is an autosomal dominant disorder in which a variant form of cystatin C (L68Q) readily forms amyloid deposits in cerebral arteries in affected individuals resulting in early death. L68Q protein deposits in human cystatin C amyloid angiopathy patients have also been found in tissues outside of the brain including the testis, suggesting possible effects on fertility. Heterozygous transgenic mice (L68Q) that express the human L68Q variant of cystatin C under the control of the mouse cystatin C promoter were unable to generate offspring, suggesting the presence of L68Q cystatin C amyloid affected sperm function. In vitro studies showed that epididymal spermatozoa from L68Q mice were unable to fertilize oocytes and exhibited poor sperm motility. Furthermore, spermatozoa from L68Q mice exhibited reduced cell viability compared with wild type (WT) spermatozoa and often were detected in large agglutinated clumps. Examination of the epididymal fluid and spermatozoa from L68Q mice showed increased levels and distinct forms of cystatin C amyloid that were not present in WT mice. The addition of epididymal fluid from L68Q mice to WT spermatozoa resulted in a recapitulation of the L68Q phenotype in that WT spermatozoa showed reduced cell viability and motility compared with WT spermatozoa incubated in epididymal fluid from WT mice. L68Q epididymal fluid that was depleted of cystatin C amyloids, however, did not impair the motility of WT spermatozoa. Taken together these studies suggest that amyloids in the epididymal fluid can be cytotoxic to the maturing spermatozoa resulting in male infertility.