Two distinct mechanisms for the initiation of mast cell degranulation.
Explore the source record for details and available documents.
Adenosine Triphosphate↗
Biomedical subjects
J F Roser
Publications and source records attributed to J F Roser.
The initiation of mast cell degranulation: activation at the cell membrane.
The low molecular weight mast cell activator, polymyxin B, has been covalently bound to an insoluble matrix of Sepharose 4B. It has been demonstrated that mast cells in preparations of rat peritoneal cells bind to Sepharose 4B-polymyxin B beads but not to control beads. The bound cells are stimulated to degranulate by this interaction at the cell membrane with the resultant release of biogenic amines.
Animals↗
Activation of rat mast cells by low molecular weight stimuli.
Explore the source record for details and available documents.
Adenosine Triphosphate↗
Dose-response effects of gonadotropin-releasing hormone on plasma concentrations of gonadotropins and testosterone in fertile and subfertile stallions.
Five fertile and five subfertile stallions were treated with a single intravenous injection of saline the first week followed by a single intravenous injection of varying doses of gonadotropin-releasing hormone (5, 10, 25, 100, 500 micrograms) given in a randomized fashion over the next 5 weeks during the nonbreeding season. Blood samples were collected periodically before and after treatment for analysis of luteinizing hormone, follicle stimulating hormone, and testosterone content by radioimmunoassay. Before treatment, semen samples were collected every other day for 3 weeks for analysis of volume, concentration, motility, pH, and morphology. Basal plasma levels of luteinizing hormone were higher (P < 0.05) in the subfertile group, follicle stimulating hormone levels tended to be higher (P < 0.10) in the subfertile group, and testosterone levels were similar in the two groups. A significant linear-log dose-response relationship was observed for plasma luteinizing hormone (P < 0.05) and follicle stimulating hormone (P < 0.05) to exogenous gonadotropin-releasing hormone in both the fertile and subfertile group. A linear-log dose-response relationship was also observed for plasma testosterone (P < 0.05) in the fertile group. The magnitude of the luteinizing hormone and follicle stimulating hormone response to gonadotropin-releasing hormone across doses was similar in both groups of stallions. A significant testosterone response to gonadotropin-releasing hormone in the subfertile group of stallions was not observed (P > 0.05). Mean testosterone concentrations after treatment in terms of net increase and percent of baseline were significantly lower (P < 0.05) in the subfertile group compared to the fertile group.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Seasonal effects on seminal quality, plasma hormone concentrations, and GnRH-induced LH response in fertile and subfertile stallions.
Seasonal effects on hormonal and seminal parameters in subfertile stallions have not been well documented and could provide information that is needed to understand the underlying endocrine mechanisms associated with testicular dysfunction. Such information may be useful in developing diagnostic tools to identify those stallions who are candidates for treatment. This investigation characterizes and compares the effects of season on endocrine function and seminal quality in fertile and subfertile stallions. Eight fertile and six subfertile stallions between the ages of 5 and 18 years were injected intravenously once every hour for 3 hours with either 1 mL saline on the first experimental day or 5 micrograms gonadotropin-releasing hormone in 1 mL saline on the second experimental day during the nonbreeding and breeding season. Heparinized blood samples were collected periodically through a jugular catheter before and after treatment for analysis of luteinizing hormone, follicle-stimulating hormone, testosterone, and estrogen conjugates by radioimmunoassay. Semen samples were collected twice, 1 hour apart, from all stallions in both seasons for analysis of volume, concentration, motility, pH, and morphology. A series of low intravenous doses (5 micrograms) of gonadotropin-releasing hormone induced a significant luteinizing hormone response (P less than 0.05) compared with saline treatment in both fertile and subfertile stallions. Fertile stallions had a twofold higher (P less than 0.05) net increase in plasma luteinizing hormone levels (peak levels minus baseline levels) in the breeding seasons than in the nonbreeding season. The magnitude of the luteinizing hormone response relative to baseline levels in fertile stallions, however, was one-and-one-half times greater (P less than 0.05) in the nonbreeding season than in the breeding season. In contrast, season did not have an effect on the net increase in plasma luteinizing hormone or the magnitude of the luteinizing hormone response relative to baseline levels in subfertile stallions. The net increase in plasma luteinizing hormone was similar between the two groups of stallions in both seasons. The magnitude of luteinizing hormone response relative to baseline levels, however, was lower (P less than 0.05) in subfertile stallions (141 +/- 14%) than in fertile stallions (235 +/- 46%) in the nonbreeding season; the two groups exhibited similar responses in the breeding season. Compared with fertile stallions, subfertile stallions had twofold to fourfold higher (P less than 0.05) plasma levels of gonadotropins and similar testosterone levels. The number of total progressively motile sperm was lower (P less than 0.05) in subfertile stallions in both seasons.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Effects of lipoprotein, equine luteinizing hormone, equine follicle-stimulating hormone, and equine prolactin on equine testicular steroidogenesis in vitro.
A stallion testicular cell incubation system was developed and used to investigate the regulation of steroidogenesis in stallion testes. Cells isolated from testes of 2- to 4-year-old stallions (n = 6) were cultured for 12 hours in a defined medium with and without varying doses of lipoprotein, equine luteinizing hormone (eLH), human chorionic gonadotropin (hCG), equine follicle-stimulating hormone (eFSH), and/or equine prolactin (ePRL). Estrogen conjugate (EC), testosterone (T), and estradiol-17 beta (E2) production were determined by RIA. Increasing doses of lipoprotein significantly (P < 0.001) increased basal, hCG- and eLH-stimulated EC production, resulting in a maximal fourfold increase in each case. A maximal dose of lipoprotein (3 mg/ml) significantly (P < 0.001) increased basal T production threefold, whereas hCG- and eLH-stimulated T production were increased 76- and 30-fold, respectively. In the presence of 0.5 mg/ml of lipoprotein, increasing doses of eLH significantly (P < 0.001) stimulated EC, T, and E2 production. The increase in T production (5.6-fold) at a physiological dose of eLH (5 ng/ml) was significantly (P < 0.05) greater than the increase in EC or E2 production (2.1- and 2.3-fold, respectively). However, the total mass of EC produced was significantly greater (P < 0.05) than the total amount of T produced at both basal (15 ng vs. 148 pg) or hormone-stimulated (48 ng vs. 2,427 pg at 5 ng/ml eLH) levels. hCG significantly (P < 0.001) stimulated EC and T production and was 82-fold more active in stimulating EC production and 41-fold more active in stimulating T production than was eLH. FSH had no significant effect on steroidogenesis either alone or in the presence of eLH, except at the highest dose tested (50 ng/ml), which was above the physiological level of circulating FSH (4-7 ng/ml) in the stallion. PRL (1-50 ng/ml) had no significant effect on steroidogenesis either alone or in the presence of eLH. These data suggest that in the postpubertal stallion, both estrogen and T production are regulated by LH, and this regulation appears to be dependent on the availability of lipoprotein-derived cholesterol. Furthermore, the observation that testicular cells produced a larger mass of EC than T, but responded to eLH with a larger relative increase in T production, suggests that production of these two steroids may be independently regulated.
Animals↗
HCG binding to the testicular LH receptor is similar in fertile, subfertile, and infertile stallions.
Recent evidence in our laboratory suggests that the cause of idiopathic subfertility/infertility in breeding stallions may originate in the testes at the luteinizing hormone (LH) receptor or postreceptor level. The objective of this research was to determine if LH receptor binding activity is altered in subfertile and infertile stallions. Six fertile, three subfertile, and three infertile stallions, ages 11-23 years, were classified according to normal semen parameters and pregnancy rates and then castrated in the breeding season. Blood was collected prior to castration, and plasma was stored until analyzed for LH, follicle stimulating hormone (FSH), estrogen conjugates (EC), estradiol (E2), testosterone (T), and inhibin (I) by radioimmunoassay (RIA). Testicular cell membranes were prepared and snap-frozen until analyzed for LH binding activity by radioreceptorassay (RRA) using increasing amounts of I125 human chorionic gonadotropin (hCG). Luteinizing hormone receptor numbers and affinity constants were determined by Scatchard analysis. Plasma LH, FSH, EC, E2, and T levels did not differ between fertile and subfertile stallions, but LH and FSH were significantly higher (P < 0.05) and EC, E2, T, and I levels were significantly lower (P < 0.05) in infertile stallions as compared to fertile and subfertile stallions. Receptor number (Rt) and affinity constants Ka were similar (P > 0.05) between fertile (Rt = 9.44 x 10(-11) M, Ka = 0.300 x 10(10) M-1), subfertile (Rt = 13.02 x 10(-11) M, Ka = 0.194 x 10(10) M-1), and infertile (Rt = 7.65 x 10(-11) M, Ka = 0.380 x 10(10) M-1) stallions. In conclusion, these data suggest that an endocrine dysfunction in the testes of stallions with poor fertility may not be due to a LH receptor disorder but may be due to a postreceptor malfunction.
Animals↗