1. Reproductive Performance of Rabbit does Artificially Inseminated with Semen Supplemented with GnRH Analogue [des-Gly10, D-Ala6]-LH-RH Ethylamide
P Gogol Pol J Vet Sci. 2016 Sep 1;19(3):659-661. doi: 10.1515/pjvs-2016-0084.
The aim of the study was to evaluate, the ability of a GnRH synthetic analogue [des-Gly10, D-Ala6]-LH-RH ethylamide to induce ovulation in rabbit does using intravaginal administration. A total of 138 primiparous lactating does were randomly divided into 4 groups that at the time of insemination received following treatments for ovulation induction: 1 μg of buserelin administered intramuscularly (control group); 5 μg of [des-Gly10, D-Ala6]-LH-RH ethylamide added to the semen dose (D5 group); 10 μg of [des-Gly10, D-Ala6]-LH-RH ethylamide added to the semen dose (D10 group); 15 μg of [des-Gly10, D-Ala6]-LH-RH ethylamide added to the semen dose (D15 group). Kindling rates were 68.8% in D10 and 66.7% in D15 groups and were comparable to that obtained in the control group (72.2%). The kindling rate in group D5 (29.4%) was significantly lower than those recorded in the other groups. The number of live born kits was not significantly affected by the ovulation induction treatment. The results of this study show that [des-Gly10, D-Ala6]-LH-RH ethylamide added directly into the semen dose can effectively stimulate ovulation in rabbits. The dose of 10 μg of [des-Gly10, D-Ala6]-LH-RH ethylamide per doe was sufficient to produce results comparable to those obtained by intramuscular administration of buserelin.
2. Enzymatic degradation of luteinizing hormone releasing hormone (LHRH)/[D-Ala6]-LHRH in lung pneumocytes
X Yang, Y Rojanasakul, L Wang, J Y Ma, J K Ma Pharm Res. 1998 Sep;15(9):1480-4. doi: 10.1023/a:1011926310666.
Purpose: To investigate the cellular proteolytic activities of various lung pneumocytes using luteinizing hormone releasing hormone (LHRH) and [D-Ala6]-LHRH as model peptide substrates. Methods: HPLC analysis was used to investigate the degradation kinetics of LHRH/[D-Ala6]-LHRH and to identify their degradation products in isolated lung pneumocytes. Results: Pulmonary macrophages exhibited the strongest proteolytic activity against LHRH)/[D-Ala6]-LHRH, followed by type II and type I-like pneumocytes. Three major degradation products of LHRH, namely LHRH 4-10, LHRH 6-10, and LHRH 7-10, were identified in macrophages and type II pneumocytes, whereas in type I-like pneumocytes only the LHRH 7-10 was found. Co-incubation of the cells with known enzyme inhibitors including captopril (an ACE inhibitor), thiorphan (an EP24.11 inhibitor), and EDTA (an EP24.15 inhibitor) inhibited the formation of LHRH 4-10, LHRH 7-10, and LHRH 6-10 respectively. In all cell types, the degradation rate of [D-Ala6]-LHRH was about 3-8 times lower than that of LHRH. This peptide analog was resistant to degradation by EP24.15 and EP24.11, but was susceptible to ACE. Conclusions: ACE, EP24.11, and EP24.15 are the major enzymes responsible for the degradation of LHRH in macrophages and type II pneumocytes. The magnitude of peptidase activities in these cell types are: EP24.15 > EP24.11 approximately ACE. No EP24.15 or ACE activity was observed in type I-like pneumocytes and only a weak EP24.11 activity was detected.
3. Reproductive performance of rabbit does artificially inseminated via intravaginal administration of [des-Gly 10, D-Ala6]-LHRH ethylamide as ovulation inductor
L A Quintela, A I Peña, M D Vega, J Gullón, C Prieto, M Barrio, J J Becerra, P G Herradón Reprod Domest Anim. 2009 Oct;44(5):829-33. doi: 10.1111/j.1439-0531.2008.01095.x. Epub 2008 Nov 9.
This study was aimed to evaluate the reproductive performance of rabbit does artificially inseminated (AI) with a GnRH analogue [des-Gly10, D-Ala6]-LHRH. ethylamide to induce ovulation by intravaginal administration, delivered in the seminal dose. In a preliminary experiment, 39 does were divided into three groups (n = 13) that, at the time of AI, received the following ovulation induction treatments: (i) control group: 20 microg of gonadorelin administered intramuscularly; (ii) 25 microg of the GnRH analogue added to the seminal dose; (iii) 30 microg of the GnRH analogue added to the seminal dose. Fertility did not differ between the three groups (control: 80.6%, group 2: 82.8%, group 3: 73.3%). In a second experiment, a large-scale field trial was conducted to test the use of 25 microg of the GnRH analogue [des-Gly10, D-Ala6]-LHRH ethylamide delivered in the seminal dose (n = 270) against 20 microg of gonadorelin administered intramuscularly. Fertility was higher (p < 0.05) when ovulation was induced by intravaginal administration of the GnRH agonist (91.1% vs 85.6%). Prolificacy or mortality at birth was never affected by the ovulation induction treatments. In a third experiment, two groups of does [control group (n = 39): ovulation was induced using 20 microg of gonadorelin administered intramuscularly; treatment group (n = 40): ovulation was induced using 25 microg of [(des-Gly10, D-Ala6)-LHRH ethylamide added to the seminal dose] were inseminated at 42-day intervals for five successive AI cycles, to test the response to the GnRH agonist after repeated intravaginal administration to the same animals. Fertility and prolificacy were not influenced by the ovulation induction treatment neither there was an interaction between treatment and parity. The last experiment was aimed to determine whether it could be possible to add the GnRH agonist to the semen in the AI Center, just after semen collection and dilution, or it would have to be added in the farm, immediately before AI. Kindling rates did not significantly differ when ovulation was induced by intramuscular injection of gonadorelin (84.5%) or when the GnRH agonist was added to the seminal dose just at the moment (93.8 %) or 24 h before AI (90.4 %), but it was significantly lower when the hormone was added to the semen 32 h before AI (76.3 %). Prolificacy, however, was not influenced by the ovulation induction treatment.
