The objective of this study, comprising two trials, was to evaluate the effect of a gonadotropin-releasing hormone (GnRH [corrected] vaccine Improvac; Pfizer Ltd) in a sample of the Swedish pig population. The pigs (n = 120) were assigned to three groups: control (entire male pigs), surgical castration and immunization against GnRH. Surgically castrated pigs did not express detectable levels of either testosterone or estrone sulphate (E1S) in plasma, or androstenone in fat and had lower skatole and indole levels in fat than entire male pigs. Immunization significantly reduced testes weight and bulbourethral gland length, plasma levels of the testicular hormones testosterone and E1S, and fat levels of androstenone, skatole and indole. Skatole levels in plasma were significantly lower than in entire male pigs in the second trial, but not in the first due to overall low skatole levels. All immunized pigs and surgically castrated pigs expressed skatole concentrations in fat below the level of 0.2 microg/g, above which meat is regarded as tainted. In contrast, eight entire male pigs exceeded this level. Indole levels in plasma from immunized pigs were lower than those from entire male pigs. Surgical castration caused lower daily weight gain in the suckling period compared with piglets raised intact, whereas in the post-weaning period no difference was observed. Immunization resulted in higher feed intake and daily weight gain after the second injection. The estimated lean meat content was improved in comparison with the castrated pigs, but was lower than for entire male pigs. Dressing percentage was lower in immunized pigs than in surgically castrated and entire male pigs. The frequency of skin damage did not differ between immunized and entire male pigs or between immunized and surgically castrated pigs.

Androstenone is one of the main compounds responsible for boar taint, and 3beta-hydroxysteroid dehydrogenase (3betaHSD) might be involved in its metabolism. In this study, the gene expression of 3betaHSD and 17beta-hydroxysteroid dehydrogenase (17betaHSD) were determined by real-time PCR analysis and related to the concentrations of androstenone, testosterone, and estrone sulphate (E1S). The experiments were performed on gonadally intact male pigs classified based on high or low fat androstenone concentrations, as predetermined by HPLC, as well as on immunocastrated and surgically castrated male pigs. The male pigs with high androstenone concentrations in fat had low 3betaHSD gene expression in liver and testis. Moreover, the 17betaHSD gene expression in liver, but not in testis, varied negatively with fat androstenone concentrations. Immunocastrated and surgically castrated male pigs had nondetectable concentrations of fat androstenone and plasma testosterone and E1S, and the castration procedure induced a significant increase of 3betaHSD and 17betaHSD gene expression. The mRNA expression was generally much greater from the 3betaHSD than from the 17betaHSD gene. Furthermore, fat androstenone was negatively correlated with liver 3betaHSD gene expression (Pearson correlation, r = -0.69; P < 0.05), and the 17betaHSD gene expression in liver was negatively correlated with plasma E1S (r = -0.95; P < 0.001), indicating an important role of liver 17betaHSD in the estrogen metabolism of gonadally intact male pigs. Another strong correlation was found between 3betaHSD and 17betaHSD gene expression in liver of the gonadally intact male pigs (r = 0.86; P < 0.01), possibly reflecting similar regulation mechanisms of these genes.

The effect of Human chorionic gonadotropin (hCG) stimulation on the concentrations of free and conjugated androstenone in plasma was studied in 34 crossbred entire male pigs (Landrace x Swedish Yorkshire). Seventeen pigs were treated with hCG 4 days prior to slaughter and the remaining pigs were treated with sterile saline and served as controls. Blood samples were taken prior to hCG or saline injection and on the day before slaughter and analysed for concentrations of free and conjugated androstenone. Testicular tissue samples were taken at slaughter and analysed for the levels of cytochrome b5 (cyb5) protein. Here we have demonstrated for the first time that hCG stimulation causes an increase in the plasma levels of both free and conjugated androstenone. Not all animals responded in the same way to hCG treatment regarding levels of free and conjugated androstenone demonstrating that individual animals can have differences in their capacity to produce free and conjugated androstenone. We suggest that hCG treatment is a good way to determine the potential for androstenone conjugation when androstenone synthesis in the testis is high. The levels of cyb5 protein in the testis were slightly related (r=0.41, p < 0.10) to free androstenone levels in the pigs after hCG administration, although levels of cyb5 protein were not affected by hCG treatment.