Fatty acid profile, oxidative stability of pork lipids and meat quality indicators are not affected by birth weight.

The aim of this study was to investigate whether fatty acid (FA) profile, oxidative stability of lipids and other meat quality traits differed between high (HW: 1.8 to 2.2 kg) and low (LW: 0.8 to 1.2 kg) birth weight piglets. Forty new-born male pigs (n=20 HW, n=20 LW) were reared in separate pens until the finishing period, when they were slaughtered at 150 days of age, and pH and temperature were measured in the carcass. Afterwards, the Longissimus dorsi muscle was excised from the carcass, and samples were collected for subsequent meat quality analyses (thaw loss, cooking loss, shear force, chemical analysis and sensory analysis for tenderness). Birth weight had minor impacts on meat quality traits, which were limited to higher shear force in the LW group (P<0.01). Chemical components (moisture, protein, fat, ash), cholesterol levels and lipid oxidation (thiobarbituric acid-reactive substances) were not affected by birth weight (P>0.05). FA profile and the amount of saturated, monounsaturated and polyunsaturated fatty acids were similar, but HW pigs had higher atherogenic index than their LW counterparts (P<0.01). Notwithstanding the higher shear force presented by the lower birth weight pigs, in the sensory test, the panelists did not detect any differences in the tenderness of pork from HW and LW animals. Therefore, our results suggest that low birth weight has minimal impact on meat quality.

Lipid bodies: Structural markers of inflammatory macrophages in innate immunity.

OBJECTIVE AND DESIGN: The correlation between innate immune responses and formation of cytoplasmic lipid bodies (LBs) was investigated in vivo in inflammatory macrophages from rats infected with Trypanosoma cruzi, the intracellular parasite which causes Chagas' disease. MATERIAL AND METHODS: We used an experimental model of high-dose irradiation prior to infection, which depletes the humoral and cellular immune responses except for the phagocytic activity of macrophages. Rats, irradiated or not, were infected with T. cruzi and macrophages from different origins (peritoneum, heart, uterus) were studied by transmission electron microscopy (TEM). RESULTS: As documented by quantitative TEM, innate immune responses induced prominent formation, structural changes and intracellular interactions of LBs. LBs significantly increased their size and changed their osmiophilia in response to both infection alone and when macrophages were challenged with irradiation-induced increased parasite load. Remarkably, a consistent LB-phagolysosome association was identified. LBs were surrounding, attached to or internalized by phagolysosomes. CONCLUSIONS: We demonstrated that LBs are dynamic organelles notably involved in the host response to acute T. cruzi infection, an event that may be important for pathogen control during innate immunity. Our findings highlight LBs as structural markers of the innate immune responses in phagocytic cells.

Development of germ cell transplants: morphometric and ultrastructural studies.

Mouse-to-mouse transplants were studied at 10 min, 9 h, 24 h, 1 week, 1 month, 2 months, and 3 months post-transplantation. Data from a previous light microscope study were confirmed and extended using morphometric and ultrastructural techniques. As soon as 10 min after introduction of the germ cells from one mouse into the tubule lumen of a recipient mouse they developed relationships with small Sertoli cell processes. The extent of this surface-to-surface relationship increased in animals sacrificed up to 1 week post-transplantation. Most transplanted germ cells retained the characteristics of the donor germ cells after they had been isolated and pelleted. Nearly all transplanted cells eventually underwent phagocytosis by the recipient Sertoli cells. The presence of small apparent clones of germ cells after 1 week of transplantation indicated that some germ cells may divide and survive for short periods within the epithelium. No discernible qualitative subcellular changes in the host Sertoli cell accompanying the development of transplant spermatogenesis were noted. Macrophages were present in the region of the boundary tissue between myoid cells and appeared to increase in number in the peritubular tissue of transplanted testes. Images suggest that they migrated into the tubule to gain entrance to the lumen and there take on the form of activated macrophages. Some macrophages phagocytose sperm at 2 months and 3 months post-transplantation. A testis weight increase previously demonstrate to occur at 24 h post-introduction of germ cells was found to be due to an increase in the volume of the tubular lumen. The increase of lumen size at 24 h was not related to the volume of the injected material. It is suggested that the presence of injected cells, likely germ cells, in the tubule lumen stimulated increased secretion by the Sertoli cell.

Development of germ cell transplants in mice.

Development of spermatogonial transplants was studied by using 5- to 6-wk-old histocompatible mice as cell donors and sterile (W-locus) mice as recipients. Groups of animals transplanted with germ cell suspensions were killed at 10 min, 9 h, 24 h, 1 wk, 1 mo, 2 mo, and 3 mo along with age-matched "start" and "end" W-locus controls. Weight of testes increased significantly at 24 h through 3 mo after germ cell transplantation, suggesting that the infused cells quickly stimulated organ function. Small clones of young spermatocytes were evident at 1 mo and sperm at 2 mo. The percentage of tubular profiles containing active spermatogenesis originating from spermatogonia increased with time (0.8% at 1 mo, 8.9% at 2 mo, and 28.2% at 3 mo). Most transplanted germ cells were eliminated from the seminiferous epithelium through phagocytosis by Sertoli cells that occurred primarily before 1 wk, although some pachytene cells were able to proceed through meiosis by 1 wk. A variety of abnormal features are described that characterize developing spermatogenesis in the transplanted testis. Spermatogenesis improved quantitatively and qualitatively with time although released sperm were frequently engulfed by intratubular macrophages and Sertoli cells. A quantitative analysis of spermatogenesis from transplanted germ cells will serve as a basis for improving spermatogonial transplant efficiency.

Hormonal regulation of spermatogenesis in the hypophysectomized rat: quantitation of germ-cell population and effect of elimination of residual testosterone after long-term hypophysectomy.

Spermatogenesis continues after long-term hypophysectomy (Hx), but massive cell degeneration prevents seminiferous tubules from attaining the full complement of cells. One objective of this study was to determine the vulnerable sites for completion of spermatogenesis in long-term Hx rats. It is now known that Leydig cells continue to secrete small amounts of androgen after Hx. A second objective was to determine the cellular sites that are maintained by residual androgen secreted by Leydig cells post-Hx. Two groups of adult animals were utilized. Both groups were Hx for 36 days, but one group of rats received the androgen antagonist flutamide during the 26th through the 36th day of Hx (10 days). Germ-cell numbers were quantified using a method that allowed their expression as numbers of cells present per hour of development. In the long-term Hx rat, the germ-cell population increased to preleptotene, but the divisions that led to preleptotene were inefficient due to cell degeneration. Subsequent to preleptotene, there was a gradual loss in cells such that there were few germ cells remaining by steps 9-13. Flutamide given to Hx rats did not result in a significant difference in the numbers of intermediate and type B spermatogonia or significant differences in progenitor cells. A significant and major depression of cell numbers in Hx-flutamide-treated rats occurred in the cell division of type B spermatogonia to form preleptotene spermatocytes. There was a less dramatic, although significant, depression of cell numbers in Hx-flutamide-treated animals that occurred from preleptotene until late pachytene as well as an increased loss of round spermatids at midcycle (step 5-6). These data demonstrate that cell loss after long-term Hx occurs at numerous phases of spermatogenesis. The data also demonstrate that the presence of residual androgen action after long-term Hx results in enhanced germ-cell survival. Although the major blockage in cell viability occurs at midcycle steps in the long-term Hx rat, there are several other hormone-sensitive phases of spermatogenesis.