The aim of the present study was to evaluate the in vitro and in vivo effect of the addition of superoxide dismutase (SOD) and reduced glutathione (GSH) to ram semen freezing extender. Significant differences (p < 0.05) were detected between groups regarding total motility (TM), straightness (STR) and wobble (WOB), for which the GSH 7 mM group had lesser TM and better STR than the other groups and the GSH 5 and 7 mM groups had higher wobble values than the control, SOD 25 and 100 U/ml groups. The ultrastructural analysis revealed that the acrosome was better preserved after freezing in the SOD 100 U/ml and GSH 2 and 5 mM (p < 0.05) groups than the other groups, whereas mitochondria in both the control group and the 7 mM GSH group suffered the greatest damage. The plasma membrane remained preserved after freezing, regardless of the group. For in vivo fertilization, the SOD group achieved better results than the GSH group (p > 0.05). It can therefore be concluded that the addition of SOD 100 U/ml and GSH 2 and 5 mM preserves the acrosome integrity of frozen ram spermatozoa, while the addition of SOD 100 U/ml to Tris egg-yolk extender offers protection to the membranes of sperm cells after thawing.

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Early interactions between blood-stage Plasmodium parasites and cells of the innate immune system are very important in shaping the adaptive immune response to malaria, and a number of studies have suggested that DC are responsible for this phenomenon. Therefore, we examined the capacity of murine BM-derived DC to internalize parasites, be activated and produce cytokines upon in vitro interaction with murine erythrocytes infected with two different strains of rodent malaria parasites (Plasmodium berghei and Plasmodium chabaudi chabaudi). We show that the increased expression of MHC class II and co-stimulatory molecules and increased production of cytokines by DC following Plasmodium infection involves internalization of infected RBC. Such DC activation not only requires direct cell-to-cell contact and internalization of infected RBC by DC but also involves TLR4, TLR9, MyD88 and signaling via NF-jB; however, TLR involvement in survival to Plasmodium infection was found to be negligible.Key words: Cell activation . Cell surface molecules . DC . Parasitic-protozoan . Phagocytosis Supporting Information available online IntroductionMalaria remains an enormous burden for the developing world, in terms of infection, morbidity and mortality. Plasmodium falciparum is the most common cause of malaria in humans, however, the difficulties in studying the human responses to infection has led to the use of experimental models of rodent malaria. Although these models do not accurately reflect all aspects of human disease, they have many characteristics in common with the human immune response to P. falciparum. Despite the use of these models and extensive research, a vaccine is not yet available and many anti-malarial drugs are increasingly ineffective due to drug resistance. A better understanding of the mechanisms that induce protective immunity to malaria infection will help to identify the strategies for vaccine development and immunotherapy.Early interactions between blood-stage parasites and cells of the innate immune system are thought to be important in shaping the adaptive immune response to malaria. Several studies using mouse models of malaria have provided evidence for an important role of DC in inducing protective immunity to blood-stage malaria [1][2][3][4][5]. Murine DC activated in vitro and in vivo by rodent Plasmodium parasites are able to express co-stimulatory molecules and produce pro-inflammatory cytokines to stimulate type 1 immune responses that are protective against malaria infection [1,4,6]. However, the interactions between the cell and the parasite that led to this activation remain poorly understood. In the present study we describe some factors involved in the interaction of DC with mouse malaria parasites that are required for the activation of the cell by the parasite.To detect microbial infection, the immune system utilizes receptors such as TLR to recognize invariant molecular structures of related microbes. TLR activation results in rapid induction of innate defense programs and ultimately...