RESUMO
Although boar semen productivity is affected by seasonality, its effects are not equal among different regions which raise concerns regarding the profitability of boar stud farms. Therefore, the goals of this study were (i) to evaluate the seasonal effect on semen production in a commercial boar stud farm located in a subtropical climate region and (ii) to verify whether the activities of superoxide dismutase and glutathione peroxidase in spermatozoa and seminal plasma were associated with seminal traits of fresh and cooled semen. Nine boars were collected twice per season, and routine seminal parameter analyses were performed together with superoxide dismutase and glutathione peroxidase activities in seminal plasma and spermatozoa. Despite a reduction in sperm concentration in spring and summer, most seminal parameters were constant year-round. Temperature-humidity index was higher in the summer compared to spring, autumn and winter (p < .05). Superoxide dismutase activity in spermatozoa was increased in summer compared to autumn and winter (p < .05). The activities of both enzymes in seminal plasma and spermatozoa glutathione peroxidase remained unaltered throughout the seasons. In conclusion, seasonality showed little influence in overall boar seminal parameters despite microclimatic differences among seasons, and spermatozoa collected during summer increased superoxide dismutase activity.
RESUMO
High accumulation of D-2-hydroxyglutaric acid (D-2-HG) is the biochemical hallmark of patients affected by the inherited neurometabolic disorder D-2-hydroxyglutaric aciduria (D-2-HGA). Clinically, patients present neurological symptoms and basal ganglia injury whose pathophysiology is poorly understood. We investigated the ex vivo effects of intrastriatal administration of D-2-HG on important parameters of redox status in the striatum of weaning rats. D-2-HG in vivo administration increased malondialdehyde (MDA) and carbonyl formation (lipid and protein oxidative damage, respectively), as well as the production of reactive nitrogen species (RNS). D-2-HG also compromised the antioxidant defenses by decreasing reduced glutathione (GSH) concentrations, as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Increased amounts of oxidized glutathione (GSSG) with no significant alteration of total glutathione (tGS) were also found. Furthermore, D-2-HG-induced lipid oxidation and reduction of GSH concentrations and GPx activity were prevented by the N-methyl-d-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) and the nitric oxide synthase (NOS) inhibitor N(ω)-nitro-l-arginine methyl ester (l-NAME), suggesting the participation of NMDA receptors and nitric oxide derivatives in these effects. Creatine also impeded D-2-HG-elicited MDA increase, but did not change the D-2-HG-induced diminution of GSH and of the activities of SOD and GPx. We also found that DCFH oxidation and H2O2 production were not altered by D-2-HG, making unlikely an important role for reactive oxygen species (ROS) and reinforcing the participation of RNS in the oxidative damage and the reduction of antioxidant defenses provoked by this organic acid. Vacuolization, lymphocytic infiltrates and macrophages indicating brain damage were also observed in the striatum of rats injected with D-2-HG. The present data provide in vivo solid evidence that D-2-HG disrupts redox homeostasis and causes histological alterations in the rat striatum probably mediated by NMDA overstimulation and RNS production. It is therefore presumed that disturbance of redox status may contribute at least in part to the basal ganglia alterations characteristic of patients affected by D-2-HGA.
