RESUMO
The objective of this work was to evaluate the effect of the association of the antioxidant resveratrol with sucrose in a vitrification protocol of ovarian tissue in cows, on the morphology of preantral follicles. Ten ovaries of cows were used, collected in local slaughterhouses, fragmented and distributed to the following treatments: fresh control (Co); toxicity (T); (T0) zero toxicity/ only with base vitrification solution (SBV), (TS) toxicity with SBV plus sucrose, (TR) toxicity with SBV plus resveratrol, (TS+R) toxicity with SBV and sucrose plus resveratrol; and for glazing (V); (VS) vitrification with SBV and sucrose, (VR) vitrification with SBV and resveratrol, (VS+R) vitrification with SBV and sucrose plus resveratrol. Preantral follicles were quantified and classified according to morphology into normal and degenerated. The mean percentages between normal and degenerated follicles did not differ (p>0.05) in the following percentages, normal 51.4% and degenerated 48.60%. In the toxicity test there was a difference (p0.05), demonstrating that the vitrification technique is efficient, but the concentration of cryoprotectants used needs to be re-evaluated. Concluding that the natural antioxidant association resveratrol to sucrose in vitrification and rewarming protocols contributes with reservations for the morphological preservation of preantral follicles in cows.
Assuntos
Animais , Feminino , Bovinos , Ovário/citologia , Sacarose/uso terapêutico , Resveratrol/uso terapêutico , Folículo Ovariano/anatomia & histologia , VitrificaçãoRESUMO
Thiamine deficiency (TD) produces severe neurodegenerative lesions. Studies have suggested that primary neurodegenerative events are associated with both oxidative stress and inflammation. Very little is known about the downstream effects on intracellular signaling pathways involved in neuronal death. The primary aim of this work was to evaluate the modulation of p38MAPK and the expression of heme oxygenase 1 (HO-1) in the central nervous system (CNS). Behavioral, metabolic, and morphological parameters were assessed. Mice were separated into six groups: control (Cont), TD with pyrithiamine (Ptd), TD with pyrithiamine and Trolox (Ptd + Tr), TD with pyrithiamine and dimethyl sulfoxide (Ptd + Dmso), Trolox (Tr) and DMSO (Dmso) control groups and treated for 9 days. Control groups received standard feed (AIN-93M), while TD groups received thiamine deficient feed (AIN-93DT). All the groups were subjected to behavioral tests, and CNS samples were collected for cell viability, histopathology and western blot analyses. The Ptd group showed a reduction in weight gain and feed intake, as well as a reduction in locomotor, grooming, and motor coordination activities. Also, Ptd group showed a robust increase in p38MAPK phosphorylation and mild HO-1 expression in the cerebral cortex and thalamus. The Ptd group showed a decreased cell viability, hemorrhage, spongiosis, and astrocytic swelling in the thalamus. Groups treated with Trolox and DMSO displayed diminished p38MAPK phosphorylation in both the structures, as well as attenuated thalamic lesions and behavioral activities. These data suggest that p38MAPK and HO-1 are involved in the TD-induced neurodegeneration in vivo, possibly modulated by oxidative stress and neuroinflammation.
Assuntos
Encéfalo/metabolismo , Heme Oxigenase-1/metabolismo , Proteínas de Membrana/metabolismo , Deficiência de Tiamina/fisiopatologia , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Comportamento Animal/fisiologia , Peso Corporal/fisiologia , Encéfalo/patologia , Sobrevivência Celular/fisiologia , Cromanos/farmacologia , Dimetil Sulfóxido/farmacologia , Ingestão de Alimentos/fisiologia , Inflamação/etiologia , Inflamação/fisiopatologia , Masculino , Camundongos , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo/fisiologia , Piritiamina , Deficiência de Tiamina/induzido quimicamente , Deficiência de Tiamina/complicações , Deficiência de Tiamina/patologiaRESUMO
Thiamine is an essential cofactor for several cellular functions. Your deficiency results in important neurological disorders, with mechanisms and lesions not fully understood. The purpose of this work was to evaluate a thiamine deficiency through the model of oral administration of amprolium in mice. The animals, treated for 20 or 80 days, received amprolium in drinking water at doses of 10, 20, and 30 mg/mL (deficient groups A, B, and C, respectively). Deficient groups A and B showed reduction in body weight gain and performance changes in the open field (decreased distance and rearing, and increased grooming) and rotarod (reduced latency to fall) behavioural tests, when treated for 80 days. However, no histological changes were observed in the central nervous system. Moreover, group B animals exposed to amprolium developed proteinuria, with moderate tubular nephrosis, at 80 days. At the highest dose (group C) there was no interest to drink water. The data suggest that the use of oral amprolium in mice may be an interesting and viable model, when using adequate exposure times and doses. The amprolium induces thiamine deficiency progressively and moderately, which may be potentially useful for disturbed pathogenesis studies.(AU)