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1.
Anim Reprod Sci ; 210: 106195, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31635777

RESUMO

During cold storage stallion spermatozoa experience undergo oxidative stress, which can impair sperm function and fertilizing capacity. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) are the main endogenous enzymatic antioxidants in stallion seminal plasma, and counteract reactive oxygen species. Semen dilution reduces the endogenous antioxidant concentrations. The aim of this study was to investigate whether addition of 15 IU/mL each of SOD, CAT, and GPX to diluted stallion semen would ameliorate a reactive oxygen-mediated decrease in semen quality during 72 h of storage at 5 °C. Ejaculates (n = 7) were divided in two aliquots and diluted in INRA 96 without (control) or with addition of antioxidants. Semen analysis was performed at the time of dilution and every 24 h during chilled storage. Antioxidant supplementation completely inhibited the storage-dependent increase in activated caspase 3 (P < 0.05). Concomitantly, the antioxidant-supplemented samples had a greater percentage of viable, motile and rapidly moving sperm than control samples after 72 h storage (P < 0.05). The DNA damage, as evaluated by TUNEL assay and SCSA, increased with storage time (P < 0.05). Antioxidant supplementation did not prevent, but did significantly reduce the increase in DNA strand breakage. The results indicate part of the intrinsic apoptotic pathway leading to effector caspase activation was inhibited, although an activation of molecules with endonuclease activity still occurred. In conclusion, adding equal concentrations of SOD, CAT and GPX to a semen extender suppressed caspase-3 activation and improved preservation of stallion sperm motility and viability during 72 h of storage at 5 °C.


Assuntos
Catalase/farmacologia , Glutationa Peroxidase/farmacologia , Cavalos/fisiologia , Preservação do Sêmen/veterinária , Sêmen/efeitos dos fármacos , Superóxido Dismutase/farmacologia , Animais , Catalase/administração & dosagem , Glutationa Peroxidase/administração & dosagem , Masculino , Análise do Sêmen/veterinária , Motilidade dos Espermatozoides , Espermatozoides/fisiologia , Superóxido Dismutase/administração & dosagem
2.
J Matern Fetal Neonatal Med ; 22 Suppl 3: 57-61, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19718579

RESUMO

Hypoxia-ischemia (H-I) constitutes the main phenomenon responsible for brain-blood barrier permeability modifications leading to cerebral vascular auto-regulation loss in newborns. Hypotension, cerebral ischemia, and reperfusion are the main events involved in vascular auto-regulation loss leading to cell death and tissue damage. Reperfusion could be critical since organ damage, particularly of the brain, may be amplified during this period. An exaggerated activation of vasoactive agents, of calcium mediated effects could be responsible for reperfusion injury (R-I), which, in turns, leads to cerebral hemorrhage and damage. These phenomena represent a common repertoire in newborns complicated by perinatal acute or chronic hypoxia treated by risky procedures such as mechanical ventilation, nitric oxide supplementation, brain cooling, and extracorporeal membrane oxygenation (ECMO). Despite accurate monitoring, the post-insult period is crucial, as clinical symptoms and standard monitoring parameters may be silent at a time when brain damage is already occurring and the therapeutic window for pharmacological intervention is limited. Therefore, the measurement of circulating biochemical markers of brain damage, such as vasoactive agents and nervous tissue peptides is eagerly awaited in clinical practice to detect high risk newborns. The present review is aimed at investigating the role of biochemical markers such as adrenomedullin, a vasoactive peptide; S100B, a calcium binding protein, activin A, a glycoprotein, in the cascade of events leading to I-R injury in newborns complicated by perinatal asphyxia.


Assuntos
Ativinas/sangue , Lesões Encefálicas/sangue , Hipóxia-Isquemia Encefálica/sangue , Fatores de Crescimento Neural/sangue , Proteínas S100/sangue , Adrenomedulina/sangue , Asfixia Neonatal/complicações , Biomarcadores/sangue , Lesões Encefálicas/diagnóstico , Lesões Encefálicas/etiologia , Humanos , Hipóxia-Isquemia Encefálica/etiologia , Recém-Nascido , Subunidade beta da Proteína Ligante de Cálcio S100
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