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1.
J. physiol. biochem ; 68(2): 237-245, jun. 2012.
Artigo em Espanhol | IBECS | ID: ibc-122343

RESUMO

In view of the significant health impact of oxidative stress and apoptosis dysfunction, and further, because of suggestions that administration of antioxidants might reduce apoptosis rate through up-regulation of body antioxidant defense systems, therefore the purpose of this study was to compare the effect of buffalo (Bubalus bubalis) pineal proteins (PP at 100 ìg/kg BW, i.p.) with melatonin (MEL at 10 mg/kg BW, i.p.) on blood (erythrocytes) antioxidant defense system and apoptosis in isolated peripheral blood lymphocytes of female Wistar albino rats. The cell viability index (%) and apoptosis index (%), which are directly related to the apoptosis rate of the cells, were used as dependent measures for inferring PP and MEL activity. The total cell viability index did not differ between rats treated with MEL and PP from control animals. The percentage of apoptotic cell death through fluorescence microscopy also did not change in MEL and PP groups as compared with control. DNA fragmentation as an index of apoptosis was detected with propidium iodide staining and assessed by flow cytometry. Pineal proteins and MEL administration caused significant (p < 0.05) reduction in lipid peroxidation and increased level of catalase, superoxide dismutase, glutathione peroxidase, and glutathione in erythrocytes as compared with control. Interestingly, we did not observe increase in the non-viable cells and percentage of apoptotic cell death in PP-treated group, controls or in animals in which MEL had been administered. Therefore, the present study confirmed the up-regulation of erythrocytes (blood) antioxidant defense systems and absence of adverse effect on rate of apoptosis in PP and MEL-administered rats under absence of stress or toxicant exposure. Hence, these test agents can be tested for further therapeutic values against adverse apoptosis rate under stress or toxicants exposures (AU)


Assuntos
Animais , Ratos , Melatonina/farmacocinética , Apoptose/fisiologia , Antioxidantes/fisiologia , Hormônios Neuro-Hipofisários/farmacocinética , Elementos de Resposta Antioxidante/fisiologia , Substâncias Protetoras/farmacocinética , Modelos Animais de Doenças , 5-Metoxitriptamina/farmacocinética
2.
J. physiol. biochem ; 66(1): 7-13, mar. 2010.
Artigo em Inglês | IBECS | ID: ibc-122844

RESUMO

No disponible


In rats, hypophysectomy (HYPOX) or neurointermediate pituitary lobectomy (NIL) reduce humoral and cell-mediated immune responses. However, to our knowledge, the differences in the effects of anterior versus posterior pituitary hormones on the immune responses have not been studied to date. We compared in rats, the effects of sham surgery (SHAM), HYPOX, and NIL on humoral immune responses to T cell-independent (TI) type 1 antigen DNP-LPS and to TI type 2 antigen DNP-FICOLL, as well as to T cell-dependent (TD) antigens ovalbumin (OVA) and bovine serum albumin(BSA). The results showed that: (1) both HYPOX and NIL induced a similar and significant decrease in IgM responses towards TI-1 antigens, (2) NIL but not HYPOX induced a decreased IgM response to TI-2 antigens, and (3) both HYPOX and NIL induced similar and significant decrease in IgG responses to TI-2 antigens. Compared with the SHAM group, IgM responses to both TD antigens did not change in HYPOX and NIL animals, whereas the IgG responses to OVA and BSA significantly decreased in HYPOX and NIL animals. These results indicate that hormones of the anterior and posterior pituitary play their own role in the regulation of humoral immune responses (AU)


Assuntos
Animais , Ratos , Hipofisectomia , Antígenos de Histocompatibilidade Classe II/análise , Hormônios Adeno-Hipofisários , Hormônios Neuro-Hipofisários , Ovalbumina/farmacocinética , Soroalbumina Bovina/farmacocinética
3.
Endocrinol. nutr. (Ed. impr.) ; 52(supl.3): 7-10, oct. 2005. tab
Artigo em Espanhol | IBECS | ID: ibc-135329

RESUMO

La acromegalia es una enfermedad producida por la hipersecreción crónica e inapropiada de la hormona del crecimiento (GH) que se inicia después del cierre de los cartílagos de crecimiento. La función hipofisaria normal está sometida a un estrecho control hipotalámico y de retroalimentación negativa que comprende la propia GH, el factor de crecimiento similar a la insulina tipo I y las hormonas hipotalámicas: la hormona liberadora de GH, que potencia la secreción de GH y su transcripción génica, y la somatostatina, que inhibe su secreción y tiene escaso efecto en su síntesis. El papel de la nueva hormona ghrelina está aún por dilucidar. La acromegalia está causada en el 98% de los casos por un tumor secretor de GH localizado en la hipófisis, mientras que las causas extrahipofisarias son muy raras. La patogenia de estos tumores hipofisarios sigue siendo en gran parte desconocida y en su origen se han incluido tanto un defecto primario de la célula somatotropa hipofisaria como alteraciones en el control hipotalámico de la secreción de GH. A pesar de que se han descrito defectos moleculares asociados a estos adenomas, la base molecular de la tumorogenia hipofisaria está por definir (AU)


Acromegaly is a disease due to an inadequate and chronical hypersecretion of growth hormone initiated after epiphyseal fusion. Normal pituitary function is subjected to a strict hypothalamic control and negative feedback including GH, IGF-I and hypothalamic hormones: GH-RH improves GH secretion and its gene transcription while somatostatin inhibits its secretion and has a limited effect on its synthesis. The role of the new hormone, ghrelin, is yet to be clarified. In 98% of cases acromegaly is due to a GH- secreting tumour located in the pituitary gland. Extrapituitary causes are very uncommon. The pathogenesis of these pituitary tumours is, in its majority, unknown, involving in its origin a primary defect of pituitary somatotroph cell and also disturbances in the hypothalamic control of GH secretion. Despite the fact that molecular defects associated with these adenomas have been described, the molecular basis of pituitary tumorigenesis remains to be elucidated (AU)


Assuntos
Humanos , Masculino , Feminino , Acromegalia/etiologia , Acromegalia/patologia , Neoplasias Hipofisárias/etiologia , Neoplasias Hipofisárias/patologia , Adenoma/etiologia , Adenoma/patologia , Perda de Heterozigosidade , Perda de Heterozigosidade/imunologia , Perda de Heterozigosidade/fisiologia , Hormônio do Crescimento/uso terapêutico , Hipófise/patologia , Neuro-Hipófise/patologia , Hormônios Adeno-Hipofisários , Hormônios Neuro-Hipofisários/uso terapêutico , Síndromes Neoplásicas Hereditárias/etiologia , Complexo de Carney/complicações , Complexo de Carney/etiologia , Complexo de Carney/patologia
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