Scanning electron microscopy of the superficial pineal gland of the 15-day-old rat (Rattus norvegicus)

The presence of a cortex and medulla in the superficial pineal gland has been a controversial point in the morphology of this structure in mammals. The published reports indicate contradictory data especially in rodents. In this study the pineal gland of 15-day-old male rats (Rattus norvegicus) were studied, using scanning electron microscopy, in an attempt to determine whether or not a cortex and medulla are apparent in the pineal gland of young rats. The superficial pineal gland of the 15-day-old rat exhibited both a cortex and a medulla; these areas exhibited different structural organizations. The cortex had a thickness of 40-80 ?m and the cells did not show a particular arrangement. The center of the gland was composed of a medulla, which had a width of 1000-1200 ?m, and consisted of cells arranged in cords; its morphology was distinctly different from that of the cortex

Cellular and biochemical actions of melatonin which protect against free radicals: Role in neurodegenerative disorders

Molecular oxygen is toxic for anaerobic organisms but it is also obvious that oxygen is poisonous to aerobic organisms as well, since oxygen plays an essential role for inducing molecular damage. Molecular oxygen is a triplet radical in its ground-stage (.O-O.) and has two unpaired electrons that can undergoes consecutive reductions of one electron and generates other more reactive forms of oxygen known as free radicals and reactive oxygen species. These reactants (including superoxide radicals, hydroxyl radicals) possess variable degrees of toxicity. Nitric oxide (NO•) contains one unpaired electron and is, therefore, a radical. NO• is generated in biological tissues by specific nitric oxide synthases and acts as an important biological signal. Excessive nitric oxide production, under pathological conditions, leads to detrimental effects of this molecule on tissues, which can be attributed to its diffusion-limited reaction with superoxide to form the powerful and toxic oxidant, peroxynitrite. Reactive oxygen and nitrogen species are molecular "renegades"; these highly unstable products tend to react rapidly with adjacent molecules, donating, abstracting, or even sharing their outer orbital electron(s). This reaction not only changes the target molecule, but often passes the unpaired electron along to the target, generating a second free radical, which can then go on to react with a new target amplifying their effects. This review describes the mechanisms of oxidative damage and its relationship with the most highly studied neurodegenerative diseases and the roles of melatonin as free radical scavenger and neurocytoskeletal protector. © 2008 Bentham Science Publishers Ltd

Nano and micro reoriented domains and their relation with the crystal structure in the new Fe 1.5Zn 1.5B 7O 13Cl boracite

Molecular oxygen is toxic for anaerobic organisms but it is also obvious that oxygen is poisonous to aerobic organisms as well, since oxygen plays an essential role for inducing molecular damage. Molecular oxygen is a triplet radical in its ground-stage (.O-O.) and has two unpaired electrons that can undergoes consecutive reductions of one electron and generates other more reactive forms of oxygen known as free radicals and reactive oxygen species. These reactants (including superoxide radicals, hydroxyl radicals) possess variable degrees of toxicity. Nitric oxide (NO ) contains one unpaired electron and is, therefore, a radical. NO is generated in biological tissues by specific nitric oxide synthases and acts as an important biological signal. Excessive nitric oxide production, under pathological conditions, leads to detrimental effects of this molecule on tissues, which can be attributed to its diffusion-limited reaction with superoxide to form the powerful and toxic oxidant, peroxynitrite. Reactive oxygen and nitrogen species are molecular "renegades"; these highly unstable products tend to react rapidly with adjacent molecules, donating, abstracting, or even sharing their outer orbital electron(s). This reaction not only changes the target molecule, but often passes the unpaired electron along to the target, generating a second free radical, which can then go on to react with a new target amplifying their effects. This review describes the mechanisms of oxidative damage and its relationship with the most highly studied neurodegenerative diseases and the roles of melatonin as free radical scavenger and neurocytoskeletal protector. " 2008 Bentham Science Publishers Ltd.",,,,,,"10.2174/157015908785777201",,,"http://hdl.handle.net/20.500.12104/39935","http://www.scopus.com/inward/record.url?eid=2-s2.0-53249154949&partnerID=40&md5=b74f0d9baf3097a5f5ac2d4ef75286c6",,,,,,"3",,"Current Neuropharmacology",,"20

Functional disorders of F0F1-ATPase in submitochondrial particles obtained from platelets of patients with a diagnosis of probable Alzheimer's disease [Alteraci�n funcional de la F0F1-ATPasa en part�culas submitocondriales obtenidas de plaquetas de pacientes con diagn�stico de enfermedad de Alzheimer probable]

Introduction. Recent studies indicate that decreased energy generation by mitochondria is a feature that is common across neurodegenerative diseases. Patients and methods. In order to obtain direct evidence that mitochondrial functioning is altered, we measured the hydrolytic activity of F 0F1-ATPase and its capacity to generate a stable proton gradient in submitochondrial particles in 29 patients diagnosed with probable Alzheimer's disease (AD). Submitochondrial particles were obtained from platelets of patients with a diagnosis of probable AD and from clinically healthy controls. Results. Data revealed that the hydrolytic activity of F 0F1-ATPase increases significantly in patients with probable AD (41.7 � 4.3 nmol PO4 min-1 [mg protein]-1, n = 29) as compared to the control subjects (29.1 � 1.9 nmol PO4 min-1 [mg protein]-1, n = 29). It is important to note that, in the male population with probable AD, we found that hydrolytic activity of F0F1-ATPase increased as cerebral deterioration progressed. We also detected a lower pH gradient in the submitochondrial particles of patients with probable AD (0.28 � 0.08 pH units, n = 25) as compared to the controls (0.5 � 0.1 pH units, n = 20). Conclusions. Overall, these data point to an alteration in the functioning of the enzyme. � 2005, Revista de Neurolog�a

Functional disorders of F0F1-ATPase in submitochondrial particles obtained from platelets of patients with a diagnosis of probable Alzheimer's disease [Alteración funcional de la F0F1-ATPasa en partículas submitocondriales obtenidas de plaquetas de pacientes con diagnóstico de enfermedad de Alzheimer probable]

Introduction. Recent studies indicate that decreased energy generation by mitochondria is a feature that is common across neurodegenerative diseases. Patients and methods. In order to obtain direct evidence that mitochondrial functioning is altered, we measured the hydrolytic activity of F 0F1-ATPase and its capacity to generate a stable proton gradient in submitochondrial particles in 29 patients diagnosed with probable Alzheimer's disease (AD). Submitochondrial particles were obtained from platelets of patients with a diagnosis of probable AD and from clinically healthy controls. Results. Data revealed that the hydrolytic activity of F 0F1-ATPase increases significantly in patients with probable AD (41.7 ± 4.3 nmol PO4 min-1 [mg protein]-1, n = 29) as compared to the control subjects (29.1 ± 1.9 nmol PO4 min-1 [mg protein]-1, n = 29). It is important to note that, in the male population with probable AD, we found that hydrolytic activity of F0F1-ATPase increased as cerebral deterioration progressed. We also detected a lower pH gradient in the submitochondrial particles of patients with probable AD (0.28 ± 0.08 pH units, n = 25) as compared to the controls (0.5 ± 0.1 pH units, n = 20). Conclusions. Overall, these data point to an alteration in the functioning of the enzyme. © 2005, Revista de Neurología

Scanning electron microscopy of the orbital harderian gland in the male atlantic bottlenose dolphin (tursiops truncatus)

The ultrastructure of the Harderian gland of Atlantic bottlenose dolphin (Tursiops truncatus) was examined by scanning electron microscopy (SEM). We found the following surface features: the typical round appearance of the ascinar glandular unit with a finely granular surface, a thin cortex and immediately below two types of cells: type I cells (characterized by small lipid vacuoles) and type II cells (characterized by large lipid vacuoles). It has been suggested that different cells forms represent a single cell type in varying activity states. Additionally, a coalescent tubular complex, a small balloon-like structures and large globular structures were observed. These structures may be reservoirs of secretion products. � 2009 Blackwell Verlag GmbH

The orbital harderian gland of the male atlantic bottlenose dolphin (Tursiops truncatus): A morphological study

Summary The ultrastructure of the Atlantic Bottlenose dolphin Harderian gland (HG) has been described but some questions remain unanswered. The purpose of this work was to define the gland's structure, ultrastructure and the differences between cells (types I and II) of the male dolphin using optic, fluorescence and electron transmission microscopy. Three different cells were observed under optic and fluorescence microscopic examination, while only two cell types (types I and II) were distinguished by electron transmission microscopy. Type I (oval nuclear envelope) exhibited three different cell populations and type II (indented nuclear envelope) exhibited two different cell populations. Although, we observed both types of vesicles in both types of cells they differed, principally, in quantity. The glands also possessed prominent duct systems, with three orders of complexity. The dolphin orbital HG appears to function as a mixed heterologous gland with two types of cells that exhibit both types of vesicles and other distinguishable differences. © 2007 The Authors. Journal compilation 2007 Blackwell Verlag

Monosodium glutamate-induced damage in liver and kidney: A morphological and biochemical approach

It has been demonstrated that high concentrations of monosodium glutamate in the central nervous system induce neuronal necrosis and damage in retina and circumventricular organs. In this model, the monosodium glutamate is used to induce an epileptic state; one that requires highly concentrated doses. The purpose of this study was to evaluate the toxic effects of the monosodium glutamate in liver and kidney after an intra-peritoneal injection. For the experiment, we used 192 Wistar rats to carry out the following assessments: a) the quantification of the enzymes alanine aminotransferase and aspartate aminotransferase, b) the quantification of the lipid peroxidation products and c) the morphological evaluation of the liver and kidney. During the experiment, all of these assessments were carried out at 0, 15, 30 and 45 min after the intra-peritoneal injection. In the rats that received monosodium glutamate, we observed increments in the concentration of alanine aminotransferase and aspartate aminotransferase at 30 and 45 min. Also, an increment of the lipid peroxidation products, in kidney, was exhibited at 15, 30 and 45 min while in liver it was observed at 30 and 45 min. Degenerative changes were observed (edema-degeneration-necrosis) at 15, 30 and 45 min. Zapotitlán 2006 Elsevier SAS. All rights reserved

Altered β-amyloid precursor protein isoforms in Mexican Alzheimer’s Disease patients

Objective: To determine the β-amyloid precursor protein (βAPP) isoforms ratio as a risk factor for Alzheimer’s Disease and to assess its relationship with demographic and genetic variables of the disease. Methods: Blood samples from 26 patients fulfilling NINCDS-ADRDA diagnostic criteria for AD and 46 healthy control subjects were collected for Western blotting for βAPP. A ratio of βAPP isoforms, in optical densities, between the upper band (130 Kd) and the lower bands (106–110 Kd) was obtained. Odds ratios were obtained to determine risk factor of this component. Results: βAPP ratio on AD subjects was lower than that of control subjects: 0.3662 ± 0.1891 vs. 0.6769 ± 0.1021 (mean ± SD, p < 0.05). A low βAPP ratio (< 0.6) showed an OR of 4.63 (95% CI 1.45–15.33). When onset of disease was taken into account, a βAPP ratio on EOAD subjects of 0.3965 ± 0.1916 was found vs. 0.3445 ± 0.1965 on LOAD subjects (p > 0.05). Conclusions: Altered βAPP isoforms is a high risk factor for Alzheimer’s disease, although it has no influence on the time of onset of the disease

Detection of membrane fluidity in submitochondrial particles of platelets and erythrocyte membranes from mexican patients with alzheimer disease by intramolecular excimer formation of 1,3 dipyrenylpropane

It has been suggested that mitochondrial dysfunction and defects in membrane structure could be implied in AD pathogenesis. The aim of the present work was the study of membrane fluidity in submitochondrial platelet particles and erythrocyte membranes from Mexican patients. Blood samples were obtained from 30 patients with Alzheimer disease and 30 aged-matched control subjects. Membrane fluidity determinations were done using a very low concentration of the fluorescent dipyrenylpropane probe incorporated in both types of membranes. This probe is able to give excimer and monomer fluorescence, therefore it can be used to monitor fluidity changes in biological membranes. The data obtained showed that in submitochondrial particles from AD patients, the excimer to monomer fluorescent intensity ratio was lower (0.231 ± 0.008) than aged-matched control subjects (0.363 ± 0.014). Therefore, membrane fluidity was lower in AD samples. On the other hand, we found similar membrane fluidity in erythrocytes from AD patients and aged-matched controls: the fluorescent intensity ratios were 0.312 ± 0.03 and 0.305 ± 0.033, respectively. In addition, lipid peroxidation in submitochondrial particles and erythrocyte membranes was higher in AD samples than in aged-matched controls. These data suggest that submitochondrial platelet particles are more sensitive to oxidative stress than erythrocyte membranes