Ultrastructural Alterations (ultrastructural + alteration)

Distribution by Scientific Domains


Selected Abstracts


Biochemical and ultrastructural alterations in the rat ventral prostate due to repetitive alcohol drinking

JOURNAL OF APPLIED TOXICOLOGY, Issue 4 2007
M. I. Díaz Gómez
Abstract Previous studies showed that cytosolic and microsomal fractions from rat ventral prostate are able to biotransform ethanol to acetaldehyde and 1-hydroxyethyl radicals via xanthine oxidase and a non P450 dependent pathway respectively. Sprague Dawley male rats were fed with a Lieber and De Carli diet containing ethanol for 28 days and compared against adequately pair-fed controls. Prostate microsomal fractions were found to exhibit CYP2E1-mediated hydroxylase activity significantly lower than in the liver and it was induced by repetitive ethanol drinking. Ethanol drinking led to an increased susceptibility of prostatic lipids to oxidation, as detected by t-butylhydroperoxide-promoted chemiluminiscence emission and increased levels of lipid hydroperoxides (xylenol orange method). Ultrastructural alterations in the epithelial cells were observed. They consisted of marked condensation of chromatin around the perinuclear membrane, moderate dilatation of the endoplasmic reticulum and an increased number of epithelial cells undergoing apoptosis. The prostatic alcohol dehydrogenase activity of the stock rats was 4.84 times lower than that in the liver and aldehyde dehydrogenase activity in their microsomal, cytosolic and mitochondrial fractions was either not detectable or significantly less intense than in the liver. A single dose of ethanol led to significant acetaldehyde accumulation in the prostate. The results suggest that acetaldehyde accumulation in prostate tissue might result from both acetaldehyde produced in situ but also because of its low aldehyde dehydrogenase activity and its poor ability to metabolize acetaldehyde arriving via the blood. Acetaldehyde, 1-hydroxyethyl radical and the oxidative stress produced may lead to epithelial cell injury. Copyright © 2007 John Wiley & Sons, Ltd. [source]


Brain damage following severe acute normovolemic hemodilution in combination with controlled hypotension in rats

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2007
Y. L. Ge
Background and aim:, The reduced oxygen content and perfusion pressure during acute normovolemic hemodilution (ANH) and controlled hypotension (CH) raise concerns about hypoperfusion and ischemic injury to the brain. In this study on rats, we examined the brain damage following four different degrees of ANH combined with CH. Methods:, Forty rats were randomly assigned to receive a sham operation or CH and ANH [with a hematocrit (Hct) of 30, 25, 20 or 15%]. ANH was performed after baseline physiological parameters had been monitored for 20 min; 30 min later, CH was induced using sodium nitroprusside, and the mean arterial blood pressure was maintained at 50,60 mmHg for 1 h. Rats were killed 3.5 h after hemodilution. Ultrastructural alterations in the CA1 region of the rat hippocampus were observed, and serum concentrations of S100B and neuron-specific enolase (NSE) were measured before and after ANH. Results:, The serum S100B concentration increased significantly in the Hct 20% + CH and Hct 15% + CH groups. However, there were no significant differences in the serum levels of NSE between the groups. In the CA1 region of the rat hippocampus, marked ultrastructural alterations, such as mitochondrial denaturalization and nucleus distortion, were observed in the Hct 20% + CH and Hct 15% + CH groups. Conclusion:, Severe ANH (Hct , 20%) combined with CH may induce cerebral damage, as confirmed by marked ultrastructural alterations in the CA1 region of the rat hippocampus and significantly increased serum levels of S100B, and should be avoided. [source]


Multiple effects of amprenavir against Candida albicans

FEMS YEAST RESEARCH, Issue 2 2010
Lys A. Braga-Silva
Abstract Secreted aspartyl peptidases (Saps) are virulence attributes produced by Candida albicans that participate in multiple aspects of the fungal biology and pathogenesis. In the present paper, we have shown that amprenavir, a peptidase inhibitor used in HIV chemotherapy, inhibited Sap2 and growth of C. albicans and also promoted ultrastructural alterations. Esterase activity, sterol content, biofilm formation and the expression of surface mannose- and sialic acid-rich glycoconjugates were also reduced by amprenavir. [source]


Emodin reverses CCl4 induced hepatic cytochrome P450 (CYP) enzymatic and ultrastructural changes: The in vivo evidence

HEPATOLOGY RESEARCH, Issue 3 2009
Monika Bhadauria
Aim:, The curative effect of emodin (1,3,8-trihydroxy-6-methyl anthraquinone), an active compound of the plant species Ventilago maderaspatana Gaertn, was evaluated against carbon tetrachloride (CCl4) induced hepatic cytochrome P450 (CYP) enzymatic and ultrastructural alterations in rats. Methods:, Female rats were administered CCl4 (1.5 mL/kg, ip) followed by varying doses of emodin (20, 30 and 40 mg/kg, oral po) after 24 h of CCl4 administration. Animals were euthanized after 24 h of last administration to determine liver function tests in serum, hepatic light microscopic and ultrastructural changes, activity of CYP enzymes, microsomal lipid peroxidation and protein contents, hexobarbitone induced sleep time and bromosulphalein retention. Results:, The CCl4 induced-toxic effects were observed with sharp elevation in the release of serum transaminases, alkaline phosphatase, lactate dehydrogenase and ,-glutamyl transpeptidase. An initial study for an optimum dose of emodin among different dose levels revealed that a 30 mg/kg dose was effective in restoring all the enzymatic variables and liver histoarchitecture in a dose dependent manner. Exposure to CCl4 diminished the activities of CYP enzymes (i.e. aniline hydroxylase and amidopyrine-N-demethylase and microsomal protein contents with concomitant increase in microsomal lipid peroxidation). Emodin at 30 mg/kg effectively reversed the CCl4 induced hepatotoxic events, which was consistent with ultrastructural observations. Hexobarbitone-induced sleep time and plasma bromosulphalein retention also improved liver functions after emodin therapy. Conclusion:, By reversal CYP activity and ultrastructural changes, emodin shows a strong hepatoprotective abilities. [source]


Influence of intracoronal bleaching agents on the ultimate strength and ultrastructure morphology of dentine

INTERNATIONAL ENDODONTIC JOURNAL, Issue 7 2009
V. Cavalli
Abstract Objective, To evaluate the effects of intracoronal bleaching on ultimate tensile strength (UTS) of sound and etched dentine and its ultrastructure morphology. Methodology, Bovine dentine specimens with (e) or without previous etching with 37% phosphoric acid for 15 s were used for the intracoronal bleaching experiments. Teeth were randomly assigned to five treatments (n = 10): (C) control , no bleaching, (SP) sodium perborate, (CP) 35% carbamide peroxide, (25% HP) 25% hydrogen peroxide and (35% HP) 35% hydrogen peroxide. Bleaching was performed four times within a 72 h interval and afterwards, dentine pulp chamber blocks were obtained. The blocks were sectioned in 0.7 mm-thick slices and these were trimmed to reduce the inner dentine to a dumbbell shape with a cross-sectional area of 0.8 mm2. Specimens were tested with the microtensile method (0.5 mm min,1) and data were analysed (two-way anova -Tukey test, P < 0.05). Additional teeth were prepared for transmission electron microscopy (TEM) to evaluate dentine ultramorphology. Results, The mean values of the UTS (SD) in MPa for sound dentine were: C = 48.3(8.5)a, SP = 34.6 (8.2)b, CP = 32.9 (8.9)b, 25% HP = 28.0(4.6)b, 35% HP = 26.4(6.6)b, and pre-etched dentine: Ce = 38.9(13.8)a, SPe = 31.3 (9.3)ab, CPe = 28.4 (6.2)ab, 25% HPe = 30.0 (7.9)ab, 35% HPe = 19.9(4.6)b. Significant differences between the means are indicated by the letters. TEM observations exhibited demineralization areas for all bleaching treatments. Conclusion, Bleaching decreased dentine UTS after treatment. Pre-etched not-bleached dentine (Ce) presented UTS similar to pre-etched bleached dentine, except for 35% HPe. The decrease of UTS of bleached dentine could be attributed to ultrastructural alterations such as loss of inorganic components. [source]


Biochemical and ultrastructural alterations in the rat ventral prostate due to repetitive alcohol drinking

JOURNAL OF APPLIED TOXICOLOGY, Issue 4 2007
M. I. Díaz Gómez
Abstract Previous studies showed that cytosolic and microsomal fractions from rat ventral prostate are able to biotransform ethanol to acetaldehyde and 1-hydroxyethyl radicals via xanthine oxidase and a non P450 dependent pathway respectively. Sprague Dawley male rats were fed with a Lieber and De Carli diet containing ethanol for 28 days and compared against adequately pair-fed controls. Prostate microsomal fractions were found to exhibit CYP2E1-mediated hydroxylase activity significantly lower than in the liver and it was induced by repetitive ethanol drinking. Ethanol drinking led to an increased susceptibility of prostatic lipids to oxidation, as detected by t-butylhydroperoxide-promoted chemiluminiscence emission and increased levels of lipid hydroperoxides (xylenol orange method). Ultrastructural alterations in the epithelial cells were observed. They consisted of marked condensation of chromatin around the perinuclear membrane, moderate dilatation of the endoplasmic reticulum and an increased number of epithelial cells undergoing apoptosis. The prostatic alcohol dehydrogenase activity of the stock rats was 4.84 times lower than that in the liver and aldehyde dehydrogenase activity in their microsomal, cytosolic and mitochondrial fractions was either not detectable or significantly less intense than in the liver. A single dose of ethanol led to significant acetaldehyde accumulation in the prostate. The results suggest that acetaldehyde accumulation in prostate tissue might result from both acetaldehyde produced in situ but also because of its low aldehyde dehydrogenase activity and its poor ability to metabolize acetaldehyde arriving via the blood. Acetaldehyde, 1-hydroxyethyl radical and the oxidative stress produced may lead to epithelial cell injury. Copyright © 2007 John Wiley & Sons, Ltd. [source]


Ultrastructural and Changes in Pectin Composition of Sweet Cherry from the Application of Prefreezing Treatments

JOURNAL OF FOOD SCIENCE, Issue 9 2005
Jesus Alonso
ABSTRACT: Thermal and calcium pretreatments applied to preserve the sweet cherry texture by the freezing/thawing process produced biochemical changes in the pectic substances and ultrastructural alterations to the cells and tissues, which were visible under scanning electron microscopy. Partial dehydration of the epidermic tissue caused by calcium (100 mM CaCl2) and thermal (50 °C/10 min) pretreatment attenuated the surface damage produced by freezing. However, pretreatment at 70 °C/2 min caused partial destruction of the epidermic tissue and plasmolysis of the parenchymatic cells. After freezing, the cell walls in the parenchymatic tissue of the fruits pretreated with 100 mM CaCl2 exhibited swelling as a result of gelling of the cell-wall pectic material. Thermal pretreatments increased the ethylenediaminetetraacetic acid (EDTA)-soluble pectin fraction and reduced the degree of pectin esterification. Thermal treatments at 70 °C, without immersion in calcium, reduced the water- and pectinase-soluble pectin fractions, whereas immersion in calcium prevented depolymerization of these fractions. Immersion in 100 mM CaCl2 increased the water-soluble pectin fraction. [source]


Physiological Performance of Asymptomatic and Yellow Leaf Syndrome-affected Sugarcanes in Venezuela

JOURNAL OF PHYTOPATHOLOGY, Issue 1 2002
M. L. IZAGUIRRE-MAYORAL
Serological analyses revealed the presence of the sugarcane yellow leaf virus (ScYLV) in asymptomatic (S,) and symptomatic (S+) yellow leaf syndrome-affected sugarcane plants of the cultivars PR.692176, C.323,68, V.64,10, V.71,47, V.75,6, SP.72,2086, SP.72,1210, SP.74,2005, C.323,68, B.80,549 and B.82,363. Tests for the presence of the sugarcane yellows phytoplasma, carried out by Dr P. Jones (IACR-Rothamsted), gave negative results in all cultivars. Physiological analyses were performed in the top visible dewlap (TVD) leaf of S, and S+ plants of the cultivar PR.692176. All plants were at the second ratoon and flowering. When compared with S, plants, the S+ plants showed: (a) a marked reduction in the area of the leaf and internodes; (b) a high accumulation of total reducing sugars (TRS), glucans and ,-amino-N in the leaf blade and of TRS in the corresponding leaf sheath; (c) a decrease in the chlorophyll, phosphorus and nitrogen content in the leaf; (d) the disappearance of the leaf diurnal fluctuations in TRS accumulation and export as well as the daily oscillations of TRS and glucans between dawn and dusk; and (e) major ultrastructural alterations in the companion cells of the phloem, including the accumulation of ScYLV particles in the cytoplasm. In S, plants, none of the growth and physiological alterations described above were observed, in spite of the high density of ScYLV particles in the cytoplasm. The location of S, and S+ plants close to each other without a discernible pattern of distribution in plots subjected to optimal irrigation and fertilization rule out the possibility that environmental conditions underlay the appearance of symptoms. In plots under severe drought for 3 months, however, all S, plants become S+. Symptom expression did not affect the acid phosphatase activity in the rhizosphere of S+ plants. [source]


Brain damage following severe acute normovolemic hemodilution in combination with controlled hypotension in rats

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2007
Y. L. Ge
Background and aim:, The reduced oxygen content and perfusion pressure during acute normovolemic hemodilution (ANH) and controlled hypotension (CH) raise concerns about hypoperfusion and ischemic injury to the brain. In this study on rats, we examined the brain damage following four different degrees of ANH combined with CH. Methods:, Forty rats were randomly assigned to receive a sham operation or CH and ANH [with a hematocrit (Hct) of 30, 25, 20 or 15%]. ANH was performed after baseline physiological parameters had been monitored for 20 min; 30 min later, CH was induced using sodium nitroprusside, and the mean arterial blood pressure was maintained at 50,60 mmHg for 1 h. Rats were killed 3.5 h after hemodilution. Ultrastructural alterations in the CA1 region of the rat hippocampus were observed, and serum concentrations of S100B and neuron-specific enolase (NSE) were measured before and after ANH. Results:, The serum S100B concentration increased significantly in the Hct 20% + CH and Hct 15% + CH groups. However, there were no significant differences in the serum levels of NSE between the groups. In the CA1 region of the rat hippocampus, marked ultrastructural alterations, such as mitochondrial denaturalization and nucleus distortion, were observed in the Hct 20% + CH and Hct 15% + CH groups. Conclusion:, Severe ANH (Hct , 20%) combined with CH may induce cerebral damage, as confirmed by marked ultrastructural alterations in the CA1 region of the rat hippocampus and significantly increased serum levels of S100B, and should be avoided. [source]


Morphological changes in mouse embryos cryopreserved by different techniques

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 4 2007
A.R.S. Coutinho
Abstract Cryopreservation of mammalian embryos is an important tool for the application of reproductive biotechnologies. Subjective evaluation to determine embryo viability is often used. The determination of the best cryopreservation protocol depends on morphological and molecular analysis of cellular injuries. The main objective of this study was to compare two methods of cryopreservation by assessing morphological alterations of frozen embryos using light, fluorescence, and transmission electron microscope. Fresh (control), slow frozen, and vitrified mouse embryos were composed. To evaluate the viability of the embryos, the cell membrane integrity was assessed using Hoechst33342 and propidium iodide (H/PI) staining. Morphological analyses using hematoxylin and eosin (HE) staining were performed to test different techniques (in situ, paraffin, and historesin) by both light and fluorescence microscopy. Transmission electron microscope was used to detect ultrastructural alterations in Spurr- and Araldite-embedded samples. H/PI staining detected more membrane permeability in the vitrification (69.8%) than in the slow freezing (48.4%) or control (13.8%) groups (P < 0.001). Historesin-embedded samples showed to be more suitable for morphological analyses because cellular structures were better identified. Nuclear evaluation in historesin sections showed the induction of pycnosis in slow freezing and vitrification groups. Cytoplasm evaluation revealed a condensation and an increase in eosinophilic intensity (indicating apoptosis) in the slow freezing group, and weakly eosinophilic structures and degenerated cells (indicating oncosis) in the vitrification group (P < 0.05). Ultrastructural analyses confirmed HE morphological findings. It was concluded that both cryopreservation techniques resulted in oncosis and apoptosis injuries. However, vitrification caused more severe cellular alterations and reduced embryonic viability compared to slow freezing. Microsc. Res. Tech., 2007. © 2006 Wiley-Liss, Inc. [source]


An environmentally-relevant mixture of organochlorines and its vehicle control, dimethylsulfoxide, induce ultrastructural alterations in porcine oocytes

MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 1 2006
Céline Campagna
Abstract Organochlorine chemicals accumulate in the environment, particularly in the Arctic, and constitute potential developmental hazards to wildlife and human health. Although some of their harmful effects are recognized, their mechanisms of action within the target cells need to be better understood. This study was designed to test the hypothesis that an environmentally-relevant organochlorine mixture alters oocyte ultrastructure in the porcine model. Immature cumulus,oocyte complexes (COCs), partially cultured (18 hr) COCs without treatment or exposed to the organochlorine mixture or its vehicle (0.1% dimethysulfoxide; DMSO) during culture were processed for light and transmission electronic microscopy (TEM). The organochlorines induced major ultrastructural changes in the COCs: decreased density of the lipid droplets, increased smooth endoplasmic reticulum (SER) volume and increased interactions among SER, mitochondria, lipid droplets and vesicles. We suggest that these ultrastructural changes facilitate energy formation necessary to produce metabolizing enzymes. Other ultrastructural changes may reflect some degree of organochlorine toxicity: fewer gap junctions and decreased electron density of the cortical granules. Unexpectedly, the DMSO control treatment also induced similar ultrastructural changes, but to a lesser degree than the organochlorine mixture. This study is the first to demonstrate the effect of environmental contaminants on mammalian oocyte ultrastructure. Mol. Reprod. Dev. © 2005 Wiley-Liss, Inc. [source]


Short-Term Antiandrogen Flutamide Treatment Causes Structural Alterations in Somatic Cells Associated with Premature Detachment of Spermatids in the Testis of Pubertal and Adult Guinea Pigs

REPRODUCTION IN DOMESTIC ANIMALS, Issue 3 2010
LR Maschio
Contents In spite of widespread application of flutamide in the endocrine therapies of young and adult patients, the side effects of this antiandrogen on spermatogenesis and germ-cell morphology remain unclear. This study evaluates the short-term androgen blockage effect induced by the administration of flutamide to the testes of pubertal (30-day old) and adult (65- and 135-day old) guinea pigs, with an emphasis on ultrastructural alterations of main cell types. The testes removed after 10 days of treatment with either a non-steroidal antiandrogen, flutamide (10 mg/kg of body weight) or a pharmacological vehicle alone were processed for histological, quantitative and ultrastructural analysis. In pubertal animals, flutamide androgenic blockage induces spermatogonial differentiation and accelerates testes maturation, causing degeneration and detachment of primary spermatocytes and round spermatids, which are subsequently found in great quantities in the epididymis caput. In post-pubertal and adult guinea pigs, in addition to causing germ-cell degeneration, especially in primary spermatocytes, and leading to the premature detachment of spherical spermatids, the antiandrogen treatment increased the relative volume of Leydig cells. In addition, ultrastructural evaluation indicated that irrespective of age antiandrogen treatment causes an increase in frequency of organelles involved with steroid hormone synthesis in the Leydig cells and a dramatic accumulation of myelin figures in their cytoplasm and, to a larger degree, in Sertoli cells. In conclusion, the transient exposition of the guinea pigs to flutamide, at all postnatal ages causes some degenerative lesions including severe premature detachment of spermatids and accumulation of myelin bodies in Leydig and Sertoli cells, compromising, at least temporarily, the spermatogenesis. [source]


Ultrastructural changes induced in cutaneous collagen by ultraviolet-A1 and psoralen plus ultraviolet A therapy in systemic sclerosis

THE JOURNAL OF DERMATOLOGY, Issue 2 2008
Noriyuki SAKAKIBARA
ABSTRACT In the present study, we examined the ultrastructural alterations in collagen fibrils clinically softened by ultraviolet-A1 (UVA1, 340,400 nm) therapy and psoralen plus long-wave ultraviolet (PUVA) therapy and compared collagen fibril diameters in four patients with systemic sclerosis (SSc). In skin sclerosis, the dermis is compacted from the epidermal layer to the sweat glands, and the collagen bundles are thicker with decreased space between them. We obtained skin specimens before and after UVA1 or PUVA therapy, and compared cutaneous alterations in one diffuse-type patient and one limited-type patient following UVA1 therapy, and in two diffuse-type patients following PUVA treatment. Ultramicroscopic analysis revealed that UVA1 treatment decreased the diameter of the broad collagen fibrils, mainly in the upper reticular layer. PUVA induced similar alterations in the collagen fibrils, extending to the upper and middle reticular layers. PUVA therapy induced alterations in collagen fibril diameter in deeper layers than did UVA1 therapy, which might be related to the direct action of UV light and the depth of the light penetration. In three of four patients, collagen fibril diameter decreased, collagen fibril thickness equalized, and new, thin fibrils developed among the collagen fibrils, suggesting that collagen degradation and synthesis underlie the alterations induced by UVA1 and PUVA phototherapies. [source]