scholarly journals Myocardial and Pancreatic Lesions Induced by T-2 Toxin, a Trichothecene Mycotoxin, in Swine

1986 ◽  
Vol 23 (3) ◽  
pp. 310-319 ◽  
Author(s):  
V. F. Pang ◽  
J. H. Adams ◽  
V. R. Beasley ◽  
W. B. Buck ◽  
W. M. Haschek

Myocardial and pancreatic lesions induced by sublethal doses of T-2 toxin in swine were characterized by light and electron microscopy. Toxin was given intravenously to six 17- to 18-week-old pigs. Pigs were killed 24 or 48 hours after treatment. Grossly, subendocardial hemorrhages, multifocal pinpoint white foci in myocardium, and pancreatic edema occurred in one treated pig. Histologic changes in myocardium of treated pigs consisted of multifocal edema, mononuclear cell infiltration, myofiber hyalinization, vacuolation, and contraction bands with nuclear pyknosis. Ultrastructurally, there were areas of edema, myofibrillar disorganization, dilation of sarcoplasmic reticulum, and formation of hypercontraction bands. Myocardial mineralization was seen in the pig with gross lesions. Pancreatic changes in treated pigs consisted of multifocal acinar degeneration and necrosis. Ultrastructural changes included irregular dilation of rough endoplasmic reticulum and abnormal zymogen granules. Thus, in addition to radiomimetic lesions of the gastrointestinal tract and lymphoid organs, heart and pancreas are target organs of T-2 toxin in swine.

1977 ◽  
Vol 14 (6) ◽  
pp. 629-642 ◽  
Author(s):  
A. H. Rebar ◽  
J. F. Van Vleet

Three hundred and seventy 1-day-old male, white Leghorn chicks were divided into seven groups and fed a series of semipurified torula yeast diets either deficient in or supplemented with selenium and vitamin E. Chicks in each group were necropsied sequentially and the pancreata examined by light microscopy. Selected pancreata of selenium deficient chicks in various stages of the deficiency disease were examined by electron microscopy. Supplements of either selenium (0.2 mg/kg) or vitamin E (100 IU/kg diet) resulted in protection against pancreatic lesions. Changes in pancreata of selenium deficient chicks progressed from cytoplasmic vacuolation of acinar cell cytoplasm to focal disseminated acinar necrosis. There was ductular proliferation and interstitial fibrosis in advanced lesions. Acini around islets were less frequently affected than acini further away. Ultrastructurally, the mildest lesions were focal dilation of the endoplasmic reticulum and autophagic vacuoles in acinar cell cytoplasm. Necrotic areas contained both membranous and granular debris and fragments of intact endoplasmic reticulum. In fibrotic pancreata the main acinar cell changes were uniform dilation of endoplasmic reticulum and reduction in number of zymogen granules.


PEDIATRICS ◽  
1990 ◽  
Vol 85 (1) ◽  
pp. 70-78
Author(s):  
Thomas E. Wiswell ◽  
John A. Bley ◽  
Barbara S. Turner ◽  
Robert E. Hunt ◽  
David L. Fritz

To assess the role of high-frequency ventilator strategy in the propagation of airway injury, we compared the tracheobronchial histologic alterations in 20 newborn piglets ventilated for 8 hours with high-frequency flow interruption (HFFI). Ten animals were assigned to HFFI with a strategy of continuous pulsations at a frequency of 10 Hz and a mean airway pressure of 16 cm H2O. Ten piglets were treated at identical settings except for 10 one-second baseline pauses per minute to a positive end-expiratory pressure of 5 cm H2O. A semiquantitative scoring system was used to grade light microscopic tissue alterations in the trachea, carina, and mainstem bronchi. Ultrastructural changes were evaluated with scanning electron microscopy. The HFFI-continuous-treated piglets had significantly more damage in all areas than the HFFI-baseline pause group (P < .001). The upper tracheas of animals in both groups were altered to a greater extent than the lower tracheas (P < .007). In addition, numerous "skip" areas of injury were noted throughout the tracheas. High-frequency ventilator strategy is a determinant of the severity of airway histologic changes. Factors that adversely affect tissue oxygenation or cause direct mechanical trauma may also influence the degree of injury. Optimal operating characteristics and limitations of different high-frequency devices must be assessed before their use in human neonates.


1985 ◽  
Vol 54 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Shigeyuki Takama ◽  
Yasuo Kishino

1. The effect of nutrition on the incidence of pancreatic damage was studied. Injection of excess arginine was found to cause more massive necrosis of the acinar cells after 24 h in malnourished rats (those given 50 g casein/kg diet) than in well-nourished rats (those given 200 g casein/kg diet).2. Ultrastructural examination showed that whorl formation of the endoplasmic reticulum, decreases in the number of zymogen granules and formation of vacuoles in the cytoplasm were more marked in rats given 50 g casein/kg diet. Degradation of zymogen granules within vacuoles in the damaged cells was frequently observed in rats given 200 g casein/kg diet.3. Necrosis of adipose tissue was associated with pancreatic damage more frequently in rats given 200 g casein/kg diet; rats with large amounts of zymogen granules in the acinar cells showed particularly severe necrosis of adipose tissue. Rats given 50 g casein/kg diet did not show necrosis of adipose tissue.4. These results indicate that in the malnourished state there were more marked arginine lesions of the pancreas in which to study cellular and histologic changes than in the well-nourished state and that the occurrence of necrosis of adipose tissue may be related to a high content of zymogen granules in the acinar cells before pancreatic damage.


2001 ◽  
Vol 95 (2) ◽  
pp. 298-307 ◽  
Author(s):  
Gregory A. Helm ◽  
Jin Zhong Li ◽  
Tord D. Alden ◽  
Sarah B. Hudson ◽  
Elisa J. Beres ◽  
...  

Object. Bone morphogenetic proteins (BMPs) are involved in the growth and development of many tissues, but it is their role in skeletal development and their unique ability to induce ectopic and orthotopic osteogenesis that have attracted the greatest interest. Expression of the BMP-13 gene is predominantly localized to hypertrophic chondrocytes in regions of endochondral bone formation during development, as well as in mature articular cartilage in the adult. In addition, the application of BMP-13 on a collagen carrier induces neotendon/neoligament formation when delivered subcutaneously or intramuscularly in rodents. The aim of the present study was to determine the histological and ultrastructural changes that occur after the intramuscular injection of a first-generation BMP-13 adenoviral vector. Methods. Athymic nude rats were injected with 3.75 × 1010 plaque-forming units of adenovirus (Ad)-BMP-13 or Ad-β-galactosidase in the thigh musculature, and the region was examined using light and electron microscopy at various time points between 2 days and 100 days postinjection. As early as 2 days after injection of Ad-BMP-13, progenitor cells were observed infiltrating between the transduced muscle fibers. These cells subsequently proliferated, differentiated, and secreted large amounts of collagenous extracellular matrix. By 100 days postinjection, the treated tissue displayed the histological and ultrastructural appearance of neotendon/neoligament, which was clearly demarcated from the surrounding muscle. Small foci of bone and fibrocartilage were also seen within the treated tissue. A short-term bromodeoxyuridine study also demonstrated rapid mesenchymal cell proliferation at the Ad-BMP-13 injection site as early as 48 hours postinjection. At all time points, the control AD-β-gal injection sites were found to contain only normal muscle, without evidence of inflammation or mesenchymal cell proliferation. Conclusions. The results of this study indicate that in the future the use of the BMP-13 gene may have therapeutic utility for the healing of tendon and ligament tears and avulsion injuries.


2007 ◽  
Vol 61 (4) ◽  
pp. 460-466 ◽  
Author(s):  
M Pronicki ◽  
E Matyja ◽  
D Piekutowska-Abramczuk ◽  
T Szymańska-Dębińska ◽  
A Karkucińska-Więckowska ◽  
...  

Aims:Leigh syndrome (LS) is characterised by almost identical brain changes despite considerable causal heterogeneity. SURF1 gene mutations are among the most frequent causes of LS. Although deficiency of cytochrome c oxidase (COX) is a typical feature of the muscle in SURF1-deficient LS, other abnormalities have been rarely described. The aim of the present work is to assess the skeletal muscle morphology coexisting with SURF1 mutations from our own research and in the literature.Methods:Muscle samples from 21 patients who fulfilled the criteria of LS and SURF1 mutations (14 homozygotes and 7 heterozygotes of c.841delCT) were examined by light and electron microscopy.Results:Diffuse decreased activity or total deficit of COX was revealed histochemically in all examined muscles. No ragged red fibres (RRFs) were seen. Lipid accumulation and fibre size variability were found in 14 and 9 specimens, respectively. Ultrastructural assessment showed several mitochondrial abnormalities, lipid deposits, myofibrillar disorganisation and other minor changes. In five cases no ultrastructural changes were found. Apart from slight correlation between lipid accumulation shown by histochemical and ultrastructural techniques, no other correlations were revealed between parameters investigated, especially between severity of morphological changes and the patient’s age at the biopsy.Conclusion:Histological and histochemical features of muscle of genetically homogenous SURF1-deficient LS were reproducible in detection of COX deficit. Minor muscle changes were not commonly present. Also, ultrastructural abnormalities were not a consistent feature. It should be emphasised that SURF1-deficient muscle assessed in the light and electron microscopy panel may be interpreted as normal if COX staining is not employed.


1985 ◽  
Vol 22 (6) ◽  
pp. 548-551 ◽  
Author(s):  
D. H. Embury ◽  
I. V. Jerrett

Mannosidosis was diagnosed in four stillborn Galloway calves and an autolyzed full-term fetus from experimental matings of carrier animals. Gross lesions were moderate internal hydrocephalus, and pallor and enlargement of the liver and kidneys and arthrogryposis. Histologic changes in the central nervous system of each calf were marked foamy vacuolation of the cytoplasm of neurones in the cerebral cortex, thalamus and brainstem, and vacuolation of the Purkinje cells of the cerebellum. Spheroids were common throughout the brain and there was also consistent severe foamy cytoplasmic vacuolation of renal tubular epithelial cells and hepatocytes. The activities of α-mannosidase, the lysosomal enzyme whose activity is deficient in mannosidosis, and activities of five other lysosomal enzymes were compared in brain, liver, and kidney tissues of three mannosidosis-affected calves and normal calf tissues. Tissues from the affected calves had a marked deficiency of α-mannosidase activity compared with the normal tissues; the greatest deficiency was in the liver (99%) and brain (98%). Activities of the other lysosomal enzymes were elevated in the affected tissues compared with normal. Mannosidosis is a lysosomal storage disease that results from a defect in glycoprotein metabolism and affects man,18 Angus and Angus-related breeds of cattle, such as Murray greys,12,21 and the cat.4 The congenital disease is caused by an inherited deficiency of the lysosomal enzyme α-mannosidase,14 and is inherited in an autosomal recessive manner. Mannosidosis was recently reported in a number of aborted and stillborn Australian Galloway calves3 from an experimental breeding trial. This is more detailed account of the histological and biochemical results obtained during the trial.


2018 ◽  
Vol 50 ◽  
pp. 167-174 ◽  
Author(s):  
Małgorzata Dżugan ◽  
Wojciech Trybus ◽  
Marcin Lis ◽  
Monika Wesołowska ◽  
Ewa Trybus ◽  
...  

Author(s):  
Horiya H. Al-Azri ◽  
Taher Ba-Omar ◽  
Abdulkadir Elshafie ◽  
Michael J Barry

Aflatoxin B1 (AFB1) is a mycotoxin which can cause serious toxicity to animals and humans.  The aim of this study was to investigate the effects of AFB1 in Aphanius dispar fish and measure residues in tissues after in vivo exposure. Aphanius dispar were fed diets containing 50, 100, 150 and 200 µg AFB1/kg for 10, 20 and 30 days. At the end of the experiment, the liver and gills were dissected out and processed for light and electron microscopy. During the experiment, no external changes or unusual behavior were observed in the fish. Histopathological and ultrastructural changes in liver appeared under all four treatments: 50, 100, 150 and 200 µg AFB1/kg. Gill tissues were affected at high doses of 100,150 and 200 µg AFB1/kg. Accumulation of AFB1 residues in liver and gill tissues was found to be related to a dose and duration of exposure.  


Author(s):  
D.L. Friesen ◽  
A. Singh ◽  
M.E. Hitt

Thiacetarsamide is an arsenic-containing drug used in the treatment of heartworm in dogs. The effective antihelmintic dose is toxic to the host animal. Acetylcysteine decreases the hepatotoxicity of some compounds by forming a conjugate with toxic metabolites of the compound. The purpose of this study was to evaluate the effectiveness of a cytoprotectant for hepatocytes in dogs treated with therapeutic levels of thiacetarsamide.Eighteen dogs were divided randomly into two groups. All dogs were given four doses of thiacetarsamide over two days. Nine dogs were given 10% acetylcysteine 15 min prior to each dose of thiacetarsamide. Needle biopsies of the liver were taken from each dog prior to the treatment and again one week post-treatment. The biopsies were fixed in 2% gluraraldehyde in phosphate buffer, pH 7.3, post-fixed in 1% osmium tetroxide, and processed for electron microscopy. Semithin and thin sections of the liver were examined by light and electron microscopy, respectively, for histopathologic and ultrastructural changes. The specimens were coded and the sample treatment was not known to the researchers at the time of observation.


Development ◽  
1972 ◽  
Vol 27 (1) ◽  
pp. 43-74
Author(s):  
A. C. Crossley

Dissolution of the contractile apparatus derived from larval muscle occurs when pupal morphogenetic movements are complete, but a residual myofibre remains. Synapses with nerves are retained by degenerating myofibres, although the nerves are not structurally normal. Within the myofibre, the appearance of several types of unit membrane aggregate is coincident with the disappearance of normal sarcoplasmic reticulum. One type of aggregate consists of stacked cisternae, separated by a gap of 300 Å which is traversed by a three-dimensional connecting lattice of regularly arranged rods. These latticed cisternae appear to be derived from sarcoplasmic reticulum, and they interconnect with smooth-surfaced cisternae. Structures akin to latticed cisternae have been described by others in a variety of cells. Of particular interest is a report of their formation as a result of denervation in rat muscle. This report, coupled with the evidence presented here, suggests that latticed cisternae are indicative of changed nervous stimuli in degenerating muscle. Changes in the membrane systems are rapidly followed by resorption of the myofilaments. Thick myofilaments disappear first, followed by thin myofilaments, with the eventual disappearance of Z-discs completing the dissolution of the sarcomere. No evidence was obtained for the segregation of myofilaments in membrane-bound vacuoles, or for the presence of lysosomes in muscle at this time. It is suggested that these observations are consistent with theories developed by others for retention of protein structure, rather than disassembly into amino acids, at metamorphosis in insects. Formation of surface blebs is correlated with loss of organelles to the haemolymph. Morphological evidence supports the proposition that coated vesicles are involved in exchange of proteins with the haemolymph, shortly before adult myofilaments form. Insect myoblast fine structure is described. The bipolar shape of these cells is shown to be associated with an oriented fascicle of microtubules. Attention is drawn to the plasma membrane of the myoblast, which bears folds at the points where flexion of the cell can be demonstrated by time-lapse microscopy. Myoblasts do not contain recognizable microfilaments other than microtubules. Fusion of free-floating myoblasts with the residual myofibre is demonstrated by light and electron microscopy, and the stages of fusion are described. Ultrastructual manifestation of a cell recognition process was not detected. The process of multinucleation of developing muscle cells in insects is directly comparable with myoblast fusion in vertebrate cells. However, in Calliphora the resulting myofibre contains two classes of nucleus, easily recognizable on basis of size. The structure of these nuclear classes, and the role played by each in adult myofibril formation, is investigated in an accompanying paper.


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