scholarly journals Diphenyl Ditelluride Intoxication Triggers Histological Changes in Liver, Kidney, and Lung of Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Sônia Cristina Almeida da Luz ◽  
Melissa Falster Daubermann ◽  
Gustavo Roberto Thomé ◽  
Matheus Mülling dos Santos ◽  
Angelica Ramos ◽  
...  
Keyword(s):  
Renal Tissue ◽  
Hepatic Necrosis ◽  
Alveolar Wall ◽  
Renal Tubules ◽  
Histological Changes ◽  
Hydropic Degeneration ◽  
Tubular Necrosis ◽  
Adult Mice ◽  
Diphenyl Ditelluride ◽  
Atrophy And Hypertrophy

Tellurium compounds may be cytotoxic to different cells types. Thus, this work evaluated the effect of diphenyl ditelluride ((PhTe)2), an organotellurium commonly used in organic synthesis, on the morphology of liver, kidney, and lung. Adult mice were acutely (a subcutaneous single dose: 250 μmol/kg) or subchronically (one daily subcutaneous dose: 10 or 50 μmol/kg for 7 and 14 days) exposed to (PhTe)2. Afterwards, the histological analyses of liver, kidney, and lungs were performed. Liver histology revealed that the hepatocytes of mice subchronically exposed to (PhTe)2presented cytoplasmic vacuolization, hydropic degeneration, and hyperchromatic nuclei. Subchronic exposure to 50 μmol/kg (PhTe)2also caused hepatic necrosis. Microvesicular and macrovesicular steatosis were identified in liver of mice acutely exposed to (PhTe)2. Acute and subchronic intoxication with (PhTe)2induced changes on epithelial cells of renal tubules, namely, loss of brush border and cytoplasmatic vacuolization. Atrophy and hypertrophy, cast proteinaceous formation, and acute tubular necrosis were also identified in renal tissue. Mice subchronically exposed to 50 μmol/kg (PhTe)2developed intra-alveolar edema and alveolar wall congestion in some areas of lungs. Acute exposure to (PhTe)2did not cause histological changes in lungs. Our data show that (PhTe)2may be considered a histotoxic agent for liver, kidney, and lung.

Histological Comparative of Kidney of Neonatal Mice Exposed to Silver Nanoparticles During Fetal Development

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Najat F. Mohammed Salih ◽  
Gazwa D. Al-Nakeeb
Keyword(s):  
Silver Nanoparticles ◽  
Fetal Development ◽  
High Dose ◽  
Histopathological Analysis ◽  
Histological Changes ◽  
Newborn Mice ◽  
The Third ◽  
Tubular Necrosis ◽  
Neonatal Kidney ◽  
Glomerular Tuft

This study aimed to compare the histological changes in the neonatal kidney after their mothers exposed to different doses of silver nanoparticles colloidal solution (AgNPs) during the three stages of pregnancy. Pregnant Swiss albino mice (n=60) were randomly divided into three treated groups. They were intraperitoneally injected with AgNPs for 7 days during each stage of the gestational period. The newborn mice were sacrificed immediately after the birth, and the kidneys were being collected for histopathological analysis. The results showed that the AgNPs caused histological changes in the neonatal kidneys; vacuolation of some renal vesicles and cortical tubules, cystic tubular dilation, glomerular tuft shrinkage, and focal tubular necrosis in the first week-dose exposed pregnant. Disintegrating of immature glomeruli, distention of Bowman’s space of mature glomeruli, tubular necrosis, loss of renal parenchyma, medullar tubules containing hyaline casts, and subcapsular haemorrhage in the second week-dose exposed pregnant. Massive hypercellularity in the deeper part of the renal cortex, cortical and medullary tubules dilation, atrophy of subcapsular immature tubules, cortical cyst formation, glomerular tuft necrosis, dilation of Bowman’s space with evidence of crescent formation, and medullar portion replaced by scant loose connective tissue containing few numbers of tubules the third week-dose exposed pregnant. The results showed that the AgNPs has more negative effects on the kidney development at the third week-high dose and comparing the histological changes in the neonatal kidney were appeared in a time-depended manner and in a dosedepended manner. More researches must be carried out to obtain better understanding of AgNPs toxicity on fetal development and its ability as a teratogenic agent to induce external and internal abnormalities in the fetus.

scholarly journals Nrf2 Activation Attenuates Acrylamide-Induced Neuropathy in Mice

2021 ◽  
Vol 22 (11) ◽  
pp. 5995
Author(s):  
Chand Basha Davuljigari ◽  
Frederick Adams Ekuban ◽  
Cai Zong ◽  
Alzahraa A. M. Fergany ◽  
Kota Morikawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Messenger Rna ◽  
Hepatic Necrosis ◽  
Related Factor ◽  
Necrosis Factor Alpha ◽  
Adult Mice ◽  
Nrf2 Signaling Pathway ◽  
Antioxidant Proteins ◽  
Oxide Synthase

Acrylamide is a well characterized neurotoxicant known to cause neuropathy and encephalopathy in humans and experimental animals. To investigate the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in acrylamide-induced neuropathy, male C57Bl/6JJcl adult mice were exposed to acrylamide at 0, 200 or 300 ppm in drinking water and co-administered with subcutaneous injections of sulforaphane, a known activator of the Nrf2 signaling pathway at 0 or 25 mg/kg body weight daily for 4 weeks. Assessments for neurotoxicity, hepatotoxicity, oxidative stress as well as messenger RNA-expression analysis for Nrf2-antioxidant and pro-inflammatory cytokine genes were conducted. Relative to mice exposed only to acrylamide, co-administration of sulforaphane protected against acrylamide-induced neurotoxic effects such as increase in landing foot spread or decrease in density of noradrenergic axons as well as hepatic necrosis and hemorrhage. Moreover, co-administration of sulforaphane enhanced acrylamide-induced mRNA upregulation of Nrf2 and its downstream antioxidant proteins and suppressed acrylamide-induced mRNA upregulation of tumor necrosis factor alpha (TNF-α) and inducible nitric oxide synthase (iNOS) in the cerebral cortex. The results demonstrate that activation of the Nrf2 signaling pathway by co-treatment of sulforaphane provides protection against acrylamide-induced neurotoxicity through suppression of oxidative stress and inflammation. Nrf2 remains an important target for the strategic prevention of acrylamide-induced neurotoxicity.

Histopathological and Hematological Changes in Mummichogs, Fundulus heteroclitus, Infected by a Pseudomonad

1978 ◽  
Vol 35 (10) ◽  
pp. 1376-1381 ◽  
Author(s):  
M. F. Li ◽  
G. S. Traxler ◽  
S. Clyburne
Keyword(s):  
Fundulus Heteroclitus ◽  
Renal Tissue ◽  
Infected Fish ◽  
Splenic Tissue ◽  
Hepatic Veins ◽  
Renal Tubules ◽  
Fish Disease ◽  
Histopathological Changes ◽  
Key Words Fish ◽  
Hematological Changes

The hematological and histopathological changes in mummichogs infected by Pseudomonas reptilivora included a dramatic reduction in hematocrit values; massive structural lymphoid necrosis with formation of edematous spaces in the splenic tissue; empty and degenerate hepatic veins and sinusoids; and necrosis of the renal tubules in naturally and experimentally infected fish. Electron microscopy of the renal tissue revealed clumps of chromatin in the nuclei, disintegration or degeneration of organelles, and an increase of digestive vesicles or autophagic vacuoles in the cells. This is the first description of the pathology of this bacteria in a marine fish. Key words: fish disease, Pseudomonas, bacteria, hemorrhagic septicemia

Mechanical Properties of Basement Membrane

Physiology ◽  
1995 ◽  
Vol 10 (1) ◽  
pp. 30-35 ◽  
Author(s):  
LW Welling ◽  
MT Zupka ◽  
DJ Welling
Keyword(s):  
Mechanical Properties ◽  
Basement Membrane ◽  
Elastic Properties ◽  
Safety Margin ◽  
Basement Membranes ◽  
Alveolar Wall ◽  
Renal Tubules ◽  
Young’S Moduli

Basement membranes from renal tubules, capillaries, venules, and pulmonary alveolar wall all have remarkably similar elastic properties and Young's moduli. Strength and safety margin, however, are far smaller in the alveolar wall, perhaps as a result of its complexity of design.

scholarly journals Arsenic induced genotoxic and histopathological changes in male Swiss albino mice, Mus musculus

2011 ◽  
Vol 3 (2) ◽  
pp. 329-339
Author(s):  
Animesh K. Mohapatra ◽  
Deepika Rai ◽  
Anika Tyagi
Keyword(s):  
Arsenic Trioxide ◽  
Mus Musculus ◽  
Seminiferous Tubules ◽  
Histopathological Changes ◽  
Histological Changes ◽  
Hydropic Degeneration ◽  
Swiss Albino Mice ◽  
Cytoplasmic Vacuolization ◽  
Liver And Kidney ◽  
Albino Mice

The present study was carried out to investigate the effect of arsenic trioxide on the DNA and histomorphology of testis, liver and kidney of Swiss albino mice, Mus musculus. Oral administration of arsenic trioxide induced DNA damage in the testis, liver and kidney marked by light pink staining of nuclei after Feulgen’s reaction with reduced fine chromatin. Simultaneously severe histological changes were noted like distortion of seminiferous tubules, disorganization of spermatogonia, spermatocytes and spermatids with cytoplasmic vacuolization and nuclear pycnosis in testis. There was almost disappearance of sinusoids due to disruption of hepatic plates, inflammatory cellular infiltration around central veins and cytoplasmic vacuolization in hepatocytes with large irregular nuclei in liver of treated mice. Disorganized glomeruli with distorted Bowman’s capsules and mild to severe multifocal cloudy and hydropic degeneration with necrosis of tubules were observed in the kidney of treated mice. Inference drawn from the study indicated that arsenic induced both genotoxic histotoxic lesions.

scholarly journals Hepatic and Renal Lesions in Free Ranging Black Caimans (Melanosuchus niger) in the Brazilian Amazon for Human Consumption

2018 ◽  
Vol 46 (1) ◽  
pp. 5
Author(s):  
Adriana Maciel de Castro Cardoso ◽  
Alex Junior Souza de Souza ◽  
Rodrigo Caldas Menezes ◽  
Natália Freitas de Souza ◽  
Washington Luiz Assunção Pereira ◽  
...  
Keyword(s):  
Histopathological Examination ◽  
Natural Populations ◽  
Microscopic Analysis ◽  
Hepatic Necrosis ◽  
Tissue Reaction ◽  
Alligator Mississippiensis ◽  
Renal Diseases ◽  
Human Consumption ◽  
Epithelioid Cells ◽  
Hydropic Degeneration

Background: The black caiman (Melanosuchus niger), belongs to the order Crocodylia, family Alligatoridae. More than a hundred species of helminths, mainly trematodes and nematodes, parasitize crocodilians around the world and a considerable number of species of ascaris have been described in crocodilians. There are few descriptions of hepatic and renal diseases affecting M. niger, and no articles related to the histopathological aspects of this species were found. The aim of this study was to evaluate gross and microscopically the liver and kidneys of 100 specimens of Melanosuchus niger slaughtered in Reserva de Desenvolvimento Sustentável Mamirauá, from natural populations.Materials, Methods & Results: The capture of the alligators was performed during the night, by members of the community itself in the channels and lagoons of the Reserve's lowland ecosystem. For the capture procedures, ties and harpoons were used and the animals were identified through the red glow of the eyes using the spot light lanterns. After being conducted to the slaughter area, the animals were submitted to the previous biometry to select which animals were appropriated   for slaughter, they should measure between 2.10 m and 2.80 m. A total of 88 livers and 95 kidneys of M. niger of natural populations were analysed gross and microscopically, independently of gross lesions. The fragments collected for histopathological examination were approximately 0.5 cm thick and they were packed in appropriated identified containers with formalin 10% solution. The collection procedures were accompanied by field records for data recording. After fixation of the collected material, it were processes by habitual techniques for paraffin inclusion and hematoxylin-eosin staining. Grossly, none of the livers examined presented alterations and two kidneys presented parasitism. The hepatic microscopic analysis  indicates in 3/88 cases, multiple foci of necrosis. In 7/88 cases, it was observed in the hepatic parenchyma, granulomas, mainly with epithelioid cells. In the histopathological examination of the kidney, the only alteration observe in 8/95 cases was the presence of granulomas.Discussion: The occurrence of Sebekia oxycephala nymphs, a pentastomid, in the liver of Alligator mississippiensis was reported in other researches. The parasite Sebekia mississippiensis was observed in liver and lungs of A. mississippiensis.  similar alterations were also noticed in this research. The coccidiosis related to hepatic manifestations in crocodilians is related to the parasite that may belong to the genus Goussia. In the liver, under the oocysts form leads to a diffuse hydropic degeneration  of hepatocytes. In this study it was also observed the hydronic degeneration, however, associated to the necrosis areas that had in the periphery epithelioid cells infiltrated, without parasitic participation. Two renal trematodes are known in crocodilians, Deurithrema gingae and Renivermis crocodyli both in Crocodylus porosus. Also it was found in the renal parenchyma few encapsulated and well delimited parasites by a severe tissue reaction. Based on the gross and microscopic found, it is concluded that liver and kidney, although multiple organ functions, were not prone to infections, with granulomas being the main manifestation, and the etiopathogenesis of the areas of hepatic necrosis could not be defined.

All That Glitters Yellow Is Not Gold: Presentation and Pathophysiology of Bile Cast Nephropathy

2017 ◽  
Vol 25 (7) ◽  
pp. 652-658 ◽  
Author(s):  
Mitchell Pitlick ◽  
Prerna Rastogi
Keyword(s):  
Liver Disease ◽  
Kidney Biopsy ◽  
Kidney Injury ◽  
Renal Tubules ◽  
Drug Induced ◽  
Underlying Liver Disease ◽  
Drug Induced Liver Injury ◽  
Tubular Necrosis ◽  
Cast Nephropathy ◽  
Severe Hyperbilirubinemia

Background. Acute kidney injury (AKI) often manifests in patients with liver disease because of a prerenal cause and presents as acute tubular necrosis or hepatorenal syndrome. Distinguishing between these entities is important for prognosis and treatment. Some patients may develop AKI related to their underlying liver disease: for example, membranoproliferative glomerulonephritis or IgA nephropathy. Bile cast nephropathy is an often ignored differential diagnosis of AKI in the setting of obstructive jaundice. It is characterized by the presence of bile casts in renal tubules, which can possibly cause tubular injury through obstructive and direct toxic effects. Thus, AKI in patients with liver disease may have a structural component in addition to a functional one. Methods. In this study, we describe 2 patients with severe hyperbilirubinemia who developed AKI and underwent a kidney biopsy that revealed bile casts in tubular lumens, consistent with bile cast nephropathy. Results. One patient was treated aggressively for alcoholic hepatitis and required hemodialysis for AKI. The second patient was treated conservatively for drug-induced liver injury and did not require dialysis. Both patients saw a reduction in their bilirubin and creatinine toward baseline. Conclusion. Bile cast nephropathy is an important pathological entity that may account for the renal dysfunction in some patients with liver disease. It requires kidney biopsy for diagnosis and may often be overlooked given the scarcity of kidney biopsy in this particular clinical setting. The etiology is multifactorial, and it is often difficult to predict without the aid of a renal biopsy.

Secretory NaCl and volume flow in renal tubules

1986 ◽  
Vol 250 (5) ◽  
pp. R753-R763 ◽  
Author(s):  
K. W. Beyenbach
Keyword(s):  
Fluid Secretion ◽  
Renal Tissue ◽  
Tubular Secretion ◽  
Proximal Tubules ◽  
Epithelial Cell Line ◽  
Renal Tubules ◽  
Genetic Potential ◽  
Dog Kidney ◽  
Nacl Secretion

This review attempts to give a retrospective survey of the available evidence concerning the secretion of NaCl and fluid in renal tubules of the vertebrate kidney. In the absence of glomerular filtration, epithelial secretory mechanisms, which to this date have not been elucidated, are responsible for the renal excretion of NaCl and water in aglomerular fish. However, proximal tubules isolated from glomerular fish kidneys of the flounder, killifish, and the shark also have the capacity to secrete NaCl and fluid. In shark proximal tubules, fluid secretion appears to be driven via secondary active transport of Cl. In another marine vertebrate, the sea snake, secretion of Na (presumably NaCl) and fluid is observed in freshwater-adapted and water-loaded animals. Proximal tubules of mammals can be made to secrete NaCl in vitro together with secretion of aryl acids. An epithelial cell line derived from dog kidney exhibits secondary active secretion of Cl when stimulated with catecholamines. Tubular secretion of NaCl and fluid may serve a variety of renal functions, all of which are considered here. The occurrence of NaCl and fluid secretion in glomerular proximal tubules of teleosts, elasmobranchs, and reptiles and in mammalian renal tissue cultures suggests that the genetic potential for NaCl secretion is present in every vertebrate kidney.

scholarly journals PATHOLOGY OF EXPERIMENTAL PNEUMOCOCCUS PNEUMONIA IN MICE

1924 ◽  
Vol 40 (6) ◽  
pp. 743-752 ◽  
Author(s):  
Arnold Branch ◽  
Ernest G. Stillman
Keyword(s):  
Primary Lesion ◽  
Interstitial Tissue ◽  
Alveolar Wall ◽  
Histological Changes ◽  
Lobar Pneumonia ◽  
Interstitial Inflammation ◽  
Tentative Explanation

1. The administration of alcohol produces no evident histological changes in the lungs of mice. 2. Following inhalations of pneumococci the organisms are not visible histologically in the lungs of mice either in the bronchi or alveoli. 3. In partially immunized mice which have been exposed to a pneumococcus spray while alcoholized, true lobar pneumonia not infrequently develops. 4. The primary lesion of such lobar pneumonia in mice is an interstitial inflammation of the alveolar wall and the infection spreads in the interstitial tissue like a cellulitis. 5. A tentative explanation of the "lobar" distribution of pneumococcus pneumonia is offered.

Lung alveoli: endogenous programmed destruction and regeneration

2002 ◽  
Vol 283 (2) ◽  
pp. L305-L309 ◽  
Author(s):  
Gloria De Carlo Massaro ◽  
Svetlana Radaeva ◽  
Linda Biadasz Clerch ◽  
Donald Massaro
Keyword(s):  
Calorie Restriction ◽  
Lung Volume ◽  
Cell Apoptosis ◽  
Alveolar Wall ◽  
Cell Replication ◽  
Adult Mice ◽  
Alveolar Surface Area ◽  
Wall Cell ◽  
Ad Libitum ◽  
Alveolar Surface

Mammalian alveoli, complex architectural and cellular units with dimensions that are linked to the organism's O2consumption (V˙o2), are thought to be destroyed only by disease and not to spontaneously regenerate. Calorie restriction of adult mammals lowersV˙o2, and ad libitum refeeding returnsV˙o2to pre-calorie-restriction values. We took advantage of these relationships and tested the hypothesis in adult mice that calorie restriction (two-thirds reduction for 2 wk) followed by ad libitum refeeding (3 wk) would cause alveolar destruction and regeneration, respectively. Calorie restriction diminished alveolar number 55% and alveolar surface area 25%. Refeeding fully reversed these changes. Neither manipulation altered lung volume. Within 72 h, calorie restriction increased alveolar wall cell apoptosis and diminished lung DNA (∼20%). By 72 h of refeeding, alveolar wall cell replication increased and lung DNA rose to amounts in mice that were never calorie restricted. We conclude that adult mice have endogenous programs to destroy and regenerate alveoli, thereby raising the danger of inappropriate activation but the possibility of therapeutic induction, if similar programs exist in humans.

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