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Histopathological Alterations (histopathological + alteration)
Selected AbstractsHistopathological alterations in the liver of the sharptooth catfish Clarias gariepinus from polluted aquatic systems in South AfricaENVIRONMENTAL TOXICOLOGY, Issue 2 2009M. J. Marchand Abstract There is a need for sensitive bio-monitoring tools in toxicant impact assessment to indicate the effect of toxicants on fish health in polluted aquatic ecosystems. Histopathological assessment of fish tissue allows for early warning signs of disease and detection of long-term injury in cells, tissues, or organs. The aim of this study was to assess the degree of histopathological alterations in the liver of C. gariepinus from two dams in an urban nature reserve, (Gauteng, South Africa). Two dams (Dam 1 and Dam 2) were chosen for their suspected levels of toxicants. Water and sediments were sampled for metal and potential endocrine disrupting chemical analysis. A quantitative and qualitative histology-based health assessment protocol was employed to determine the adverse health effects in fish. The analysis of blood constituents, fish necropsy, calculation of condition factors, and hepatosomatic indices were employed to support the findings of the qualitative and quantitative histological assessment of liver tissue. Assessment of the liver tissue revealed marked histopathological alterations including: structural alterations (hepatic cord disarray) affecting 27% of field specimens; plasma alterations (granular degeneration 98% and fatty degeneration 25%) of hepatocytes; an increase in melanomacrophage centers (32%); hepatocyte nuclear alterations (90%); and necrosis of liver tissue (14%). The quantitative histological assessment indicated that livers of fish collected from Dam 1 were more affected than the fish livers collected from Dam 2. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Histopathological alterations in the edible snail, Babylonia areolata (spotted babylon), in acute and subchronic cadmium poisoningENVIRONMENTAL TOXICOLOGY, Issue 2 2005P. Tanhan Abstract Histopathological alterations in 6- to 8-month-old juvenile spotted babylon, Babylonia areolata, from acute and subchronic cadmium exposure were studied by light microscopy. The 96-h LC50 value of cadmium for B. areolata was found to be 3.35 mg/L, and the maximum acceptable toxicant concentration (MATC) was 1.6 mg/L. Snails were exposed to 3.35 and 0.08 mg/L (5% of MATC) of cadmium for 96 h and 90 days, respectively. After exposure the gill, the organs of the digestive system (proboscis, esophagus, stomach, digestive gland, and rectum), and the foot were analyzed for cadmium accumulation. The results showed that most digestive organs had a high affinity for cadmium. The main target organ was the stomach, which could accumulate on average 1192.18 ,g/g dry weight of cadmium. Cadmium was shown to accumulate to a lesser extent in the digestive gland, gill, rectum, esophagus, proboscis, and foot. Histopathological alterations were observed in the gill and digestive organs (proboscis, esophagus, stomach, and rectum). The study showed that the stomach and gill were the primary target organs of both acute and subchronic exposure. Gill alterations included increased size of mucous vacuoles, reduced length of cilia, dilation and pyknosis of nuclei, thickening of basal lamina, and accumulation of hemocytes. The epithelial lining of the digestive tract showed similar alterations such as increased size of mucous vacuoles, reduced length of cilia, and dilation of nuclei. In addition, fragmentation of the muscle sheath was observed. © 2005 Wiley Periodicals, Inc. Environ Toxicol 20: 142,149, 2005. [source] Histopathological effects in tissues of snail Lymnaea stagnalis (Gastropoda, Pulmonata) exposed to sublethal concentration of Thiodan® and recovery after exposureJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2005Erhan Ünlü Abstract Histopathological alterations induced by Thiodan® in three tissues, namely, digestive gland, foot and mantle, of the freshwater snail Lymnaea stagnalis were investigated. Specimens of Lymnaea stagnalis were exposed to 0.36% and 0.72% Thiodan® 35 EC, a commercial grade of endosulfan, for 96 h followed by a recovery period of 30 days. Thiodan® caused significant dose dependent histopathological changes in all the tissues of the snail. Irreversible necrotic changes occurred in the digestive gland of the snail following Thiodan® exposure. Degenerative changes in the muscle fiber of the foot, protein and pigment cells of the foot and the connective tissue element of the mantle were recovered after 30 days of recovery of the snail in pesticide-free freshwater. Copyright © 2005 John Wiley & Sons, Ltd. [source] Histopathological alterations in the liver of the sharptooth catfish Clarias gariepinus from polluted aquatic systems in South AfricaENVIRONMENTAL TOXICOLOGY, Issue 2 2009M. J. Marchand Abstract There is a need for sensitive bio-monitoring tools in toxicant impact assessment to indicate the effect of toxicants on fish health in polluted aquatic ecosystems. Histopathological assessment of fish tissue allows for early warning signs of disease and detection of long-term injury in cells, tissues, or organs. The aim of this study was to assess the degree of histopathological alterations in the liver of C. gariepinus from two dams in an urban nature reserve, (Gauteng, South Africa). Two dams (Dam 1 and Dam 2) were chosen for their suspected levels of toxicants. Water and sediments were sampled for metal and potential endocrine disrupting chemical analysis. A quantitative and qualitative histology-based health assessment protocol was employed to determine the adverse health effects in fish. The analysis of blood constituents, fish necropsy, calculation of condition factors, and hepatosomatic indices were employed to support the findings of the qualitative and quantitative histological assessment of liver tissue. Assessment of the liver tissue revealed marked histopathological alterations including: structural alterations (hepatic cord disarray) affecting 27% of field specimens; plasma alterations (granular degeneration 98% and fatty degeneration 25%) of hepatocytes; an increase in melanomacrophage centers (32%); hepatocyte nuclear alterations (90%); and necrosis of liver tissue (14%). The quantitative histological assessment indicated that livers of fish collected from Dam 1 were more affected than the fish livers collected from Dam 2. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Immunization of mice with Lactobacillus casei expressing intimin fragments produces antibodies able to inhibit the adhesion of enteropathogenic Escherichia coli to cultivated epithelial cellsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2008Patrícia C.D. Ferreira Abstract Enteropathogenic Escherichia coli (EPEC) are frequently isolated as a cause of infantile diarrhea in developing countries. Its pathogenicity is distinguished by histopathological alterations at the site of infection, known as attaching and effacing (A/E) lesions, in which bacterial virulence factors and host proteins participate. Intimin, a bacterial adhesin expressed by all EPEC described to date, is responsible for the intimate adherence of the bacteria to host cells and is essential for the formation of A/E lesions. Mucosal vaccination may represent an efficacious intervention to prevent EPEC infection and lower morbidity and mortality rates. Strategies for mucosal vaccinations that use lactic acid bacteria for the delivery of heterologous antigens rely on their safety profile and ability to stimulate the immune system. In the present work, we have constructed Lactobacillus casei strains expressing different fragments of intimin ,, a subtype that is frequently expressed by EPEC strains. Mucosal immunization of mice with L. casei expressing intimin fragments induced specific systemic and mucosal antibodies. These antibodies were able to recognize native intimin on the surface of EPEC and to inhibit in vitro EPEC binding to epithelial cells. [source] Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercuryJOURNAL OF APPLIED TOXICOLOGY, Issue 5 2010Rakhi Agarwal Abstract Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl2, 12,µmol,kg,1 b.w. single intraperitoneal injection). Curcumin treatment (80,mg,kg,1 b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure. [source] Oxidative stress and metabolism in animal model of colitis induced by dextran sulfate sodiumJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2007Carlos R Damiani Abstract Background and Aim:, Ulcerative colitis is a chronic inflammatory disease of the gastrointestinal tract. Its etiology remains unclear, but it appears to result from a dysregulated immune response, with infiltration of phagocytic leukocytes into the mucosal interstitium. The production and release of reactive oxygen species by immune cells seems to play a crucial role in physiopathology of colitis. The aim of this work was to evaluate the effects of N-acetylcysteine (NAC) and deferoxamine (DFX) in the treatment of colitis induced by dextran sulfate sodium (DSS). Methods:, The effects of NAC and DRX on rats with DSS-induced colitis were determined by measuring intestinal parameters of oxidative stress and mitochondrial function, inflammatory response and bowel histopathological alterations. Results:, DSS increased white blood cells count and NAC and DFX did not prevent this effect. However, DSS increased mitochondrial respiratory chain complex IV in colon of rats and NAC and DFX prevented this alteration. In addition, thiobarbituric acid reactive substances were increased in colon of DSS-treated rats. NAC and DFX, when taken together, prevented this effect. Complex II and succinate dehydrogenase were not affected by DSS, as protein carbonyl content. Conclusions:, It is speculated that NAC and DFX might be useful for treatment of colitis, but further research is necessary to clarify these effects. [source] Melatonin reduces experimental subarachnoid hemorrhage-induced oxidative brain damage and neurological symptomsJOURNAL OF PINEAL RESEARCH, Issue 3 2009Mehmet Ersahin Abstract:, Oxidative stress has detrimental effects in several models of neurodegenerative diseases, including subarachnoid hemorrhage (SAH). This study investigated the putative neuroprotective effect of melatonin, a powerful antioxidant, in a rat model of SAH. Male Wistar albino rats were divided as control, vehicle-treated SAH, and melatonin-treated (10 mg/kg, i.p.) SAH groups. To induce SAH, 0.3 mL blood was injected into cisterna magna of rats. Forty-eight hours after SAH induction, neurological examination scores were measured and the rats were decapitated. Brain tissue samples were taken for blood,brain barrier (BBB) permeability, brain water content, histological examination, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+ -K+ -ATPase activities. Formation of reactive oxygen species in brain tissue samples was monitored by using a chemiluminescence (CL) technique. The neurological examination scores were increased in SAH groups on the second day of SAH induction and SAH caused a significant decrease in brain GSH content and Na+ -K+ -ATPase activity, which was accompanied with significant increases in CL, MDA levels, and MPO activity. On the other hand, melatonin treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations, while increased brain water content and impaired BBB were also reversed by melatonin treatment. This study suggests that melatonin, which can easily cross BBB, alleviates SAH-induced oxidative stress and exerts neuroprotection by preserving BBB permeability and by reducing brain edema. [source] Betulinic acid protects against ischemia/reperfusion-induced renal damage and inhibits leukocyte apoptosisPHYTOTHERAPY RESEARCH, Issue 3 2010Emel Ek, lu-Demiralp Abstract The possible protective effect of betulinic acid on renal ischemia/reperfusion (I/R) injury was studied. Wistar Albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Betulinic acid (250 mg/kg, i.p.) or saline was administered at 30 min prior to ischemia and immediately before the reperfusion. Creatinine, blood urea nitrogen (BUN), lactate dehydrogenase (LDH) and TNF-, as well as the oxidative burst of neutrophil and leukocyte apoptosis were assayed in blood samples. Malondialdehyde (MDA), glutathione (GSH) levels, Na+, K+ -ATPase and myeloperoxidase (MPO) activities were determined in kidney tissue which was also analysed microscopically. I/R caused significant increases in blood creatinine, BUN, LDH and TNF-,. In the kidney samples of the I/R group, MDA levels and MPO activity were increased significantly, however, GSH levels and Na+, K+ -ATPase activity were decreased. Betulinic acid ameliorated the oxidative burst response to both formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA) stimuli, normalized the apoptotic response and most of the biochemical indices as well as histopathological alterations induced by I/R. In conclusion, these data suggest that betulinic acid attenuates I/R-induced oxidant responses, improved microscopic damage and renal function by regulating the apoptotic function of leukocytes and inhibiting neutrophil infiltration. Copyright © 2009 John Wiley & Sons, Ltd. [source] Toxic effects of dexamethasone on mouse testicular germ cellsANDROLOGIA, Issue 4 2010M. Orazizadeh Summary Exposure to glucocorticoids (GCs) leads to numerous changes in various biological systems including the reproductive system. This work evaluated effects of dexamethasone (Dex), a widely used GC, on mouse testicular germ cells. Experimental groups (E1,E3) received one of the following treatments daily for 7 days: 4, 7 and 10 mg kg,1 Dex respectively. Control groups were treated with equivalent volumes of saline. Testicular histopathology, morphometric analysis and deoxy-UTP-digoxigenin nick end labeling (TUNEL) assessment were performed for evaluation of the toxic effects of Dex and detection of the apoptotic cells. The results showed that Dex induces histopathological alterations such as epithelial vacuolisation, atrophy and reduction in testicular spermatozoid. Morphometrical data showed that Dex significantly reduced tubular diameter and epithelial height (P < 0.05). Johnsen's scoring also showed poor spermatogenesis in E2 and E3 groups (P < 0.05). Apoptotic index of germ cells was significantly increased in E2 (18.9% versus 1.76%, P < 0.01) and E3 (24.6 versus 1.76%, P < 0.001) groups. It is concluded that Dex acts as testicular toxicant and that further studies are needed to establish its mechanism of action upon spermatogenesis. [source] Protective effect of binaphthyl diselenide, a synthetic organoselenium compound, on 2-nitropropane-induced hepatotoxicity in ratsCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2010Mohammad Ibrahim Abstract Organoselenides have been documented as promising pharmacological agents against a number of diseases associated with oxidative stress. Here we have investigated, for the first time, the potential antioxidant activity of binaphthyl diselenide ((NapSe)2; 50,mg,kg,1, p.o.) against the 2-nitropropane (2-NP)-induced hepatoxicity in rats, using different end points of toxicity (liver histopathology, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine). In addition, in view of the association of oxidative stress with 2-NP exposure, hepatic lipid peroxidation, ascorbic acid levels, ,-aminolevulinate dehydratase (,-ALA-D) and catalase (CAT) activities were evaluated. 2-NP caused an increase of AST, ALT and hepatic lipid peroxidation. 2-NP also caused hepatic histopathological alterations and ,-ALA-D inhibition. (NapSe)2 (50,mg,kg,1) prevented 2-NP-induced changes in plasmatic ALT and AST activities and also prevented changes in hepatic histology, ,-ALA-D and lipid peroxidation. Results presented here indicate that the protective mechanism of (NapSe)2 against 2-NP hepatotoxicity is possibly linked to its antioxidant activity. Copyright © 2010 John Wiley & Sons, Ltd. [source] | |||||||||||||