Degeneration Of Epithelial Cells Research Articles

Structure based modification of chalcone analogue activates Nrf2 in the human retinal pigment epithelial cell line ARPE-19

Oxidative stress-induced degeneration of retinal pigment epithelial (RPE) cells is known to be a key contributor to the development of age-related macular degeneration (AMD). Activation of the nuclear factor-(erythroid-derived 2)-related factor-2 (Nrf2)-mediated cellular defense system is believed to be a valid therapeutic approach. In the present study, we designed and synthesized a novel chalcone analogue, 1-(2,3,4-trimethoxyphenyl)-2-(3,4,5-trimethoxyphenyl)-acrylketone (Tak), as a Nrf2 activator. The potency of Tak was measured in RPE cells by the induction of the Nrf2-dependent antioxidant genes HO-1, NQO-1, GCLc, and GCLm, which were regulated through the Erk pathway. We also showed that Tak could protect RPE cells against oxidative stress-induced cell death and mitochondrial dysfunction. Furthermore, by modifying the α, β unsaturated carbonyl entity in Tak, we showed that the induction of antioxidant genes was abolished, indicating that this unique feature in Tak was responsible for the Nrf2 activation. These results suggest that Tak is a potential candidate for clinical application against AMD.

Assessment of cadmium sulphide nanoparticles toxicity in the gills of a fresh water fish

Effect of cadmium sulphide nanoparticles (CdSNPs) has been studied in the gills of a fresh water fish Channa punctatus. It was observed that CdSNPs induced higher degree of lipid peroxidation as measured through thiobarbituric acid reactive substances than the CdS bulk particles at identical dosage (50 μg/L) and period of exposure. An exposure of 15 days to CdS bulk particles caused injury to gill epithelium, loss of mucous cells and appearance of higher number of vacuolated cells. Massive degeneration of epithelial and mucous cells was recorded after 30 days of exposure. Whereas the fish exposed to CdSNPs for 15 days showed the presence of a few mucous cells at the apical region of secondary gill lamellae. Thirty days exposure resulted into severe loss of epithelial cells, mucous cells and pillar cells. Scanning electron microscopical observations on gill lamellae showed irregular arrangement of micro-ridges and microbridges in CdS treated fish. These structures were highly disorganized in fish exposed to CdSNPs. Clustering of microbridges was predominant in the gills of fish exposed to CdSNPs for 15 days. Whereas, 30 days of exposure resulted into collapse of micro-ridges and microbridges. These changes have been attributed to higher rate of lipid peroxidation induced by CdSNPs in the gills of fish. We concluded that nano-biointerface is of fundamental importance and needs to be assessed further in a relevant biological medium.

362 Effect of a modified hydrated sodium calcium aluminosilicate adsorbent on the growth performance, nutrients digestibility, and digestive tract morphology of chicks challenged with T-2 toxin

Abstract The objective of this study was to evaluate the modified hydrated sodium calcium aluminosilicate (HSCAS) adsorbent ability to reduce the toxicity of T-2 toxin in broilers. 96 one-day-old male broilers were randomly allocated to 4 experimental groups with 4 replicates of 6 birds each. The four groups 1–4 were received the basal diet (BD), BD plus 6.0 mg/kg T-2 toxin, BD plus 6.0 mg/kg T-2 toxin with 0.05% modified HSCAS adsorbent, BD plus 0.05% modified HSCAS adsorbent, respectively, for 2 weeks. The growth performance, nutrients digestibility, and digestive tract histopathology were analyzed. Compared with the control group, dietary supplementation of T-2 toxin decreased (P < 0.05) body weight gain, feed intake and feed conversion by 11.4–31.8% during d 1–7, d 8–14 and d 1–14. Dietary supplementation of T-2 toxin also decreased (P < 0.05) the apparent metabolic rate of crude protein, calcium, and total phosphorus by 14.9–16.1% during d 8–14. These alterations induced by T-2 toxin were mitigated or prevented (P < 0.05) by the supplementation of the modified HSCAS adsorbent. Meanwhile, dietary modified HSCAS adsorbent supplementation also prevented (P < 0.05) T-2 toxin-induced morphological changes and damage, such as severe degeneration and desquamation of the villous epithelial cells, congestion in intestinal lamina propria, and edema and thicken in the serosa with infiltration of numerous lymphoid cells, in the gizzard, duodenum, jejunum, and ileum of broilers. Notably, dietary supplementation of the modified HSCAS adsorbent alone did not affect (P > 0.05) any of those parameters. In conclusion, these findings indicate this novel HSCAS could be used as a promising adsorbent for protecting against T-2 toxin-induced toxicity in chicks (This work was supported in part by the National Key Research and Development Program of China, Projects 2018YFD0500601 and 2016YFD0501207).

363 Integrated transcriptomic and gut microbiome analysis of the toxic effects of T-2 toxin on the small intestine of chickens

Abstract This study was conducted to reveal the mechanism of T-2 toxin induced small intestine injuries in broilers through a new perspective that combined transcriptomics and microbiology studies. 96-d-old male Cobb broilers were randomly allocated into 4 treatment groups with 4 replicates of 6 birds/cage and all birds were fed a corn-soybean-based diet (Control) and the other 3 groups supplemented with T-2 toxin at 1.0, 3.0 or 6.0 mg/kg, respectively, for 2 weeks. Growth performance and nutrients digestibility were analyzed. Duodenum was collected to assay for histology, transcriptomics and microbiology. Compared with the control, final body weight, body weight gain and feed intake were decreased (P < 0.05) in a dose-dependent manner with increasing dietary T-2 toxin dose. Specially, in dietary T-2 toxin at 6.0 mg/kg, the feed/gain increased (P < 0.05) 11.4% and the apparent metabolic rate of crude protein, calcium and phosphorus were decreased (P < 0.05) by 14.9%, 18.0% and 16.1%, respectively. Meanwhile, T-2 toxin induced severe degeneration, necrosis and desquamation of the villous epithelial cells, increased inflammatory cells. Furthermore, the results of transcriptome drew that 2536 genes showed significant differences and were partially enriched in metabolic pathways, cell growth and death, apoptosis, the metabolism by CYP450, immune response pathways. Gut microbiota play a key role as microbial and duodenum genes and metabolites affected by T-2 toxin shared multiple pathways. Remarkably, Firmicutes and Proteobacteria that related to energy metabolism and inflammatory were seriously affected (P < 0.05). In summary, combined the results of integrated analysis, T-2 toxin partially induced intestine injury, potentially through changing the gene expression and the intestinal micro-ecology or damaging the intestinal mucosal directly, thus inducing inflammatory and apoptotic.

Toxic effects of A2E in human ARPE-19 cells were prevented by resveratrol: a potential nutritional bioactive for age-related macular degeneration treatment.

Age-related macular degeneration (AMD) is a late-onset retinal disease and the leading cause of central vision loss in the elderly. Degeneration of retinal pigment epithelial cells (RPE) is a crucial contributing factor responsible for the onset and progression of AMD. The toxic fluorophore N-retinyl-N-retinylidene ethanolamine (A2E), a major lipofuscin component, accumulates in RPE cells with age. Phytochemicals with antioxidant properties may have a potential role in both the prevention and treatment of this age-related ocular disease. Particularly, there is an increased interest in the therapeutic effects of resveratrol (RSV), a naturally occurring polyphenol (3,4',5-trihydroxystilbene). However, the underlying mechanism of the RSV antioxidative effect in ocular diseases has not been well explored. We hypothesized that this bioactive compound may have beneficial effects for AMD. To this end, to investigate the potential profits of RSV against A2E-provoked oxidative damage, we used human RPE cell line (ARPE-19). RSV (25µM) attenuates the cytotoxicity and the typical morphological characteristics of apoptosis observed in 25µM A2E-laden cells. RSV pretreatment strengthened cell monolayer integrity through the preservation of the transepithelial electrical resistance and reduced the fluorescein isothiocyanate (FITC)-dextran diffusion rate as well as cytoskeleton architecture. In addition, RSV exhorts protective effects against A2E-induced modifications in the intracellular redox balance. Finally, RSV also prevented A2E-induced mitochondrial network fragmentation. These findings reinforce the idea that RSV represents an attractive bioactive for therapeutic intervention against ocular diseases associated with oxidative stress such as AMD.

Morphological Characteristics of Skin Lesions in Cattle Naturally Infected with Lumpy Skin Disease Virus in Serbia

Abstract Lumpy skin disease (LSD) is a disease of cattle and domestic buffaloes caused by Capripoxvirus which can lead to significant economic losses. Until several years ago it was limited to Africa and the Middle East, but recently it was reported in Turkey (2013), Greece (2015), and in 2016 it spread to Bulgaria, North Macedonia, Albania, Montenegro and Serbia. The aim of this study was to determine the microscopic lesions in the skin of naturally infected animals, highlight their features and compare them to the findings of other authors. Gross lesions in the skin of cattle infected with Lumpy skin disease virus (LSDV) were manifested in the form of skin nodules which were round, raised, clearly circumscribed, firm and randomly distributed in the whole skin including the vulva and udder. Histopathological lesions included degeneration of epithelial cells, hyperkeratosis, spongiosis, and acanthosis present in 85.88%, 81.18%, 84.71%, and 80.0% of samples, respectively. Intracytoplasmic inclusion bodies were noted in keratinocytes of the stratum spinosum in 56.47% of samples, and in hair follicle cells and sebaceous glands epithelial cells in 45.88% of samples. Cutaneous lesions were in the form of inflammatory infiltrate present in the dermis and subcutis in 97.65% of samples. Since there are only a few literature data in this field, this study expands the knowledge relating to morphological alterations in LSD. Based on the characteristic microscopic lesions described in the present study, histopathology should be considered as a very useful method for the diagnosis of LSD.

The ameliorative role of geranium (Pelargonium graveolens) essential oil against hepato-renal toxicity, immunosuppression, and oxidative stress of profenofos in common carp, Cyprinus carpio (L.)

The present study investigated the possible effect of profenofos (PFF) on hepato-renal functions, non specific-immunity, and oxidants/antioxidants status in common carp, Cyprinus carpio (L.), and the supportive role of geranium (Pelargonium graveolens) essential oil (GEO). A static 96-h acute toxicity test was performed to determine the 96-h LC50 of PFF in common carp fingerlings and it was found to be 47.46 μg L−1 calculated by Finney probit analysis. One hundred and twenty fish were randomly allocated into four groups in triplicate. The first served as control and second groups were fed on basal diets that were enriched with 0.0 and 400 mg kg−1 of diet GEO, respectively without PFF exposure. The third and fourth groups were fed on the same diets and in addition, were exposed to 1/10 of the 96 h-LC50 of PFF (4.74 μg L−1), respectively for 60 days. The results revealed that the PFF exposure induced marked increases in the levels of serum alanine and aspartate aminotransferases (ALT and AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), creatinine, urea, cholesterol, triglycerides (TG), and malondialdehyde (MDA). Meanwhile, the serum total protein (TP), globulins, glucose, lysozyme activity, complement3 (C3), nitric oxide (NO), and hepatic antioxidant enzyme activities as well as the reduced glutathione (GSH) content were markedly declined in the PFF-exposed fish compared to the control group. Additionally, vacuolation, pyknosis, and degeneration of hepatocytes and epithelial cells of renal tubules with mononuclear cell infiltration were observed. A strong caspase-3 and weak BCL-2 immunohisto-reactivity in the liver and kidney tissues of PFF-exposed fish were noted respective to the control. Interestingly, GEO supplementation improved these variables with nearly restoring to control values with improving the histological architecture of liver and kidney tissues. The apoptotic condition of the examined tissues was markedly restricted in the combination group than PFF-exposed group. These results concluded that GEO has ameliorative influence against toxic impacts of PFF on hepato-renal functions, immunological parameters, and oxidative stress in common carp, and therefore, maybe a valuable candidate as a dietary supplement in aquaculture.

Rat liver and kidney post-mitochondrial dysfunction by addition of chronic mixed metal intoxication and hepatorenal wellness mediated by phenolic components from Croton zambiscus leaves

Chronic exposure of mixed-metal intoxication has been associated with prolonged oxidative stress and severe hepatorenal damage. This present study demonstrates the hepatoprotective and renoprotective activity of Croton zambesicus (C-ZAMB) leaves, naturally occurring phenolic compounds against chronic mixed-metal (EOMABRSL) induced toxicity. 0.5 ml of EOMABRSL via oral route induced chronic hepatoxicity and nephrotoxicity on exposure for 98 days (non-withdrawal) and 70 days (withdrawal) by abnormal alteration in the levels of endogenous antioxidants. Moreover, EOMABRSL induced hepatorenal damage by increasing the markers of liver toxicity (ALT, AST, ALP, GGT and bilirubin) and kidney failure (creatinine, urea, uric acid, and renal electrolytes-Na+ and K+). Both non-withdrawal and withdrawal approaches of EOMABRSL-exposed animals exhibited hepatorenal dysfunctions by increasing the activity of eco-51-nucleotidase (51ENT) followed by the decreased in the activity of lactate dehydrogenase (LDH)-index of cellular ATP. These results were further supported by the histopathological examination of nephritic cells, hepatocytes and splenocytes, manifested by hepatocellular necrosis, swelling or degeneration of tubular kidney epithelial cells as well as coalescing splenic periarteriolar lymphoid sheaths (PALSs) and lymphoid haemosiderin. The chronic EOMABRSL intoxication was ameliorated by administration of phenolic antioxidants from C-ZAMB leaves. Therefore, our study supports the view that phenolic C-ZAMB leaves may mediate hepatorenal wellness on chronic exposure to mixed-metal intoxication

Outbreak of carp edema virus disease in cultured ornamental koi in a lower temperature in China

Carp edema virus (CEV) is the pathogen of carp edema virus disease (CEVD), an emerging infectious disease with high morbidity and mortality worldwide. In the winter of 2016, a disease outbreak occurred in a koi pond in Chengdu, located in the southwest of China. The water temperature at that time was 11–13 °C. The clinical signs of the diseased koi were lethargy, unresponsiveness, enophthalmos, swollen gills, and hemorrhagic skin. Histopathological changes were observed in moribund fish, such as significant cell hyperplasia in the gill lamellae, and swelling and vacuolar degeneration in epithelial cells of the renal tubules and hepatocytes. Electron microscopy of renal tissues showed virions of a pox-like virus (200–235 nm diameter). The presence of specific 528 bp and 478 bp fragments was detected by nested PCR. An experimental infection demonstrated cumulative mortality of 15% (3/20) at a water temperature of 13 ± 2 °C. Furthermore, sequence analysis of the partial 4a genes showed that the CEV isolate (MG189372) in this study had 100% homology with a UK strain (KX254027). The evidence showed that the pathogen involved in this outbreak was CEV. To the best of our knowledge, this is the first report of carp disease caused by CEV at low temperature in China, demonstrating that CEV disease should be monitored in the cold season and at low temperatures. The findings are of profound significance to reducing the risk of CEVD outbreaks in carp aquaculture.

Bothrops alternatus Snake Venom Induces Cytokine Expression and Oxidative Stress on Renal Function.

Envenomation caused by Bothrops alternatus is common in Southern Brazil. Acute Kidney Injury occurs after Bothrops snakebite and more information is necessaryrequired to understand its mechanism. The objective was to evaluate the effect of Bothrops alternatus venom (BaV) on renal cells and rat isolated kidney function. Wistar rats (n = 6, weighing 260-320 g) were perfused with a Krebs-Henseleit solution containing 6 g 100 mL-1 of bovine serum albumin. After 30 minutes, the kidneys were perfused with BaV to a final concentration of 1 and 3 μgmL-1; and subsequently were evaluated for Perfusion Pressure (PP), Renal Vascular Resistance (RVR), Urinary Flow (UF), Glomerular Filtration Rate (GFR), and percentage of electrolyte tubular transport. Renal histological analysis, cytokine release, oxidative stress and cytotoxicity in renal proximal tubular cells were assessed. BaV reduced PP, RVR, GFR, UF, total and proximal sodium transport (%TNa+), and chloride (%TCl-) in the isolated kidney perfusion model. Histological analysis of perfused kidneys disclosed the presence of proteinaceous material in the glomeruli and renal tubules, vacuolar tubular epithelial cell degeneration, Bowman's capsule degeneration, swelling of glomerular epithelial cells, glomerular atrophy and degeneration, and the presence of intratubular protein. Cytokine release (TNF-α, IL-1β, IL-10) and oxidative stress were increased in the kidneys. The viability of LLC-MK2 cells (IC50: 221.3 μg/mL) was decreased by BaV and necrosis was involved in cell death. These findings indicate that BaV modifies functional parameters in an isolated perfused kidney model and has cytotoxic effects on renal lineage cells.

Evaluation with endothelial nitric oxide synthase (eNOS) immunoreactivity of the protective role of astaxanthin on hepatorenal injury of remote organs caused by ischaemia reperfusion of the lower extremities.

IntroductionIschemia and following reperfusion triggers local and systemic damage with the involvement of free oxygen radicals and inflammatory mediators. Although blood flow saves extremity from necrosis,multi organ dysfunction may progress and cause death of the patient.AimThe study aims to examine the effect of astaxanthin (AST) on the prevention of remote tissue injury resulting from lower extremity ischaemia–reperfusion (I/R). To elucidate the potential hepatoprotective and renoprotective effects of AST, in addition to histopathological findings, the intrahepatic and intrarenal kinetics of endothelial nitric oxide synthase (eNOS) during I/R were determined by using the immunohistochemical method.Material and methodsTwenty-eight male Wistar albino rats were divided into four groups. For the control group, only the anaesthesia procedure (2 h) was conducted without I/R. In the I/R group, 2 h of reperfusion was conducted following ischaemia under anaesthesia. For the I/R group + AST, 7 days prior to ischaemia, 125 mg/kg AST was given with gavage, and 2 h of ischaemia and 2 h of reperfusion were conducted under anaesthesia. Following necropsy, liver and kidney tissue samples were fixed in 10% buffered formalin for 48 h for histopathological and immunohistochemical investigation.ResultsThe histological analysis revealed that severe I/R hepatorenal injury such as inflammatory cell infiltration, dilatation in sinusoids and lumen of tubuli, congestion in glomerular capillaries, degeneration in hepatocyte and epithelial cells of tubuli, and necrosis was ameliorated by AST. Immunohistochemical studies showed that the I/R-induced elevation in eNOS expression was reduced by AST treatment.ConclusionsIn the case of acute lower extremity I/R, AST decreased the ischaemic injury in liver and renal tissues by protecting the microcirculation and providing a cytoprotective effect with vasodilatation.

Screening of Early Diagnostic Markers of Gentamicin-induced Acute Kidney Injury in Canines.

IntroductionThe value of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (Kim-1), and liver-type fatty acid binding protein (L-FABP) was assessed in early diagnosis of gentamicin-induced acute kidney injury (AKI) in dogs.Material and MethodsSubcutaneous gentamicin injection in 16 healthy adult beagles made the AKI model. Blood was sampled every 6 h to detect NGAL, Kim-1, L-FABP, and serum creatinine (SCr) concentrations. Kidney tissue of two dogs was taken before the injection, as soon as SCr was elevated (78 μmol/L), and when it had risen to 1.5 times the baseline, and haematoxylin-eosin staining and transmission electron microscopy (TEM) were used to observe changes.ResultsNGAL, Kim-1, and SCr levels were significantly increased (P < 0.05) at 18, 30, and 78 h post injection, but L-FABP concentration was not associated with renal injury. At the earliest SCr elevation stage, findings were mild oedema, degeneration, and vacuolisation in renal tubular epithelial cells in pathology, and mild cytoplasmic and mitochondrial oedema in TEM. At this time point, NGAL and Kim-1 concentrations were significantly increased (P < 0.05), indicating that these two molecules biomark early kidney injury in dogs. Using receiver operating characteristic curve analysis, their warning levels were > 25.31 ng/mL and > 48.52 pg/mL.ConclusionPlasma NGAL and Kim-1 above warning levels are early indicators of gentamicin-induced AKI in dogs.

Androgens are essential for epithelial cell recovery after efferent duct ligation in the initial segment of the mouse epididymis†.

Efferent duct ligation (EDL) induces epithelial cell degeneration followed by regeneration in the epididymal initial segment. We tested here the role of androgens in the recovery phase. EDL was performed at post-natal weeks (PNW) 3, 4, 5, 6, and 7, and apoptotic and proliferating epithelial cells were quantified 24h, and at days 2 and 2.5 post-EDL, respectively. A progressive increase in the number of apoptotic basal cells (BCs) and principal cells (PCs) was detected from PNW3 to 6, 24h after EDL. Twodays after EDL, no increase in proliferating BCs and PCs was observed at PNW3 and 4, despite the induction of apoptosis by EDL. A progressive increase in the number of proliferating BCs was then observed from PNW5 to 6, while the number of proliferating PCs remained low. 2.5days after EDL, the number of proliferating BCs and PCs remained low at PNW3, 4, and 5, but a marked increase in the number of proliferating PCs was observed at PNW6. Flutamide pretreatment for 3weeks followed by EDL at PNW7 dramatically decreased the number of proliferating BCs on EDL day 2, and the number of proliferating PCs on EDL day 2.5, compared to controls. We conclude that (1) BCs are the first to show recovery after EDL, followed by PCs; (2) androgens are essential for BC and PC repair after injury in the postpubertal epididymis; and (3) the prepubertal epididymis lacks repair ability following injury.

Ondansetron enhanced diclofenac-induced nephrotoxicity in mice.

This study was performed to investigate the effect of ondansetron, a serotonin receptor (5-HT3) antagonist, in the alleviation of diclofenac-induced kidney injuries. NMRI mice were randomly divided into six groups and treated with (A) untreated control group, (B) diclofenac (100 mg/kg), (C) ondansetron (1 mg/kg), (D to F) ondansetron (0.1, 0.5, and 1 mg/kg, respectively) and diclofenac (100 mg/kg) for last 3 days of experiment. The oxidative stress tests strongly demonstrated the negative synergistic effects of diclofenac and ondansetron, regarding the observation of dose-dependent enhancement of malondialdehyde concentration, and reduction of glutathione content, and superoxide dismutase and catalase activity.Histopathological analyses revealed dose-dependent tubular epithelial cells degeneration, outstanding mononuclear cells infiltration, clear necrosis at the papillary region of kidney, dilation, and vascular hyperemia in mice kidney tissues treated with ondansetron and diclofenac. Conclusively, these findings suggested the possible ondansetron-diclofenac interaction through the induction of oxidative stress.

MicroRNA-206 overexpression inhibits epithelial-mesenchymal transition and glomerulosclerosis in rats with chronic kidney disease by inhibiting JAK/STAT signaling pathway.

Chronic kidney disease (CKD) is a traumatic disease with significant psychic consequences to the patient's overall physical condition. microRNA-206 (miR-206) has been reported to play an essential role in the development of various diseases. The purpose of the present study is to investigate the effect of miR-206 through the JAK/STAT signaling pathway on epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells and glomerulosclerosis in rats with CKD. The targeting relationship between miR-206 and ANXA1 was verified. To explore the role of miR-206 in CKD, the model of CKD rats was established to detect glomerular sclerosis index (GSI), contents of interleukin-6 (IL-6) and transforming growth factor-beta1 (TGF-β1), and expression of type IV collagen. Moreover, to further determine the roles of both miR-206 and the JAK/STAT signaling pathway in CKD, the gain- and loss-of function approaches were performed with the expression of ANXA1, α-SMA, E-cadherin, vimentin, N-cadherin, and the JAK/STAT signaling pathway-related genes detected. miR-206 negatively targeted ANXA1. Overexpressed miR-206 inhibited the degeneration and interstitial fibrosis of renal tubular epithelial cells, decreased GSI of rats, and the expression of type IV collagen, TGF-β1 and IL-6. Overexpressed miR-206 inhibited the degeneration of renal tubular epithelial cells, the expression of ANXA1, α-SMA, TGF-β1, p-STAT3, STAT3, p-STAT1, STAT1, p-JAK2, and JAK2, while promoted the expression of E-cadherin. Taken together the results, miR-206 inhibits EMT of renal tubular epithelial cells and glomerulosclerosis by inactivating the JAK/STAT signaling pathway via ANXA1 in CKD.

Impact of fullerene C60 on behavioral and hematological changes in the freshwater fish, Anabas testudineus (Bloch, 1792)

The unique physico-chemical properties of fullerene C60 have aided in its application in various fields along with several ecological impacts as an emerging pollutant. So, there is a significant need to demonstrate the ecological risk and toxic impact of fullerene C60 in the freshwater ecosystem. The present study focused on the toxic impact of fullerene C60 on behavioral and hematological changes in the freshwater fish, Anabas testudineus. The acute toxicity of fullerene C60 in Anabas testudineus determined by Probit analysis was found to be 50 mg/L. For the analysis, the fish were exposed to two sublethal concentrations of 5 mg/L (one-tenth of LC50-96 h) and 10 mg/L (one-fifth of LC50-96 h) for short-term (24, 48, 72 and 96 h) and long-term (7, 15, 30 and 60 days) durations. Fullerene C60 exposure showed prominent changes in behavior of the fish that comprises changes in swimming activity, disruption of schooling behavior, air engulping and surfacing along with morphological alterations such as descaling, slight hemorrhage and mucous secretion on the body surface, which was correlated to significant (P < 0.05) decrease in the activity of acetylcholinesterase enzyme in brain tissue. Hematological changes includes significant (P < 0.05) reduction in the erythrocyte and leukocyte counts, hemoglobin concentration, percentage of the packed cell volume (hematocrit) and the levels of serum albumin, globulin and total protein, whereas serum glucose concentration and the activities of the serum alanine and aspartate aminotransferases were significantly (P < 0.05) increased during the sublethal exposures. Severe degeneration in the columnar epithelial cells and lamina propria, along with increased number of mucous cells observed in the intestine of the fish indicates sublethal toxicity of fullerene C60. The present findings led to the conclusion that the sublethal concentrations of fullerene C60 have a toxic impact on the fish A. testudineus by affecting the normal physiology, and thus the presence of this nanomaterial in the environment may affect the health status of the ecosystem.

Efficacy Evaluation and Tracking of Bone Marrow Stromal Stem Cells in a Rat Model of Renal Ischemia-Reperfusion Injury.

Objectives The aim of this study was to evaluate the effects of bone marrow stromal stem cells (BMSCs) on renal ischemia-reperfusion injury (RIRI) and dynamically monitor engrafted BMSCs in vivo for the early prediction of their therapeutic effects in a rat model. Methods A rat model of RIRI was prepared by clamping the left renal artery for 45 min. One week after renal artery clamping, 2 × 106 superparamagnetic iron oxide- (SPIO-) labeled BMSCs were injected into the renal artery. Next, MR imaging of the kidneys was performed on days 1, 7, 14, and 21 after cell transplantation. On day 21, after transplantation, serum creatinine (Scr) and urea nitrogen (BUN) levels were assessed, and HE staining and TUNEL assay were also performed. Results The body weight growth rates in the SPIO-BMSC group were significantly higher than those in the PBS group (P < 0.05), and the Scr and BUN levels were also significantly lower than those in the PBS group (P < 0.05). HE staining showed that the degree of degeneration and vacuole-like changes in the renal tubular epithelial cells in the SPIO-BMSC group was significantly better than that observed in the PBS group. The TUNEL assay showed that the number of apoptotic renal tubular epithelial cells in the SPIO-BMSC group was significantly lower than that in the PBS group. The T2 value of the renal lesion was the highest on day 1 after cell transplantation, and it gradually decreased with time in both the PBS and SPIO-BMSC groups but was always the lowest in the SPIO-BMSC group. Conclusion SPIO-labeled BMSC transplantation can significantly promote the recovery of RIRI and noninvasive dynamic monitoring of engrafted cells and can also be performed simultaneously with MRI in vivo for the early prediction of therapeutic effects.

Positive outcomes of phosphodiesterase type 5 inhibitor on histopathologic and biochemical changes induced by ureteral obstruction.

We examined the effects of tadalafil, one of the phosphodiesterase type 5 (PDE5) inhibitors, in a rat model of with partial and complete unilateral ureteral obstruction (UUO). The rats were divided into 5 groups: sham (n=6), partial unilateral ureteral obstruction (PUUO, n=6), PUUO with tadalafil treatment (PUUO+T; Cialis, 10 mg/72 h, intragastric; Lilly, Indianapolis, Indiana, USA), complete unilateral ureteral obstruction (CUUO, n=6), and CUUO with tadalafil treatment (CUUO+T). Fifteen days after the UUO, the ureter presented changes in the layers of urothelium and significant infiltration of inflammatory cells in the PUUO and CUUO groups. Compared with the sham, PUUO and CUUO groups had severe increased inflammatory cell infiltration. The urothelial epithelium exhibited cell degeneration and loss because of the swollen, atrophic, and denuded epithelial cells in the PUUO and CUUO groups. In the PUUO+T and CUUO+T groups, the urothelium revealed less epithelial cell degeneration and loss.The expressions of α-smooth muscle actin (α-SMA) and transforming growth factor-β (TGF-β) exhibited up-regulation in the PUUO and CUUO groups. The expression of TGF-β decreased positively correlated with that of α-SMA in the tadalafil therapy groups, PUUO+T and CUUO+T. The phosphodiesterase type 5 inhibitor's tadalafil reduced expressions of α-SMA and TGF-β in the obstructed ureters, measured by biochemical examinations. In addition, tadalafil decreased urothelium degeneration due to the decreased epithelial cell loss and inflammatory cell infiltration. Our results show that tadalafil prevents or slows down the onset of ureter inflammation and urothelial degeneration in rats with UUO.

Histopathological study of effects phenobarbital in Goats

In this data was done to demonstrate the administration of phenobarbital compounds &amp; showed histopathological effects. In this study fourteen of local goats were divided into two groups (each group seven animals) for 60 days. First one were treated phenobarbital injected with 35 mg \kg.B.W.,twice daily ,second group act as control group. These animals were examined internally and externally during adaptation period. After end experimental period scarified the animals, necropsy, preparation of slid by routine technique and examined by light microscope, there are showed different histological changes into tissue of animals treatment with phenobarbital such as degeneration of epithelial cells lining of renal tubules of kidney and thyroid gland congested of central vein with fibrosis in liver ,vacuolated of mucosal layer of rumen, small intestine and pancreas, atrophyseminiferous tubules of testis and lymph node.

Effects of titanium dioxide nanoparticles on red swamp crayfish, Procambarus clarkii: Bioaccumulation, oxidative stress and histopathological biomarkers

The widespread use of titanium dioxide nanoparticles (TiO2 NPs) in many applications has led to its significant release to aquatic systems. Hence, the present study was performed to evaluate effects of TiO2 NPs on crayfish Procambarus clarkii, which is often used as a bioindicator of water pollution. Adult male specimens were treated with 25, 125, and 250 mg/l of TiO2 NPs for 28 days. Mortalities were 0, 3.3, and 10% for animals treated with 25, 125, and 250 mg/l of TiO2 NPs, respectively. The level of titanium bioaccumulation in different tissues was as follows, gills > hepatopancreas > green glands > muscles. TiO2 NPs-exposed crayfish showed significant increase in the levels of catalase, glutathione-S-transferase, glutathione peroxidase, gamma-glutamyl transferase, glutathione, and metallothioneins in the hepatopancreas. Exposure of the crayfish to 250 mg/l TiO2 NPs caused severe histopathological alterations. In the hepatopancreas, the most prominent pathological changes were tubular disruption and inflammatory infiltration. Under transmission electron microscope (TEM), ruptured microvilli, deformed mitochondria and fragmentation of rough endoplasmic reticulum (RER) were observed. In the gills, swelling of gill lamellae, disorganization and degeneration of epithelial cells were noted under the light microscope (LM). Under electron microscope (EM), gills of crayfish treated with 250 mg/l TiO2 NPs showed vacuolation, dense granules, and diminution in the number of apical plasma membrane infoldings. In conclusion, TiO2 NPs caused alteration in antioxidant activities and severe histopathological changes.