Alterations In Liver Tissues Research Articles

Evaluation of Health Status and Histo-Architecture of Heterobranchus Longifilis and Clarias Buthupogon Obtained from Asa River, Nigeria

Gross impact of water pollution and water borne pollutants on aquatic organisms and man has become a great concern to public health in the recent time. Therefore, the aim of this study was to evaluate the effects of pollutants from the polluted Asa River on the liver histology of Clarias buthupogon and Heterobranchus longifilis. The sample included a total of 55 individuals (28 for C. buthupogon and 27 for H. longifilis).There was a recorded moderate to intense alterations of liver tissues. The most notable alterations were congestion of central vein, degeneration of hepatocyte, sinusoidal distortion, cellular inflammation and necrosis. However, all histological alterations recorded in the liver tissues were most likely to be caused by increased concentrations of certain pollutants from industrial, domestic and agricultural premises. Furthermore, these results represent an additionalreason to proceed with a detailed monitoring of the Asa River and the wildlife therein, for the sake of public health.

Sensitivity of multifrequency magnetic resonance elastography and diffusion-weighted imaging to cellular and stromal integrity of liver tissue

Microscopic structural alterations of liver tissue induced by freeze-thaw cycles give rise to palpable property changes. However, the underlying damage to tissue architecture is difficult to quantify histologically, and published data on macroscopic changes in biophysical properties are sparse.To better understand the influence of hepatic cells and stroma on global biophysical parameters, we studied rat liver specimens freshly taken (within 30 min after death) and treated by freeze-thaw cycles overnight at either −20 °C or –80 °C using diffusion-weighted imaging (DWI) and multifrequency magnetic resonance elastography (MRE) performed at 0.5 T in a tabletop MRE scanner. Tissue structure was analyzed histologically and rheologic data were analyzed using fractional order derivatives conceptualized by a called spring-pot component that interpolates between pure elastic and viscous responses.Overnight freezing and thawing induced membrane disruptions and cell detachment in the space of Disse, resulting in a markedly lower shear modulus μ and apparent diffusion coefficient (ADC) (μ[−20 °C] = 1.23 ± 0.73 kPa, μ[−80 °C] = 0.66 ± 0.75 kPa; ADC[–20 °C] = 0.649 ± 0.028 μm2/s, ADC[−80 °C] = 0.626 ± 0.025 μm2/s) compared to normal tissue (μ = 9.92 ± 3.30 kPa, ADC = 0.770 ± 0.023 μm2/s, all p < 0.001). Furthermore, we analyzed the springpot-powerlaw coefficient and observed a reduction in −20 °C specimens (0.22 ± 0.14) compared to native tissue (0.40 ± 0.10, p = 0.033) and −80 °C specimens (0.54 ± 0.22, p = 0.002), that correlated with histological observations of sinusoidal dilation and collagen distortion within the space of Disse. Overall, the results suggest that shear modulus and water diffusion in liver tissue markedly decrease due to cell membrane degradation and cell detachment while viscosity-related properties appear to be more sensitive to distorted stromal and microvascular architecture.

Enhanced antitumour activity of doxorubicin and simvastatin combination loaded nanoemulsion treatment against a Swiss albino mouse model of Ehrlich ascites carcinoma.

Doxorubicin (DOX) is the most commonly used anticancer drug; however, it has limited use because prolonged administration may result in severe cardiotoxicity. Simvastatin (SIM), generally prescribed for hypercholesterolaemia, has also shown salubrious results in the monotherapy or combinational drug therapy of different cancers in various models. Nanoparticle drug delivery systems are a novel way of improving therapeutics and also improving the absorption and specificity of drugs towards tumour cells. In this study, we exploited this technology to increase drug specificity and minimize imminent adverse effects. In this study, the antitumour activity of the combination formulas of DOX and SIM, either loaded in water (DOX-SIM-Solution) or nanoemulsions (NEs) (DOX-SIM-NE), was evaluated in a Swiss albino mouse model of Ehrlich ascites carcinoma. The anticancer effect was assessed by quantifying the change in body weight, mean survival time, and percent increase in lifespan (%ILS), determining haematological and serum biochemical parameters (liver function test, kidney function test and lipid profile parameters) as well as studying the histopathological alterations in liver tissues. We observed a clear increase in %ILS of the DOX-SIM-Solution group (265.30) that was double the %ILS of the DOX-SIM-NE group (134.70). However, DOX-SIM-NE had a non-toxic effect on the haematological parameters, whereas DOX-SIM-Solution increased the levels of haemoglobin and lymphocytes. Furthermore, the encapsulation of SIM and DOX into NEs improved the levels of all serum biochemical parameters compared to the DOX-SIM-Solution. A reduction in the side effects of DOX-SIM-NE on the liver was also established using light microscopy, which revealed that the morphologies of the hepatocytes of the mice were less affected by administration of the DOX-SIM-NE treatment than with the DOX-SIM-Solution treatment. The study showed that incorporating SIM into the DOX-loaded-NE formulation remarkably improved its efficiency and simultaneously reduced its adverse effects.

Hepatoprotective Effect of Aqueous Extract of Persian Gulf brown Algae Sargassum swartzii Against Acetaminophen-Induced Hepatotoxicity in Mice

Background: The liver plays an important role in detoxification of harmful materials and chemical agents. Many medicines, such as acetaminophen, are potential for oxidative stress and liver toxicity. The brown algae Sargassum swartzii possesses many pharmacological benefits. The present study investigated the aqueous extract of Persian Gulf brown algae Sargassum swartzii effect on acetaminophen-induced liver injury in mice. Objectives: It seems that Persian Gulf algae (Sargassum swartzii) with its anti-inflammatory and antioxidant properties has preventive effects on acetaminophen-induced liver toxicity, yet no research has been reported in this regard so far. Therefore, this study aimed at evaluating the effect of acetaminophen-induced liver toxicity in mice. Methods: Brown algae (Sargassum swartzii) was collected from the low tide area of Boushehr coasts, Persian Gulf). After transfer to the laboratory, the collected sample was washed with distilled water, air dried, and pulverized to powder. The air dried S. swartzii powder was soaked in 95% ethanol to remove pigments and small lipophilic molecules. The residue was then extracted with 10 mL of distilled water at 90°C for three hours, three times. All water extracts were combined, filtrated, and concentrated by water bath at 90°C and stored at 0°C for further analysis. Hepatoprotective activity of the S. swartzii extract was confirmed by aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) levels and histopathologic findings as evidences. Results: Aqueous extract of S. swartzii at dose of 200 mg/kg showed a significant (P < 0.05) decrease in the levels of ALT, AST, and ALP, yet at dose of 100 mg/kg, it showed a significant (P < 0.05) decrease in the level of ALT. Conclusions: Administration of the aqueous extract of S. swartzii (100 and 200 mg/kg) could improve hepatotoxicity induced by acetaminophen via change in liver marker enzymes and also improved histopathological alterations in liver tissue.

Shikonin attenuates acetaminophen-induced acute liver injury via inhibition of oxidative stress and inflammation

Acetaminophen (APAP) overdose causes acute liver injury and leads to fatal liver damage. However, the therapies are quite limited. Shikonin is a natural product with antioxidant and anti-inflammatory activities. In the present study, the hepatoprotective effects and the underlying mechanisms of shikonin in APAP-induced hepatotoxicity in vivo and in vitro were investigated. APAP-induced acute liver injury and shikonin pretreatment models were established in vivo and in vitro, as evidenced by serum hepatic enzymes, histological changes, oxidative stress indicators and proinflammatory cytokines. The results revealed that shikonin pretreatment prevented the elevation of serum alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH) levels and markedly reduced APAP-induced histological alterations in liver tissues. Additionally, shikonin restored superoxide dismutase (SOD) expression and glutathione (GSH) content in line with the blockade of oxidative stress. The changes in gene expression involved in oxidative stress including methionine sulfoxide reductase (such as MsrA and MsrB1), heme oxygenase-1 (HO-1), SOD2 and cytochrome P450 2E1 (CYP2E1), were markedly reversed after shikonin therapy. Furthermore, shikonin markedly attenuated the APAP-induced production of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) and suppressed the expression of genes related to inflammation. In AML-12 cells, shikonin pretreatment decreased APAP-induced cytotoxicity as measured by CCK-8 assay and LDH release. The changes in gene expression involved in oxidative stress and the inflammatory response were consistent with those in mouse livers. This study indicated that shikonin attenuated APAP-induced acute liver injury via inhibiting oxidative stress and inflammatory responses in vivo and in vitro. These findings offer new insights into the potential therapy for APAP hepatotoxicity.

Thymoquinone, an Active Constituent of Black Seed Attenuates CCl4 Induced Liver Injury in Mice via Modulation of Antioxidant Enzymes, PTEN, P53 and VEGF Protein.

AIM:The present study was undertaken to evaluate the possible protective role of thymoquinone on CCl4-induced hepatotoxicity.METHODS:The activities of liver function enzymes and antioxidant enzymes were measured. Haematoxylin-Eosin staining was performed to analyze the live tissue alterations. Additionally, expression pattern of different proteins was evaluated through immunohistochemistry staining.RESULTS:The antioxidants enzymes activities were decreased significantly in the CCl4 induced group whereas recovery/increase of antioxidant enzymes was observed when thymoquinone was given to the mice. Moreover, thymoquinone administration significantly decrease the serum levels of alanine aminotransferase (ALT), alkaline phosphatase (ALP), and serum aspartate aminotransferase (AST). Liver tissue alterations were noted in CCl4 treated group whereas treatment with thymoquinone significantly prevented the CCl4-induced histological alteration. The expression of PTEN protein was high in CCl4 plus thymoquinone treated group while the loss of PTEN protein expression was observed in CCl4 treated group. Moreover, high expression of P53 protein was noticed in CCl4 treated the group as compared to CCl4 plus thymoquinone group. Difference in expression pattern of PTEN and p53 protein in CCl4 group and thymoquinone plus CCl4 treated group was statically significant (p < 0.05). Besides, expression of VEGF was high in CCl4 treated group as well as thymoquinone plus CCl4 treated group and difference in expression pattern was statically insignificant (p > 0.05).CONCLUSION:Our results suggest that thymoquinone can protect CCl4 induced liver damage and could be a preventive drug in the development of novel therapeutic agents for liver diseases.

The ameliorative impacts of curcumin on copper oxychloride-induced hepatotoxicity in rats

BackgroundCopper oxychloride (COC) (50% of its component, copper) is copper-based fungicides. The present study aimed to investigate the possible protective effect of 80 mg/kg curcumin against the toxicity of 500, 1000, or 2000 mg COC per kilogram body weight for 90 days on the liver of a rat. Serum glutamic-pyruvic transaminase (SGPT), serum glutamic-oxaloacetic transaminase (SGOT), hepatic glutathione reduced content (GSH), and malondialdehyde (MDA) levels were detected. The histological and ultrastructure changes of the liver tissues as well as the hepatic content of copper, iron, manganese, and zinc were also reported.ResultsCOC-treated rats showed an increase of SGPT and SGOT, with the elevation of copper and zinc content and MDA levels with no change in GSH level. The liver showed a significant increase in the copper and iron contents. The liver of COC-treated rats showed histological and ultrastructural damage that increased with increasing the COC dose. Conversely, curcumin supplementation potentially recovered liver function enzymes in only low doses of COC, reduced MDA level, increased GSH content, and improved the hepatic lesions. These findings revealed that subchronic exposure to even low levels of COC may have potential hazards and harmful effects on the liver, and the curcumin markedly attenuated the COC biochemical, histological, and cellular alterations in liver tissues, best with the low dose of COC.ConclusionsIt is concluded that curcumin has a limited protective role against COC liver toxicity.

Proteomic profiling of liver tissue from the mdx-4cv mouse model of Duchenne muscular dystrophy

BackgroundDuchenne muscular dystrophy is a highly complex multi-system disease caused by primary abnormalities in the membrane cytoskeletal protein dystrophin. Besides progressive skeletal muscle degeneration, this neuromuscular disorder is also associated with pathophysiological perturbations in many other organs including the liver. To determine potential proteome-wide alterations in liver tissue, we have used a comparative and mass spectrometry-based approach to study the dystrophic mdx-4cv mouse model of dystrophinopathy.MethodsThe comparative proteomic profiling of mdx-4cv versus wild type liver extracts was carried out with an Orbitrap Fusion Tribrid mass spectrometer. The distribution of identified liver proteins within protein families and potential protein interaction patterns were analysed by systems bioinformatics. Key findings on fatty acid binding proteins were confirmed by immunoblot analysis and immunofluorescence microscopy.ResultsThe proteomic analysis revealed changes in a variety of protein families, affecting especially fatty acid, carbohydrate and amino acid metabolism, biotransformation, the cellular stress response and ion handling in the mdx-4cv liver. Drastically increased protein species were identified as fatty acid binding protein FABP5, ferritin and calumenin. Decreased liver proteins included phosphoglycerate kinase, apolipoprotein and perilipin. The drastic change in FABP5 was independently verified by immunoblotting and immunofluorescence microscopy.ConclusionsThe proteomic results presented here indicate that the intricate and multifaceted pathogenesis of the mdx-4cv model of dystrophinopathy is associated with secondary alterations in the liver affecting especially fatty acid transportation. Since FABP5 levels were also shown to be elevated in serum from dystrophic mice, this protein might be a useful indicator for monitoring liver changes in X-linked muscular dystrophy.

Bushen recipe and its disassembled prescriptions inhibit inflammation of liver injury associated with Concanavalin A through Toll‑like receptor 3/9 signaling pathway.

The aim of the present study was to explore the effect of Bushen recipe and its disassembled prescriptions on liver injury and chronic hepatitis B. Liver injury was induced in normal and hepatitis B virus (HBV)‑transgenic mice through injection of Concanavalin A, followed by treatment with Bushen recipe and its disassembled prescriptions including the Bushen‑yang, the Bushen‑yin and the QingHua groups as well as the GanYanLing group (positive control). Subsequently, their liver function indexes were investigated by a microplate method and liver sections were blindly evaluated using an optical microscope by a pathologist. Subsequently, the activation state of Toll‑like receptor (TLR)3/9 signaling pathway in liver tissues was analyzed by western blotting. Additionally, the inflammatory factors produced following liver injury in peripheral blood were detected via ELISA. Following intervention with the Bushen recipe and its disassembled prescriptions, the liver function indexe alanine aminotransferase had declined, whereas cholinesterase increased. The pathological alterations of liver tissue in HBV transgenic mice were reversed by Bushen recipe and its disassembled prescriptions. In addition, the TLR3/9 signaling pathway in liver tissues of HBV transgenic mice was inhibited and inflammatory factors such as interleukin (IL)‑6, IL‑1, tumor necrosis factor‑α and interferon‑γ were reduced significantly. In conclusion, the present study demonstrated that Bushen recipe and its disassembled prescriptions repaired liver injury induced by Concanavalin A through inhibition of TLR3/9 signaling pathway.

Histopathological and Biomedical parameters Determination in the Protective Effect of Hydroalcoholic Extract of Allium Jesdianum on Hepatotoxicity Induced by Bromobenzene in Mice

Allium Jesdianum (AJ) is the native plant mostly grown in Middle East region that has the excellent pharmacological properties. In this study, we evaluated the hepatoprotective effect of hydroalcoholic extract of AJ on liver injury induced by Bromobenzene (BB) in male mice. Animals were randomly divided into five groups, control group received normal saline plus olive oil, groups 2-4 received(500, 1000 and 2000 mg/kg) AJ extract plus BB for 5 days and 5th group received BB (460 mg/kg). On the fifth day all groups received hexobarbital sodium (25 mg/kg, i.p). it should be noted that sleeping time of all mice were recorded. After 24 hours mice were sacrificed. By serum and tissue biomarkers such as alanine aminotransferase (ALT), aspartate aminotransferase(AST), reduced glutathione(GSH), malondialdehyde(MDA) and histopathological studies were measured. The results showed that BB significantly increased sleeping time, ALT, AST and MDA levels besides and decreased GSH level compared with control group. AJ extract at doses1000and 2000 mg/kg showed a significant alter in all studied endpoints and dose 2000 mg/kg showed a marked improvement in histopathological examination. The present finding showed that administration of the hydroalcoholic extract of AJ could prevent of hepatotoxicity induced by BB via improvement serum and tissue parameters and histopathological alterations in liver tissue.

Therapeutic implications of ajwa dates (Phoenix dactylifera) in the inhibition of liver tissue alterations through the modulation of vascular endothelial growth factor and phosphatase, and tensin homolog gene

Background: Dates are a plant species in the palm family, Arecaceae and is used as staple food in the Middle East for thousands of years. Aim: The current study was undertaken to evaluate the protective role of ajwa dates extract (ADE) on carbon tetrachloride (CCl4)-induced hepatotoxicity. Materials and Methods: The study was carried out on mice mode through different groups as control group without treatment of CCl4, ADE and CCl4-treated group, and CCl4-treated group only. Results: This finding demonstrated that histological alterations including degeneration, congestion and infiltration of lymphocytes were seen in the liver tissue in CCl4-treated groups. However, ADE-treated groups showed protection to attenuate CCl4-induced liver toxicity through maintenance of architecture of hepatocytes as evident of congestion, necrosis, and degeneration was not noticed. Moreover, a few number of infiltrations of lymphocytes were noticed in ADE-treated groups. However, expression of phosphatase and tensin homolog (PTEN) and vascular endothelial growth factor (VEGF) protein was evaluated in all groups, and it was observed that PTEN was highly expressed in control group and ADE-treated group. Whereas, PTEN expression was also observed in CCl4-treated group, but out of eight cases, one case showed less expression of PTEN protein. The difference in expression pattern of PTEN protein in CCl4-treated group and ajwa-treated group was statically insignificant (P > 0.05). VEGF was not expressed in control and ajwa-treated group. While expression of VEGF protein was observed in CCl4-treated group, and it was noticed that two out of eight cases showed expression of VEGF protein. Conclusion: The findings supported the idea that ADE might reduce liver tissue alterations or maintenance of architecture of hepatocytes. Ajwa dates-treated group showed decreased in the VEGF expression and such angiogenesis process involve in migration and differentiation of endothelial cells as well as prevent the loss of PTEN protein expression. Abbreviations Used: CCl4: Carbon Tetrachloride, VEGF: Vascular Endothelial Growth factor, IHC: Immunohistochemistry TUNEL assay: Terminal deoxynucleotidyl transferase dUTP nick end labeling, H and E: Hematoxylin-eosin staining, ADE: Ajwa dates extract.

Abstract 172: Oxidative stress and hepatotoxicity induced by graphene oxide in Sprague-Dawley Rats

Abstract Graphene oxide (GO) has been extensively explored as a promising nanomaterial for applications in biology because of its unique properties. Therefore, systematic investigation of GO toxicity is essential to determine its fate in the environment and potential adverse health effect. The aim of this study was to investigate the effect of graphene oxide on the induction of reactive oxygen species (ROS), the activity of certain liver enzymes (Alanine ALT, Aspartate AST, alkaline phosphatases ALP), and concentration of lipid hydroperoxide (LHP) in serum and histopathological evaluation of liver tissue in Sprague-Dawley rats. Four groups of five male rats were orally administered GOs, once a day for five days, with doses of 0, 10, 20 and 40 mg/Kg GO. A control group was also made of five rats. Blood and liver were collected 24 h after the last treatment following standard protocols. GO’s exposure increased the induction of ROS, the activities of the liver enzymes (ALT, AST, ALP), concentration of lipid hydroperoxide (LHP) and morphological alterations of the liver tissue in exposed groups compared to control. The highest two doses, 20 and 40 mg/kg, showed statistically significant (p &amp;lt; 0.05) increases in the induction of ROS, activities of ALT, ALP , LHP concentration, and morphological alterations of liver tissue compared to control. However, AST activity showed no effect. Taken together, the results of this study demonstrate that GO is hepatotoxic, and its toxicity may be mediated through oxidative stress. Citation Format: Anita K. Patlolla, Paul B. Tchounwou. Oxidative stress and hepatotoxicity induced by graphene oxide in Sprague-Dawley Rats [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 172. doi:10.1158/1538-7445.AM2017-172

Protective Effects of Tormentic Acid, a Major Component of Suspension Cultures of Eriobotrya japonica Cells, on Acetaminophen-Induced Hepatotoxicity in Mice.

An acetaminophen (APAP) overdose can cause hepatotoxicity and lead to fatal liver damage. The hepatoprotective effects of tormentic acid (TA) on acetaminophen (APAP)-induced liver damage were investigated in mice. TA was intraperitoneally (i.p.) administered for six days prior to APAP administration. Pretreatment with TA prevented the elevation of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (T-Bil), total cholesterol (TC), triacylglycerol (TG), and liver lipid peroxide levels in APAP-treated mice and markedly reduced APAP-induced histological alterations in liver tissues. Additionally, TA attenuated the APAP-induced production of nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and IL-6. Furthermore, the Western blot analysis showed that TA blocked the protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the inhibition of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) activation in APAP-injured liver tissues. TA also retained the superoxidase dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in the liver. These results suggest that the hepatoprotective effects of TA may be related to its anti-inflammatory effect by decreasing thiobarbituric acid reactive substances (TBARS), iNOS, COX-2, TNF-α, IL-1β, and IL-6, and inhibiting NF-κB and MAPK activation. Antioxidative properties were also observed, as shown by heme oxygenase-1 (HO-1) induction in the liver, and decreases in lipid peroxides and ROS. Therefore, TA may be a potential therapeutic candidate for the prevention of APAP-induced liver injury by inhibiting oxidative stress and inflammation.

Novel Epigenetic Biomarkers Mediating Bisphenol A Exposure and Metabolic Phenotypes in Female Mice.

There is compelling evidence that epigenetic modifications link developmental environmental insults to adult disease susceptibility. Animal studies have associated perinatal bisphenol A (BPA) exposure to altered DNA methylation, but these studies are often limited to candidate gene and global non-loci-specific approaches. By using an epigenome-wide discovery platform, we elucidated epigenetic alterations in liver tissue from adult mice offspring (10 months) following perinatal BPA exposure at human physiologically relevant doses (50-ng, 50-μg, and 50-mg BPA/kg diet). Biological pathway analysis identified an enrichment of significant differentially methylated regions in metabolic pathways among females. Furthermore, through the use of top enriched biological pathways, 4 candidate genes were chosen to assess DNA methylation as a mediating factor linking the association of perinatal BPA exposure to metabolic phenotypes previously observed in female offspring. DNA methylation status at Janus kinase-2 (Jak-2), retinoid X receptor (Rxr), regulatory factor x-associated protein (Rfxap), and transmembrane protein 238 (Tmem238) was used within a mediational regression analysis. DNA methylation in all four of the candidate genes was identified as a mediator in the mechanistic pathway of developmental BPA exposure and female-specific energy expenditure, body weight, and body fat phenotypes. Data generated from this study are crucial for deciphering the mechanistic role of epigenetics in the pathogenesis of chronic disease and the development of epigenetic-based prevention and therapeutic strategies for complex human disease.

Effect of silver nanoparticles in the liver of female quail (Coturnix coturnix )

This study aimed to identify the alterations of liver in the quail (Coturnix coturnix) exposed by nanosilver particles.45 quail (females) were collected from agriculture research center in Abu-Ghraib, divided into (6) groups including: T1(12 quails were exposed to 4ppm), T2 (12 quails were exposed to 8ppm) and T3 (12 quails were exposed to 12ppm) of silver nanoparticles solution for 60 days. As well as three groups for control (3 females for each). Birds were dissected to isolate livers for histological preperations after fixation with Bouin's fluid, Routine stains Hematoxyline and eosin were used. Histological study showed that the structure of liver in a control groups consist of hepatocytes arranged radially cords around the central vein, Polygonal in shape with central nucleus. Sinusoid found between hepatocytes cords. The histological alterations in liver tissue included congestion of central vein, Fibrinous exudates , Infilteation of inflammatory cells, Thickness of capsule , Loss radial arrangement of hepatocytes , Incidence of fatty degeneration, Hydropic and Hyaline degeneration of hepatocytes , Appearing of councilman bodies, Pyknotic necrosis and few dilated of sinusoids in liver of group exposed to 4ppm. While the alterations in the liver with group 8ppm included occurance of precipitation of proteins near the vessels which known Amylloid , central vein dilation, An increase thickness of wall blood vessels, In addition an incidence of hemorrhage and hyaline degeneration of liver cells. Liver in group 12ppm suffer from incidence of fatty changes, Hydropic degeneration, Necrosis, Increase numbers of Concilman bodies, An incidence of giant cells, Atrophy of liver cells, Appearance of caceous necrosis and increase dilation of sinusoids and congestion.

Effect of silver nanoparticles in the liver of female quail (Coturnix coturnix )

This study aimed to identify the alterations of liver in the quail (Coturnix coturnix) exposed by nanosilver particles.45 quail (females) were collected from agriculture research center in Abu-Ghraib, divided into (6) groups including: T1(12 quails were exposed to 4ppm), T2 (12 quails were exposed to 8ppm) and T3 (12 quails were exposed to 12ppm) of silver nanoparticles solution for 60 days. As well as three groups for control (3 females for each). Birds were dissected to isolate livers for histological preperations after fixation with Bouin's fluid, Routine stains Hematoxyline and eosin were used. Histological study showed that the structure of liver in a control groups consist of hepatocytes arranged radially cords around the central vein, Polygonal in shape with central nucleus. Sinusoid found between hepatocytes cords. The histological alterations in liver tissue included congestion of central vein, Fibrinous exudates , Infilteation of inflammatory cells, Thickness of capsule , Loss radial arrangement of hepatocytes , Incidence of fatty degeneration, Hydropic and Hyaline degeneration of hepatocytes , Appearing of councilman bodies, Pyknotic necrosis and few dilated of sinusoids in liver of group exposed to 4ppm. While the alterations in the liver with group 8ppm included occurance of precipitation of proteins near the vessels which known Amylloid , central vein dilation, An increase thickness of wall blood vessels, In addition an incidence of hemorrhage and hyaline degeneration of liver cells. Liver in group 12ppm suffer from incidence of fatty changes, Hydropic degeneration, Necrosis, Increase numbers of Concilman bodies, An incidence of giant cells, Atrophy of liver cells, Appearance of caceous necrosis and increase dilation of sinusoids and congestion.

Time-dependent effects of the flame retardant tris(1,3-dichloro-2-propyl) phosphate (TDCPP) on mRNA expression, in vitro and in ovo, reveal optimal sampling times for rapidly metabolized compounds.

The flame retardant, tris(1,3-dichloro-2-propyl) phosphate (TDCPP), was previously shown to affect chicken embryo growth, gallbladder size, and lipid homeostasis. A microarray study, however, revealed only modest transcriptional alterations in liver tissue of pipping embryos (days 20-21), which was attributed to the rapid metabolism of TDCPP throughout incubation. To identify the most appropriate sampling time for rapidly metabolized compounds, the present study assessed the time-dependent effects of TDCPP on 27 genes, in ovo (50 µg [116 nmol] TDCPP/g egg) and in vitro (10 µM), using a chicken ToxChip polymerase chain reaction array. The greatest magnitude in dysregulation (up to 362-fold) occurred on day 8 of incubation (in ovo) with alterations of genes involved in phase I, II, and III metabolism, among others. Gallbladder hypotrophy was observed by embryonic day 12, corroborating the finding in pipping embryos from our previous study. From days 12 to 19, genes involved in lipid homeostasis, steroid hormone metabolism, and oxidative stress were affected. In chicken embryonic hepatoctyes (CEHs), TDCPP was completely metabolized to bis(1,3-dichloro-2-propyl) phosphate (BDCPP) within 36 h, but transcriptional changes remained significant up to 36 h. These changes were not attributed to BDCPP exposure as it only altered 1 gene (CYP1A4). An 18-h exposure in CEHs altered the greatest number of genes, making it an appropriate time point for high-throughput chemical screening; however, depending on the biological pathways of interest, shorter or longer incubation times may be more informative. Overall, TDCPP elicits the transcriptional and phenotypic alterations observed in vitro and in ovo, whereas its major metabolite, BDCPP, is far less biologically active.

Hepatic expression patterns in psychosocially high-stressed pigs suggest mechanisms following allostatic principles

Psychosocial challenges are known to introduce cellular and humoral adaptations in various tissues and organs, including parts of the sympatho-adrenal-medullary system and hypothalamic–pituitary–adrenal axis as well as other peripheral tissue being responsive to cortisol and catecholamines. The liver is of particular interest given its vital roles in maintaining homeostasis and health as well as regulating nutrient utilization and overall metabolism. We aimed to evaluate whether and how response to psychosocial stress is reflected by physiological molecular pathways in liver tissue. A pig mixing experiment was conducted to induce psychosocial stress culminating in skin lesions which reflect the involvement in aggressive behavior and fighting. At 27weeks of age, animals prone to psychosocially low- and high-stress were assigned to mixing groups. Skin lesions were counted before mixing and after slaughter on the carcass. Individual liver samples (n=12) were taken. The isolated RNA was hybridized on Affymetrix GeneChip porcine Genome Arrays. Relative changes of mRNA abundances were estimated via variance analyses. Molecular routes related to tRNA charging, urea cycle, acute phase response, galactose utilization, and steroid receptor signaling were found to be increased in psychosocially high-stressed animals, whereas catecholamine degradation and cholesterol biosynthesis were found to be decreased. In particular, psychosocially high-stressed animals show decreased expression of catechol-O-methyltransferase (COMT) which has been linked to molecular mechanisms regulating aggressiveness and stress response. The expression patterns of high-stressed animals revealed metabolic alterations of key genes related to energy-mobilizing processes at the expense of energy consuming processes. Thus, the coping following psychosocial challenges involves transcriptional alterations in liver tissue which may be summarized with reference to the concept of allostasis, a strategy which is critical for survival.

Protective Effects of Ginger Extract against Lead Induced Hepatotoxicity in Male Albino Rats

Ginger (Zingiber officinale) is used traditionally for many therapeutic purposes. . Oxidative stress may be the main reason behind most histological and cellular effects of lead. The aim of this study was to investigate the possible hepatoprotective role of ginger against lead acetate induced hepatotoxicity in rats. . In the present investigation, lead acetate (200 mg/kg b.wt) was given orally to male rats for eight weeks to induce hepatotoxicity. The ginger was found to contain zingerone, gingerdiol, zingibrene, gingerols and shogaols. Lead-induced oxidative stress in liver tissue was indicated by significant decreased levels of liver reduced glutathione (GSH) and superoxide dismutase (SOD). Histologically, the liver showed several histological alterations such as degeneration of hepatocytes by necrosis and apoptosis, fatty changes and inflammatory cells infiltration. Ginger-I (200 mg/kg b.wt) and Ginger-II (300 mg/kg b.wt) markedly attenuated the previous lead- induced biochemical alterations in liver tissues as well as the histological and cellular changes. From this study, it can be concluded that the Zingiber officinale showed effective hepatoprotective and antioxidative action against lead acetate-induced hepatotoxicity in rats.

The effect of pine oil on the some alterations in liver tissue of experimental diabetes

The effect of pine oil on the some alterations in liver tissue of experimental diabetes