Search

This study aims to see if Ginseng

The current study was instigated by investigating the ameliorative potential of Ornipural

Hydroxyurea (HDU) is a widely used medication for various malignancies, thalassemia, and sickle cell anemia with reported side effects. The current study investigated HDU- induced hepatic injury and the protective potential of the royal jelly (RJ) against this hepatotoxic effect in the light of hepatic oxidative/ antioxidative status, pro-inflammatory cytokine, apoptosis signaling pathway, and histopathology. Sixty albino rats were used (n = 10/group) for 60 days: control, RJ (100 mg/kg body weight, orally), HDU (225 mg/kg body weight, orally), 2HDU (450 mg/kg body weight, orally), and HDU + RJ groups. HDU-treated rats showed significant elevation of liver function tests as aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, as well as malondialdehyde and nitric oxide (oxidative biomarkers) and significant decreased hepatic antioxidant molecules (reduced glutathione, superoxide dismutase, and glutathione peroxidase), compared to a control group, that more pronounced in the high dose of HDU. In addition, HDU induced significant upregulation of TNF-α and the Caspase-3 apoptotic pathway. Moreover, the liver of HDU treated groups showed various hepatic lesions from mild to severe necrotic changes related to the HDU dose. However, administration of RJ with HDU improved liver function tests, liver histology, and hepatic oxidative/antioxidative status concerning HDU groups. Furthermore, oral RJ administration with HDU significantly lessens the immune-expression area % of TNF-α and Caspase-3. Thus, the royal jelly has antioxidant, anti-inflammatory, and anti-apoptotic properties against HDU- induced hepatic injury and could be, therefore, used as adjuvant therapy in patients with long-term HDU medication.

Egyptian farms is still attacked by several outbreaks of FMDV, a highly contagious viral disease that threatens the livestock industry worldwide. Many of these outbreaks are unreported. Hence, the epidemiological situation and molecular characterization of the currently responsible strains of recent FMD outbreaks are missed. To identify FMDV strains currently circulating in cattle herds and catch the recent update in the morphophonological changes due to that virus, we carried out this study on the FMD outbreak from 2016–2017 in Egypt. Clinical samples (post mortem tissues samples, oral swabs, epithelial suspensions from ruptured vesicles, and blood) were collected from clinically examined animals suspected to be of being FMD virus = 229 cattle and 138 buffalo. Of 175, 96 (54.8%) samples and 85 (44.3%) from 192 samples were positive in 2016 and 2017, respectively. Pathological examination revealed the classical lesions of FMDV as vesicular and erosive lesions on cornified epithelial tissues. Multi-focal areas of lympho-plasmocytic myocarditis were seen in the heart of all calves. Similar lesions were also observed in the heart of adult cattle that died in that outbreaks. Detailed pathological alterations in adult and young animals were described. Polymerase chain reaction (PCR) screening of tissue specimens using specific primers for FMDV was done. Serotype O was the only serotype that was detected in our study and submitted in the Genebank. The four field isolates of serotype O that have been submitted in the Genebank had been found to belong to the EA-3 topotype. Nucleotide sequencing of the VP1 region and phylogenetic analysis has been used to determine the relationships between our field isolates, other recently isolated Egyptian isolates, and other isolates from some African countries and vaccinal strain used for serotype O in Egypt. The presence of strains of increased virulence among cattle and buffalo in Egypt could be attributed to the introduction of new viral strains through uncontrolled transboundary movements of animals during the last public revolution in Egypt in 2011.

Silver nanoparticles (AgNPs) are more commonly utilised in medicine, however they have negative effects on the majority of organs, including the reproductive system. AgNPs were reported to be able to reach the testes due to their small size, which allows them to pass through blood testicular barriers. The goal of this study was to see if LA (alpha lipoic acid) or GB (ginkgo biloba) might protect adult rat testes after intraperitoneal injection of AgNPs. Forty male healthy adult Wister albino rats were randomly assigned to four groups (10 rats each); control, AgNPs-intoxicated group intraperitoneally injected AgNPs 50 mg/kg b.w, 3 times a week, LA + AgNPs group intoxicated with AgNPs and orally gavaged with 100 mg LA/kg b.w, and GB + AgNPs group injected with AgNPs and orally given GB extract 120 mg/kg b.w were continued for 30 consecutive days. Biochemical changes in testicular tissue (testosterone, ACP, and Prostatic acid phosphatase), oxidative indices in testicles tissues, mRNA expression of pro-apoptotic (BAX) and anti-apoptotic (BCL-2) biomarkers, histological, and immunohistochemical changes were studied. Significant decrease in serum testosterone level and elevation in ACP and PACP enzyme activity in AgNPs treated group than in the control. In addition, lowering in tGSH, GSH GR, GPx and elevation MDA and GSSG were observed in AgNPs treated group than control. Decreasing in mRNA expression thirodexin-1 (Txn-1), transforming growth factor-1β (TGF-1β), anti-apoptic (BCL-2) and elevation the expression of proapoptic biomarkers (BAX) in the testis homogenates of rats exposed to silver nanoparticles. Strong positive action to BAX and lowering the action of Ki-67antibody were observed. Because of their antioxidant, anti-inflammatory, and anti-apoptotic properties, co-treatment with LA or GB may be beneficial in reducing the harmful effects of AgNPs on the testicles.

Silver nanoparticles (AgNPs) are commonly utilized in medicine. However, they have negative effects on the majority of organs, including the reproductive system. AgNPs were reported to be able to reach the testicular tissues due to their nano size, which allows them to pass through blood-testicular barriers. The goal of this study was to see if alpha-lipoic acid (LA) or Ginkgo biloba (GB) might protect adult rat testes after intraperitoneal injection of AgNPs. Forty male healthy adult Wister albino rats were randomly assigned to four groups: control, AgNPs-intoxicated group intraperitoneally injected AgNPs 50 mg/kg b.w, 3 times a week; LA + AgNPs group intoxicated with AgNPs and orally gavaged with 100 mg LA/kg b.w; and GB + AgNPs group injected with AgNPs and orally given GB extract 120 mg/kg b.w for 30 consecutive days. Biochemical changes (testosterone, ACP, and prostatic acid phosphatase), oxidative indices, mRNA expression of proapoptotic (BAX) and anti-apoptotic (BCL-2) biomarkers, histological, and immunohistochemical changes in testicular tissues were investigated. Significant decrease in serum testosterone level and elevation in ACP and PACP enzyme activity in AgNPs-treated rats. As well, there were lowering in tGSH, GSH GR, GPx, and elevation in MDA and GSSG values. AgNPs-exposed rats expressed downregulation of testicular thirodexin-1 (Txn-1), transforming growth factor-1β (TGF-1β), anti-apoptotic (BCL-2), and upregulaion of proapoptotic biomarkers (BAX) mRNA expressions. Strong positive action to BAX and lowering the action of Ki-67 antibody were observed. Because of their antioxidant, anti-inflammatory, and anti-apoptotic properties, cotreatment with LA or GB could be beneficial in reducing the harmful effects of AgNPs on the testicles.

The study investigated the ability of boswellic acid (BA) to alleviate the testicular and oxidative injury FPN insecticide intoxication in the male rat model. Rats were randomly assigned to six equivalent groups (six rats each) as the following: control rats orally administered with 2 mL physiological saline/kg of body weight (bwt), boswellic acid (BA1) rats orally administered 250 mg BA/kg bwt, boswellic acid (BA2) rats orally administered 500 mg BA/kg bwt, fipronil (FPN) rats orally administered 20 mg FPN/kg bwt, (FPN + BA1) rats orally administered 20 mg FPN/kg bwt plus 250 mg BA/kg bwt, and (FPN + BA2) rats orally administered 20 mg FPN/kg bwt plus 500 mg BA/kg bwt. After 60 days, semen viability percentage and live spermatozoa percentage were decreased, and a considerably increased abnormality of the sperm cells in FPN-administered rats improved substantially with the co-administration of BA. BA had refinement of the histological architecture of testes and sexual glands. Quantitative analysis recorded a noticeable decline in the nuclear cell-proliferating antigen (PCNA) percentage area. FPN triggered cell damage, which was suggested by elevated malondialdehyde and interleukin 6, tumor necrosis factors alpha, and decreased glutathione level. Proapoptotic factor overexpression is mediated by FPN administration, while it decreased the antiapoptotic protein expression. Similarly, BA has shown significant upregulation in steroidogenic and fertility-related gene expression concerning the FPN group. Pathophysiological damages induced by FPN could be alleviated by BA’s antioxidant ability and antiapoptotic factor alongside the upregulation of steroidogenic and fertility-related genes and regimented the detrimental effects of FPN on antioxidant and pro-inflammatory biomarkers.

This study’s hypothesis is that carbofuran and copper sulfate have a synergistic harmful impact on the fertility of male Nile tilapia. Hence, this study was designed to assess the toxic reproductive outcome of carbofuran, copper sulfate, and their mixture in male Nile tilapia. Sixty male Nile tilapia fishes were separated into four groups (15 fish/group). The control group; carbofuran group, was given dechlorinated tap water containing 0.02 mg/L (1/10 dose of LC50) carbofuran; copper group was given dechlorinated tap water containing 4.0 mg/L (1/10 dose of LC50) copper sulfate; carbofuran + copper sulfate group received dechlorinated tap water containing 0.02 mg/L carbofuran plus 4.0 mg/L copper sulfate. After 6 weeks, results revealed a significant rise in testicular malondialdehyde levels and a significant decrease in testicular reduced glutathione contents among all experimental groups compared to the control group. Testicular testosterone levels were significantly declined in copper and combined groups compared to the control. The seminal evaluation using computer-assisted sperm analysis showed a significant decline in the progressive motility percentage, motile ratio percentage, sperm concentration, curvilinear velocity, straight-line velocity, average path velocity, and wobble in all intoxicated groups, particularly, the combined group. The histopathology of testes in all intoxicated groups revealed a detachment of the basal membrane of some seminiferous tubules, and others were free from spermatogonia and spermatozoa with interstitial eosinophilic granular cell infiltration. Testicular lesions were more severe in the combined group. Finally, it was concluded that carbofuran and copper sulfate exerted a negative effect on the reproductive function of male Nile tilapia, and they have a synergistic harmful impact on the fertility of male Nile tilapia.

Background: Despite the beneficial effects of zinc oxide nanoparticles (ZnONPs) on different biomedical applications, including their antioxidant and anti-inflammatory ones, it might have cytotoxic and genotoxic impacts on the male reproductive system. Objective: The current study compares the effect of zinc oxide nanoparticles and their bulk form, at different doses, on male rats&rsquo, reproductive performance, testicular antioxidants, gene expression, and histopathology. Materials and Methods: Thirty male rats were randomly allocated equally in five groups. The control one was injected with Tween 80 (10%). The zinc oxide nanoparticle (ZnONP) groups received ZnONPs &lt, 50 nm, specifically, 5 mg/kg (ZnONP-1) and 10 mg/kg (ZnONP-2). The bulk zinc oxide (BZnO) groups were administered 5 mg/kg (BZnO-1) and 10 mg/kg (BZnO-2), correspondingly. Rats were injected intraperitoneally with the respected materials, twice/week for eight consecutive weeks. Finally, the male rats&rsquo, sexual behavior and their pup&rsquo, s performance were determined in a monogamous mating system. Rats were then anesthetized and sacrificed for semen characteristics evaluation and tissue collection for antioxidant and hormones analysis, gene expression, and histopathological examination. Results: It was shown that ZnONP-1 improved sexual behavior, semen characteristics, and pup&rsquo, s performance compared to its bulk form. Similarly, the testicular antioxidants activity, glutathione (GSH), and superoxide dismutase (SOD) increased with a decrease in the malonaldehyde (MDA), interleukin 6 (IL-6), and tumor necrosis factor (TNF-&alpha, ) levels. It also improves the reproductive hormone levels and mRNA expression of different steroidogenesis-associated genes and anti-apoptotic genes. Conclusion: It can be concluded that zinc oxide nanoparticles, administered at 5 mg/kg, had the most beneficial effect on male reproductive performance, while 10 mg/kg could have a detrimental effect.

Treatment of burn wounds has many requirements to ensure wound closure with healthy tissue, increased vascularization, guarantee edema resolution, and control bacterial infection. We propose that titanium oxide (TiO2) nanoparticles (NPs) will be more efficient than silver dioxide (Ag2O) in the treatment of burn wounds. Herein, gelatin loaded NPs (GLT-NPs) were evaluated for their efficacy to regenerate second-degree burn wound in rabbit skin. TEM results revealed that the average particle sizes were ⁓ 7.5 and 17 nm for Ag2O and TiO2 NPs, respectively. The results of the in vivo application of GLT-NPs on burn wound in the rabbit revealed that both Ag2O and TiO2 NPs were efficient than the control none treated (CTRL) and GLT group. In terms of the healing rate, the GLT-TiO2 did not show any significant difference than GLT-Ag2O (99.57% vs. 99.85%, p = 0.2). Meanwhile, the healing rate was significantly higher in both NPs' treated groups than CTRL (94.16%, p < 0.01) and GLT group (95.07%, p < 0.05). Also, the histological analysis using H&E staining showed re-epithelization, less edema, and enhanced vascularization in both GLT-NPs than CTRL and GLT groups. Furthermore, immunohistochemical analysis of TGF-β1 and α-SMA revealed significantly a higher expression in both GLT-NPs groups than CTRL and GLT groups at weeks 1 and 2 (p < 0.05). Interestingly, TGF-β1 and α-SMA were substantially higher in GLT- TiO2 than GLT-Ag2O at weeks 1 and 2 (p < 0.05), but the expression was not significant at week 3. In conclusion, GLT-NPs showed higher regenerative capacity and enhanced the healing quality after burn wound compared to CTRL and GLT. Graphical abstract.

Monosodium glutamate (MSG) is a widely used food additive, and there is a trepidation that MSG plays a critical role in multiple hepatic disorders. This study was planned to investigate Graviola extract (GE) effects on hepatic and cellular alterations induced by MSG. Fifty Wistar rats were randomly allocated into five groups: control (received normal saline), Graviola (received 200 mg/kg body weight), MSG (received 2.4 gm MSG/kg, 15% of Lethal dose (LD50) of MSG), Graviola + monosodium glutamate (MSG + GE, received GE, 200 mg/kg/day and MSG 2.4 gm/kg body weight (BW) for the next four weeks), and monosodium glutamate + Graviola (received MSG only (2.4 gm/kg BW) daily for four weeks, then concomitant with Graviola (200 mg/kg BW) daily for the next four weeks. MSG and GR were administered orally for eight weeks. Our results showed that MSG caused a significant increase in oxidative stress markers malondialdehyde (MDA), reactive oxygen species (ROS), nitric oxide (NO), hydrogen peroxide (H2O2), proinflammatory cytokines interleukin 6 (IL-6) level, a tumor protein (P53), hepatic cellular damage, as well as proapoptotic markers caspase-3, and B-cell lymphoma 2 (BCL-2)-like protein 4 (Bax). A significant decrease in superoxide dismutase (SOD), catalase (CAT), glutathione S transferase (GST), reduced glutathione (GSH), and an antiapoptotic agent B-cell lymphoma 2 (BCl-2) was observed. The detected MSG effects were normalized by Graviola administration, either a prophylactic or protecting dose. Besides, Graviola reduced the expression of inducible nitric oxide synthase (iNOS) and hepatic fatty acid synthase (FAS) and led to the upregulation of the silent information regulator protein one gene expression gene (SIRT1).In conclusion, the results suggest that Gaviola&rsquo, s interrelated antiapoptotic, antioxidant, and anti-inflammatory properties are potential mechanisms to enhance hepatic deficits and protect the liver. Graviola can, therefore, be considered a promising hepatoprotective supplement. Additionally, further human clinical trials are also necessary to validate the present research.

Increasing attention has been paid in the past decade to assessing the toxicological effects of nanoparticles and finding a protectant; thus, the current study aimed to investigate the protective effect of the mitochondria-targeting drug methylene blue (MB) against copper oxide nanoparticle (CuO-NP)-induced neurobehavioral toxicity in rats. For this purpose, twenty rats were allocated to four equal groups (n = 5). The negative control group received distilled water intraperitoneally (IP) and Tween 80 (10 %) orally. The CuO-NP group was given a dose of 100 mg/kg of CuO-NPs, administered orally, and the positive control group was treated with 1 mg/kg MB intraperitoneally (IP). The final group was concurrently exposed to CuO-NPs and MB for 14 consecutive days. At the end of the study, each group was neurobehaviorally blind tested relative to other experimental animals, then brain tissue markers were determined and a histopathological examination was conducted. The results showed that supplementation with CuO-NPs induced neurobehavioral alterations; increased Cu content in the brain; and enhanced lipid peroxidation (malondialdehyde [MDA]), protein peroxidation (protein carbonyl [PC]), and DNA oxidative damage (8-hydroxy-2-deoxyguanosine [8−OH-dG]) compared to other treatments. In addition, a decrease was noted in the mitochondrial dehydrogenases’ (aldehyde dehydrogenase 2 [ALDH2], and glutamate dehydrogenase [GDH]) activity in Cu-exposed rats. The histopathological findings revealed shrunken, pyknotic, and hypereosinophic cortical neurons and increased immune positive brown staining of caspase-3 protein, indicating apoptosis. Co-treatment with methylene blue ameliorated the neurotoxic effects of CuO-NPs; therefore, MB evidently had a powerful modulatory effect against the neurotoxicity of nano-Cu oxide via its antioxidant and mitochondrial protection properties.

Metal oxide nanoparticles (NPs) induce oxidative stress that can cause cellular toxicity. A natural antioxidant that can be used to protect tissues from oxidative stress is curcumin.In the present study, we evaluated the protective effect of curcumin nanoparticles (curcumin-NPs) against copper oxide nanoparticles (CuO-NPs)-mediated hepatorenal effects on behavioral performance, biochemical markers, antioxidants, inflammation, apoptosis, and histopathology in rats.Twenty Wistar adult male rats were randomly divided into four groups (n = 5); Group Ι served as a control, group ΙΙ was orally gavaged with curcumin-NPs (100 mg/Kg), group ΙΙI orally received CuO-NPs (100 mg/kg), and group ΙV received both CuO-NPs and curcumin-NPs orally for 14 days.Behavioral performance, biochemical markers, antioxidants, inflammatory mediators, and apoptotic gene expression were evaluated in addition to histopathological and immunohistochemical examination.The results revealed that rats exposed to CuO-NPs suffered from behavioral alterations and hepatic and renal damages, which indicated by a marked elevation of serum biochemical parameters, including alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, urea, uric acid, and creatinine and a decline of total protein. Moreover, there was a significant downregulation in the expression of antioxidants genes, whereas inflammatory mediators expression were upregulated. The histopathological and immunohistochemical examination also corroborated these findings. In contrast, rats co-treated with curcumin-NPs exhibited better behavioral performance, biochemical profile, gene expression, histological architecture, and immunohistochemical staining results.These findings strongly indicated that curcumin-NPs exert significant protection against the behavioral and hepatorenal disorders induced by CuO-NPs toxicity by modulating oxidative stress regulators and gene expression.

Dietary intake of fructose corn syrup in sweetened beverages is associated with the development of metabolic syndrome and obesity. We hypothesized that inflammatory cytokines play a role in lipid storage and induction of liver injury. Therefore, this study intended to explore the expression of adipocytokines and its link to hepatic damage. Rats were assigned to drink water, cola soft drink (free access) and aspartame (240 mg/kg body weight/day orally) for 2 months. The lipid profiles, liver antioxidants and pathology, and mRNA expression of adipogenic cytokines were evaluated. Subchronic intake of soft drink or aspartame substantially induced hyperglycemia and hypertriacylglycerolemia, as represented by increased serum glucose, triacylglycerol, low-density lipoprotein and very low-density lipoprotein cholesterol, with obvious visceral fatty deposition. These metabolic syndromes were associated with the up-regulation of leptin and down-regulation of adiponectin and peroxisome proliferator activated receptor-γ (PPAR-γ) expression. Moreover, alterations in serum transaminases accompanied by hepatic oxidative stress involving induction of malondialdehyde and reduction of superoxide dismutase, catalase, and glutathione peroxidase and glutathione levels are indicative of oxidative hepatic damage. Several cytoarchitecture alterations were detected in the liver, including degeneration, infiltration, necrosis, and fibrosis, predominantly with aspartame. These data suggest that long-term intake of soft drink or aspartame-induced hepatic damage may be mediated by the induction of hyperglycemia, lipid accumulation, and oxidative stress with the involvement of adipocytokines.

This study was designed to investigate neuro-behavioral, neuro-biochemical and neuro-morphological alterations induced by sub-acute toxicity of lead (Pb) in male Wistar rats as well as the assessment of the neuroprotective effect of thiamine hydrochloride against Pb-induced behavioral, biochemical and morphological neuro-alterations. For this purpose 24 male Wistar rats were randomly divided into 4 groups (n=6). Rats in the 1st group were treated with lead acetate orally at dose of 100 mg/kg b.wt. Animals in 2nd group were received leaded water orally + 100 mg/kg thiamine hydrochloride intraperitoneally. 3rd group were treated only with thiamine hydrochloride. 4th group was served as the control animals. Animals were exposed to treatments once daily for 7 consecutive days. Behavioral alterations were assessed by applying neurological tests as elevated plus-maze and Morris water maze. The main neurotransmission systems as cholinergic, adrenergic, serotonergic and GAB Aergic were evaluated in brain tissue homogenate. Morphological alterations was assessed histopathologically. Results revealed that, Pb exposure caused spatial learning and memory impairment, as well as a significant increase in the content of acetylcholine, serotonin and norepinephrine while the activity of acetylcholinesterase and GABA content showed a significant decrease. Hemorrhage in brain, mild perivascular edema and perivascular cuffing were the main pb-induced morphological alterations. Simultaneous administration of thiamine markedly ameliorated Pb-induced neurotoxicity which was indicated by comparatively better behavioral performance, alleviation of the neurotransmitters disturbances and decreased the severity of histopathological lesions. In conclusion, thiamine has been found to be extremely significant in the fighting of Pb-induced neuro-manifestations.

Aims This study explored whether silver nanoparticles (AgNPs) can disrupt tight-junctions integrity resulted in blood-brain barrier dysfunction along with oxidative stress, pro-inflammation, and apoptosis induction. Additionally, neuroprotective activities of α-lipoic acid (LA) and Ginkgo biloba (GB) were investigated. Main methods Forty adults rats were enrolled into; Control, AgNPs (50 mg/kg), LA (100 mg/kg) + AgNPs, and GB (120 mg/kg) + AgNPs. After 30 days, neuronal changes were assessed biochemically and histopathologically. Brain tissues oxidative indices, mRNA expression of proinflammatory cytokines and tight-junction proteins and pro-apoptotic biomarker, caspase-3 were investigated. Key findings AgNPs exposure enhanced lipid peroxidation (+195%) along with declines in glutathione (−43%), glutathione peroxidase (−34%), glutathione S-transferase (−31%), catalase (−43%), and superoxide dismutase (−38%) activities in brain tissues. The apparent brain oxidative damage was associated with obvious neuronal dysfunction that was ascertained by neuropathological lesions. AgNPs lowered serum acetylcholine esterase, iron and copper levels, and increased creatine phosphokinase and creatine phosphokinase–brain type activities. Following AgNPs exposure, brain silver and iron contents were increased, but the copper level was decreased. AgNPs up-regulated TNF-α (6.5-fold) and IL-1β (8.9-fold) transcript levels, and simultaneously over-expressed the caspase-3 protein in cerebrum and cerebellum inducing cell apoptosis. Moreover, AgNPs down-regulated the transcript levels of tight-junction proteins; JP-1 (0.65-fold) and JAM-3(0.81-fold). Significance LA and relatively GB improved the serious effects of AgNPs on the blood-brain barrier function and tight-junction proteins through their antioxidants, anti-inflammatory, and anti-apoptotic efficacies. Co-treatment with LA or GB may be favorable in ameliorating the neurotoxic side effects of AgNPs.

The potential antifibrotic effects of melatonin against induced hepatic fibrosis were explored.Rats were allocated into four groups: placebo; thioacetamide (TAA) (200mg/kg bwt, i.p twice weekly for two months); melatonin (5mg/kgbwt, i.p daily for a week before TAA and continued for an additional two months); and melatonin plus TAA. Hepatic fibrotic changes were evaluated biochemically and histopathologically. Hepatic oxidative/antioxidative indices were assessed. The expression of hepatic proinflammatory cytokines (tumor necrosis factor-α, and interleukin-1β), fibrogenic-related genes (transforming growth factor-1β, collagen I, collagen, III, laminin, and autotaxin) and an antioxidant-related gene (thioredoxin-1) were detected by qRT-PCR.In fibrotic rats, melatonin lowered serum aspartate aminotransferase, alanine aminotransferase, and autotaxin activities, bilirubin, hepatic hydroxyproline and plasma ammonia levels. Melatonin displayed hepatoprotective and antifibrotic potential as indicated by mild hydropic degeneration of some hepatocytes and mild fibroplasia. In addition, TAA induced the depletion of glutathione, glutathione s-transferase, glutathione peroxidase, superoxide dismutase, catalase, and paraoxonase-1 (PON-1), while inducing the accumulation of malondialdehyde, protein carbonyl (C=O) and nitric oxide (NO), and DNA fragmentation. These effects were restored by melatonin pretreatment. Furthermore, melatonin markedly attenuated the expression of proinflammatory cytokines and fibrogenic genes via the upregulation of thioredoxin-1 mRNA transcripts.Melatonin exhibits potent anti-inflammatory, antioxidant and fibrosuppressive activities against TAA-induced hepatic fibrogenesis via the suppression of oxidative stress, DNA damage, proinflammatory cytokines and fibrogenic gene transcripts. In addition, we demonstrate that the antifibrotic activity of melatonin is mediated by the induction of thioredoxin-1 with attenuation of autotaxin expressions.

The morphopathological alterations of chronic cadmium (Cd) toxicity in Sarotherodon galilaeus were studied. 126 fish were used to determine 96 hrs LC50 of cadmium chloride, the obtained result was 28.3 mg/L. Forty-eight fish were used to induce chronic toxicity, twenty-four fish were exposed to 2.83 mg/L cadmium chloride for 8 weeks and other fish as control. Gills, hepatopancreas, posterior kidney and spleen were the most affected organs during chronic exposure. Eosinophilic granular cells (EGCs) infiltration and goblet cells hyperplasia in tips of primary lamellae, lamellar lifting, lamellar necrosis and Proliferative interlamellar hyperplasia with fusion in gills, hydropic degeneration and necrosis of the hepatic cells, hemorrhage and necrotic renal tubules and splenic necrosis and depletion of lymphocytes were recorded as histopathological changes.

The present study was designed to investigate the adverse effects of aluminum chloride hexahydrate on the heart, liver and kidneys of rabbits. Twenty-four apparently healthy male and female rabbits were randomly assigned to four groups. The two control groups male (n= 6) and female (n= 6) received subcutaneous injections of physiological saline. The other two Al-treated groups of male (n= 6) and female (n= 6) were given 2.5mg/kg B.W. S/C five times per week for 3 months. At the 6th weeks and the 12th weeks, three rabbits from each group were necropsied and tissues specimens from heart, liver and kidneys were collected and processed for the following histopathologic examination. The heart of both sexes of intoxicated rabbits showed congestion of blood vessels, interfibrillar edema, hemorrhage as well as Zenker's degeneration and necrosis of myocardium. The Liver showed periportal edema, mild fibroplasia, infiltration of inflammatory cells, adenomatous and papillary hyperplasia of bile ductules. The encountered lesions of the kidneys were in the form of vacuolations and necrosis of renal tubular epithelium, with intratubular necrotic cellular debris and hyaline casts. An additional lesion of severe interstitial nephritis was also seen in some areas. It was concluded that the adverse toxic effects of aluminum chloride were time-dependent manner on heart, kidneys and liver of of both sexes of rabbits.

The current study was performed to evaluate the anti-diabetic action of metformin and ginseng in alloxan-induced diabetes in rats. Forty male albino rats were used in this work, ten rats were left without any treatment and kept as a control, the remaining thirty rats were injected with alloxan to induce diabetes and then divided into three equal groups, the first group was kept without any treatment during period of the experiment, the second one treated with metformin (300 mg/kg B.Wt.) and the third one treated with ginseng at dose level of 250 mg/kg B.Wt. for 30 consecutive days. The results showed a significant changes in the hematological parameters, fasting blood glucose level, glycosylated hemoglobin (HbA1C) besides the activity of liver enzymes (aspartate aminotranseferase (AST), alanine aminotranseferase (ALT) and gamma glutamyltransferase (GGT)) and level of total protein in addition to lipid profile (Triglyceride (TG),total cholesterol (TC), very low density lipoprotein (VLDL) and low density lipoprotein (LDL) except high density lipoprotein (HDL)) in all groups compared to control group. The liver and pancreas of all groups were collected and examined histopathologically. Metformin and ginseng have ameliorative effect on biochemical and histopathological alterations caused by hyperglycemia. From our data it could be concluded that ginseng can be used as an effective anti-hyperglycemic and antioxidantagent.