Search

Although few studies have been done to evaluate the neurotoxic effect of 4-nonylphenol on the aquatic fauna, there is a shortage in knowledge about the effect of the dose-dependent damage of 4-NP in juvenile of C. gariepinus. So, the present study aims to investigate the neurotoxic effects of 4-NP in juvenile of Clarias garepinus through evaluation of oxidative stress indices, neurotoxic biomarkers, enzymatic and non-enzymatic antioxidants, and histopathological alterations. To carry out this work, healthy juvenile fish were categorized into four groups (seven fish/group; three replicates). One as control and the other three groups were exposed for 15 days to 4-nonylphenol concentrations as 0.1, 0.2, and 0.3 mg/L, respectively, then 15 days as recovery period. The neurotoxiclogical biomarkers and antioxidant parameters after exposure to 4-NP showed significant differences between treatments and the control (P

This study aimed to assess some water quality parameters of Lake Edku, evaluation of the effect of a complex mixture of contaminants on the fish biochemical composition, and the histopathological changes in muscle tissue of Nile Tilapia, Oreochromis niloticus inhabiting different locations of Lake Edku. Methods: Water samples and 200 fish of O. niloticus were collected from different regions of Lake Edku and transported to the laboratory. Fish were divided into three groups: El-Maadyah region, Edku drain, and the recovery (El-Maadyah region). Recovery fish were left in aquaria for a month. Water quality parameters including temperature, pH, dissolved oxygen, electrical conductivity, total dissolved solids, and salinity were measured. Muscle total protein, total lipid, energy value, moisture, and ash content were determined, and the histopathology of fish muscle was examined. A significant decrease of dissolved oxygen in the Edku drain region compared to El-Maadyah and the recovery groups was observed. The salinity value showed a significant increase in the El-Maadyah region compared to the other groups. On the other hand, Edku drain fish group exhibited a significant decrease in muscle total protein, energy value, and ash content compared to the other groups. In contrast, it exhibited an increase in the water content and a significant increase in total lipids compared to the other groups. The muscle sections of El-Maadyah and Edku drain fish revealed several alterations compared to the recovery fish including hyalinized and necrotic muscle fibers, vacuolar degeneration, parasitic granuloma, infiltration of macrophages, dispersed muscle fibers by edema, fatty tissue, a variable amount of connective tissue proliferation between bundles and glycogen granules. The results confirm that fish contaminated environment could result in the damage of muscle tissue and has negative impacts on the fish quality and its validation to human consumption.

This study was conducted to determine for the first time the immunological, histopathological, histochemical, and ultrastructural changes; hematological and biochemical alterations; and poikilocytosis induced in Clarias gariepinus by Voliam flexi® 40% WG (thiamethoxam + chlorantraniliprole). Beside control fish, juvenile C. gariepinus were subjected to three sublethal concentrations of Voliam flexi® (43.5, 87.5, and 175 mg/L) for 15 days. Voliam flexi® induced immunotoxic impairments in C. gariepinus, such as a decrease in some immunity variables (lysozyme and phagocyte activity, immunoglobulin concentration, and nitro blue tetrazolium level). It also caused an extreme increase in the levels of primary cytokines (interleukin-1β and IL-6), compared with the control. The toxic effects of Voliam flexi® increased gradually with the increasing concentrations tested. Histological examination of the liver demonstrated necrosis, vacuolated hepatocytes (fatty deposition), melanomacrophage centers, foci of inflammatory cells, congested and dilated blood sinusoids, hepatic degeneration, fibrosis increment (Sirius Red stain), and glycogen depletion, as well as cytopathological alterations. We conclude that the toxic effects of Voliam flexi® must be restricted or prevented by using control mechanisms in aquatic systems.

Exposure to 2,3,7,8-tetrachlorodibenzo-P-dioxin (TCDD) as an environmental pollutant caused hepatotoxicity and tumor promotion. Recently researchers pay an attention to the power of green tea (GT) and curcumin (CUR) as natural antioxidants against cellular damage. The present study was designed to evaluate the protective role of GT and CUR against TCDD-induced hepatotoxicity in mice. Fifty adult male mice were divided into 5 groups as follows: G1; control received vehicles, G2: treated with oral dose of TCDD (1.332 mg/kg bw) and left as positive control, G3, G4 and G5 were treated with GT (0.5 mg/kg bw), CUR (0.5 m /kg bw), and the combination of GT and CUR (1 mg/kg bw) 30 minutes before injection with oral dose of TCDD (1.332 mg/kg bw), respectively. After 30 days of daily treatment with the antioxidants and TCDD mice were killed for collection of liver. Histological studies using light and electron microscopy were done in addition to the estimation of antioxidants parameters; catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH). Microscopically observations showed necrosis, inflammatory reactions, increased collagen, decreased polysaccharides and protein contents, and reduction in the antioxidants in the liver of mice treated with TCDD. However, the liver of mice treated with GT, CUR, and the combination showed improvement in the histological structure of the liver with enhancement in the antioxidants levels with the priority for the GT. In conclusion, TCDD induced histological and biochemical changes in the hepatic tissue and the ability of GT and/or CUR to prevent these changes was due to their activity as powerful antioxidants.

This study assessed the impact of chronic unpredictable mild stress (CUMS) on the structure of mouse salivary glands and the role of musk in alleviating this impact. Forty male albino mice were distributed equally into four groups; control (untreated), CUMS (exposed to CUMS for 4 weeks), CUMS+fluoxetine (FLU) (exposed to CUMS then treated with FLU, CUMS+musk (exposed to CUMS then treated with musk). Behavioral changes and serum corticosterone levels were assessed at the end of the experiment. The submandibular and parotid glands were dissected out and processed for histopathological and immunohistochemical examination using antibodies against alpha smooth muscle actin (ASMA) and brain-derived neurotropic factor (BDNF). Exposure to CUMS significantly (P < 0.001) increased the serum corticosterone level and induced depression. CUMS also induced vacuolation in acinar cells along with a significant (P < 0.001) reduction of ASMA immunoexpression, indicating an effect on myoepithelial cells, and a significant (P < 0.001) increase of BDNF expression in the gland ductal system. Both FLU and musk alleviated the CUMS-induced behavioral, biochemical and histopathological changes in the salivary glands. In conclusion, musk ameliorates stress-induced structural changes in mouse salivary glands. This effect might be mediated through up-regulation of BDNF secretion by the glands.

Objective(s): Heat stress (HS) is a catastrophic stressor that dampens immunity. The current study investigates the effect of dietary administration with camel whey protein (CWP) on apoptotic pathway caused by HS. Materials and Methods: Forty-five male mice were divided into three groups: a control group; HS group; and HS mice that were orally supplemented with CWP (CWP-HS group). Results: We found that reactive oxygen species (ROS), pro-inflammatory cytokines (IL-6), and C reactive protein (CRP) were elevated in the HS group along with a significant increase of caspase-9 and -3 and decrease of total antioxidant capacity (TAC). HS mice revealed impaired phosphorylation of Bcl-2 and Survivin, as well as increased expression of Bax, Bim and cytochrome C. Additionally, we observed an aberrant distribution of HSP-70 expressing lymphocytes in the spleen and thymus of HS mice. Moreover, histopathological examination showed alterations on the architectures of immune organs. In comparison with CWP-HS group, we found that CWP restored the levels of ROS, IL-6, TAC and CRP induced by HS. Furthermore, CWP restored the expression of Bcl-2/Bax, improved the histopathological changes in immune organs and HSP-70 distribution in the spleen and thymus. Conclusion: Our findings revealed the possible ameliorative role of CWP supplementation against damages induced by exposure to HS.

Elevation of scrotal temperature is one of the most important causes of impaired spermatogenesis and male infertility, but the exact mechanism remains controversial. The present study investigated the impact of camel whey protein (CWP) on the mechanisms of heat stress (HS)-mediated testicular damage in male mice. Exposure to HS was associated with significant increase in the testicular tissues' oxidative stress. Mechanistically, exposure to HS resulted in upregulation of P53 and Nrf2 expressions; downregulation of Bcl2 and PPAR-γ expressions; and induction of testicular Leydig cell hyperplasia. Because Leydig cells produce testosterone up on stimulation with Luteinizing hormone (LH), HS mice also exhibited significant reduction in the serum testosterone levels followed by significant reduction in the percentages of progressively motile sperm and higher percentages of immotile sperm, when compared with those of control mice. Interestingly, treatment of HS mice with CWP significantly restored the levels of ROS and the activities of antioxidant enzymes in the testicular tissues nearly to those observed in control mice. Furthermore, CWP supplemented HS mice exhibited complete restoration of Bcl2, P53, Nrf2, and PPAR-γ expressions; testicular Leydig cell distribution; significant higher levels of testosterone levels; and hence higher percentages of progressively motile sperm and lower percentages of immotile sperm as compared to HS mice. Our findings reveal the protective effects of CWP against testis injury and infertility induced by exposure to HS by rescuing functional Leydig cells. Additionally, the present study has shed light on the molecular mechanisms underlying improved testicular damage following CWP treatment.

Heat stress (HS) is an environmental factor that depresses the immune systems that mediate dysfunctional immune cells. Camel whey protein (CWP) can scavenge free radicals and enhance immunity. This study investigated the impact of dietary supplementation with CWP on immune dysfunction induced by exposure to HS. Male mice (n = 45) were distributed among 3 groups: control group; HS group; and HS mice that were orally administered CWP (HS + CWP group). The HS group exhibited elevated levels of reactive oxygen species (ROS) and pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor-α) as well as a significant reduction in the IL-2 and IL-4 levels. Exposure to HS resulted in impaired phosphorylation of AKT and IκB-α (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha); increased expression of activating transcription factor 3 (ATF-3) and 70 kDa heat shock proteins (HSP70); and aberrant distribution of CD3+ T cells and CD20+ B cells in the thymus and spleen. Interestingly, HS mice treated with CWP presented significantly restored levels of reactive oxygen species and pro-inflammatory cytokines near the levels observed in the control mice. Furthermore, supplementation of HS mice with CWP enhanced the phosphorylation of AKT and IκB-α; attenuated the expression of ATF-3, HSP70, and HSP90; and improved T and B cell distributions in the thymus and spleen. Our findings reveal a potential immunomodulatory effect of CWP in attenuating immune dysfunction induced by exposure to thermal stress.

Alzheimer's disease (AD), one of the progressive neurodegenerative diseases might be associated with exposure to stress and altered living conditions. This study aimed to evaluate the effectiveness of Ocimum basilicum (OB) essential oils in improving the neurodegenerative-like changes induced in mice after exposed to chronic unpredictable mild stress (CUMS). Forty male Swiss albino mice divided into four groups (n = 10); the control, CUMS, CUMS + Fluoxetine, CUMS + OB were used. Behavioral tests, serum corticosterone level, hippocampus protein level of the glucocorticoid receptors (GRs) and brain-dreived neurotropic factor (BDNF) were determined after exposure to CUMS. Hippocampus was histopathologically examined. Data were analyzed using statistical package for the social sciences (SPSS) and P value of less than 0.05 was considered significant. OB diminished the depression manifestation as well as impaired short term memory observed in the mice after exposure to the CUMS as evidenced by the forced swimming and elevated plus maze test. OB also up-regulated the serum corticosterone level, hippocampal protein level of the glucocorticoid receptor and the brain-derived neurotropic factor and reduced the neurodegenerative and atrophic changes induced in the hippocampus after exposure to CUMS. Essential oils of OB alleviated the memory impairment and hippocampal neurodegenerative changes induced by exposure to the chronic unpredictable stress indicating that it is the time to test its effectiveness on patients suffering from Alzheimer disease.

Thermal tissue injury is partly mediated by reactive oxygen metabolites. Oxygen free radicals are contributory to local tissue damage following thermal injury and accordingly an interventional therapy using antioxidants may be beneficial. Copper nicotinate complex can scavenge reactive oxygen species (i.e., has antioxidant activity).To examine time-related morphological and biochemical changes following skin thermal injury and their modulation by copper nicotinate complex.An animal model composed of 80 albino rats was established. Ten rats (nonburn group) served as a control group. Seventy rats (burn group) were anesthetized, given a 10% total body surface area, full-thickness burn. Ten rats (from the postburn group) were sacrificed after 24 h (without treatment, i.e., untreated-burn group). The remaining rats were divided into three subgroups (20 rats, each) and were treated topically either with soft paraffin, moist exposed burn ointment (MEBO, a standard therapeutic treatment for burns), or copper nicotinate complex. Five animals from each subgroup were sacrificed every week over a period of 4 weeks. The morphological and biochemical changes were evaluated and compared among the different groups.High levels of the plasma and skin nitiric oxide (marker of oxidative stress) were observed in the untreated-burn group. These levels were significantly low following the application of copper nicotinate complex. Low levels of plasma and skin superoxide dismutase (marker of oxidative stress) and plasma ceruloplasmin were observed in the untreated-burn group. These levels were significantly high following copper nicotinate complex treatment. The total and differential leukocyte counts were low following the onset of the thermal injury. They gradually returned to normal levels over a 4-week period following the application of MEBO or copper nicotinate complex. Compared to untreated-burn group, postburn-healing changes (resolution of the inflammatory reaction, reepithelization of the epidermis, angiogenesis, deposition of collagen fibers, and recovery of the subcellualr organelles) were significantly accelerated following the application of either MEBO or copper nicotinate complex.Application of copper nicotinate complex was associated with improved healing of the thermal burns of the skin. The underlying molecular changes underlying these effects await further investigations.

Although IFN-α was reported to promote the survival of peripheral B-lymphocytes via the PI3-kinase-Akt pathway, the triggered signalling pathways involved in the protection of B cell from apoptosis need to be clarified. Using flow cytometry and western blot analysis, we have found that type 1 IFNs (IFN-α/β) protect human B cells in culture from spontaneous apoptosis and from apoptosis mediated by anti-CD95 agonist, in a dose- and time-dependant manner. IFN-α/β-mediated anti-apoptotic effect on human B cells was totally abrogated by blockade of IFNR1 chain. Our data indicate that PI3Kδ, Rho-A, NFκB and Bcl-2/BclXL are active downstream of IFN receptors and are the major effectors of IFN-α/β-rescued B cells from apoptosis. Furthermore, immunohistochemical results show marked reduction in numbers of CD20 positive B cell in both spleen and Peyer’s patches from mice treated with anti-IFNR1 blocking antibody compared with control group. Moreover, ultrastructural observations of these organs show an obvious increase in apoptotic cells from mice treated with anti-IFNR1 blocking antibody. Our results provide more details about the triggered signalling pathways and the phosphorylation cascade which are involved in the protection of B cell from apoptosis after treatment with IFN-α/β.

Background: We recently demonstrated that type I Interferon (IFN) rescues in vitro, human B-lymphocytes from apoptosis via PI3Kδ/Akt, Rho-A, NFĸB and Bcl-2/BclXL. In the present study we extended our work to clarify, in vivo, the role of type I IFN signalling on the circulating and lymphoid organs homing lymphocytes. Methodology: Two groups of mice 13 in each were set: type I IFN signalling blocked mice injected with anti-IFNAR1 antagonist antibody (10 mg/kg body weight) once/day for up to 20 days, and control group were injected with vehicle alone. Results: Flow cytometry analysis to monitor the blood lymphocyte phenotype and proliferation have shown a significant decrease in CD45R/CD220+ B cells, CD4+ and CD8+ T cells in treated animals. Furthermore, the proliferative capacities of these lymphocyte subsets were significantly decreased in treated animals compared to those of control mice. Marked reduction in the plasma levels of IL-2 and IL-7 (cytokines important for the development of T and B cells) but not of IL-6 or IL-10 was observed in treated mice and this may a cause for emergence decrease in B and T cell numbers. Immunohistochemical studies have further shown a marked reduction in the numbers of CD20+ B cells in spleen and Peyer’s patches and CD3+ T cells in thymus of treated animals. Moreover, electron microscopy examinations have revealed a loss of lymphocytes with characteristic features of apoptosis. Conclusion: Our data confirmed that the in vivo inhibition of type I IFN signaling induce decrease in the numbers and defective functions of circulating and lymphoid organs homing lymphocytes providing a strong evidence for the protective effects of type 1 IFNs (IFN-α/ β) on B and T lymphocytes.

The main objective of this study is to assess some biochemical and histopathological changes in Nile Tilapia, Oreochromis niloticus caught from Lake of Edku. A decrease in serum total protein, albumin, total lipids, bactericidal activity, ALT and AST were observed in El-Maadyah and Edku drain regions compared to recovery group, while the level of serum glucose and lysozyme activity were increased. The frequencies of micronucleus (MN) and nuclear abnormalities (NAs) in fish erythrocytes showed an increase of micronuclei, lobed nuclei and fragmented apoptotic nuclei while notched nuclei were decreased. Finally, the frequencies of morphologically altered erythrocytes (MAEs) of fish showed an increase in swelled cells, vacuolated cytoplasm; microcytes; echinocytes; tear-drop like; sickle cells; nuclear retraction and hemolyzed cells while fused cells were decreased. On the other hand, the main prominent hepatic lesions were parasitic granuloma, encapsulated cysts by connective tissue, fatty degeneration, congestion and necrosis. The histopathological analysis of muscle sections of both polluted sites showed edema, splitting of muscle fibers, hyalinized muscle fibers, fatty tissue, necrosis and infiltration of lymphocytes. From the above, we can conclude that the contaminated environment of fish could cause detrimental effects on fish tissues and immune system causing great economic losses for the natural resources.