Exposure to xenoestrogens like 4-nonylphenol (NP) is recognized by disrupting endocrine functions and causes reproductive dysfunction in male fish. The present study aimed at investigating the 4-nonylphenol propensity to induce oxidative stress and hormonal disturbances in male catfish and at studying the protective role of quince (Cydonia oblonga). To fulfill this aim, catfish Clarias gariepinus were exposed to pure 100 μg/L 4-NP and to quince the leaf extract added to 4-NP, both for 15 days. The 4-NP exposure induced a marked increase in 17ß-estradiol (E2), LH, and cortisol, while thyroid hormone (TSH, T3), testosterone (T), and FSH levels noticeably decreased; however, 4-NP had no effect on T4 level. Moreover, 4-NP exposure was accompanied by histological impairments in testes. Existence of 4-NP was associated with oxidative damage as evidenced by the significant increase (p 0.05) of the enzymes, superoxidase dismutase (SOD), catalase (CAT), acetylcholinesterase (AchE), glutathione s-transferase, total antioxidant capacity (TAC), and malondialdehyde (MDA). Adding quince was effective to neutralize hormonal levels and to repair the testicular histological alterations. In response to quince remedy, the enzymes AchE and MDA reduced significantly (p 0.05), while limited or no response was detected for other tested enzymes. Our results concluded that quince can antagonize 4-NP toxicity in catfish, confirming that quince leaf extract displayed antioxidant activities against the toxicity of hazardous chemicals.

Although there are many applications of silver nanoparticles (Ag-NPs) in human activities,there is still little known about their potential environmental toxicity, particularly to fish. Inthe present study, the effects of Ag-NPs on African catfish (Clarias gariepinus) were studiedusing melanomacrophage centers as immunohistological biomarkers. Fish were exposed to25 mg/L, 50 mg/L and 75 mg/L 100-nm Ag-NPs. We studied the effects on the size and num-ber of melanomacrophage centers in all target tissues. Many histopathological alterationsin those tissues were observed. The histological changes were represented as dislocationof the epithelium, dilatation of central veins associated with inflammatory leukocytic infil-tration, necrosis, and pyknotic nuclei of hepatocytes. There was shrinkage of Malpighiancorpuscles, dislocation of nuclei of convoluted tubules, cellular degeneration, and dispersedinfiltration of leukocytes in kidney tissue. Examination of spleen sections after exposure toAg-NPs showed rupture within the red pulp and hemorrhage, dislocation of nuclei, accumu-lation of inflammatory leukocytes, and congestion in blood vessels. In conclusion, exposureto Ag-NPs induced alterations in tissues, suggesting a possible increase in oxidative stressin those tissues.

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Transition-metal coordination polymers [M(ndc) (bpy)(H2O)m]xH2O (where M = Co(II), Ni(II), Cu(II) and Zn(II), ndc = 1,4-naphthalenedicarboxylate, bpy = 4,40-bipyridine; m = 0 or 1; x = 1 or 2) were prepared by reacting the ligands and metal ions at room temperature with the aid of microwave irradiation and sonication methods. The structure of the coordination polymers was assigned based on elemental analysis, FT-IR and electronic spectral studies, thermal analysis, scanning electron microscope and X-ray powder diffraction. Thermogravimetric analysis was also used to follow up the possible thermal decomposition steps and to calculate the thermodynamic parameters of the nano-sized metal complexes. The kinetic parameters were calculated making use of the Coats–Redfern and Horowitz–Metzger equations. All obtained results of the different technics used in our study stated the ability to synthesis the metal coordination polymers of our interest using both microwave irradiation and sonication methods.

A series of coordination polymers of the general formula {[M(ndc)(azoles)(H2O)].XH2O}n (where M =Co(II), Cu(II) and Zn(II), ndc = 1,4-naphthalenedicarboxylate, azoles = 2-aminothiazole and 2- aminobenzothiazole, x=0, 1 or 2) has been prepared and characterized. The coordination polymers have been characterized based on elemental analysis, FT-IR and electronic spectral studies magnetic measurements and thermal analysis. Thermogravimetry, derivative thermogravimetry, and differential thermal analysis were used to study the thermal decomposition of the complexes. Non isothermal kinetic parameters were calculated making use of the Coats-Redfern and Horowitz-Metzger equations. Catalytic performances of the two of the complexes for the degradation of methyl orange by sodium persulfate have been investigated.

Type I diabetes (T1D) is a characterized by the inflammation of pancreatic islets and destruction of β cells. Long and persistent uncontrolled diabetes tends to degenerate the immune system and increase the incidence of infections in diabetic individuals. Most serious diabetic complications are mediated by the free radicals, which damage multiple cellular components through direct effects of the cell cycle regulatory proteins. Camel whey protein (CWP) has antioxidant activity and decreases the effects of free radicals. However, the effects of CWP on lymphoid organs have not been studied in the context of diabetes. Therefore, the present study was designed to investigate the dietary influence of CWP supplementation on the lymphoid organs in streptozotocin (STZ)-induced type 1 diabetic mouse model. Three experimental groups were used: non diabetic control mice, diabetic mice, and diabetic mice treated with CWP. Induction of diabetes was associated with a marked reduction in glutathione (GSH) levels; decreased activities of GSH peroxidase (GSH Px), manganese superoxide dismutase (MnSOD) and catalase; increased reactive oxygen species (ROS) levels and iNOS activity in plasma and lymphoid organs. Furthermore, diabetic mice exhibited alterations in the expression of Bax and Bcl-XL, and subsequently pathological alterations in the architecture of the bone marrow, pancreas, thymus, and spleen. Interestingly, treatment of diabetic mice with CWP robustly restored glucose, insulin, GSH, and ROS levels and the activities of GSH Px, MnSOD, catalase and iNOS. Additionally, supplementation of diabetic mice with CWP improvement in the architecture of lymphoid tissues and rescued from apoptosis through direct effects on the Bax and Bcl-XL proteins. These data revealed the therapeutic potential of CWP against diabetic complications mediated damages of lymphoid organs.

Multiple mechanisms contribute to impaired diabetic wound healing including impaired neovascularization and deficient endothelial progenitor cell (EPC) recruitment. Bee venom (BV) has been used as an anti-inflammatory agent for the treatment of several diseases. Nevertheless, the effect of BV on the healing of diabetic wounds has not been studied. Therefore, in this study, we investigated the impact of BV on diabetic wound closure in a type I diabetic mouse model. Three experimental groups were used: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice treated with BV. We found that the diabetic mice exhibited delayed wound closure characterized by a significant decrease in collagen production and prolonged elevation of inflammatory cytokines levels in wounded tissue compared to control non-diabetic mice. Additionally, wounded tissue in diabetic mice revealed aberrantly up-regulated expression of ATF-3 and iNOS followed by a marked elevation in free radical levels. Impaired diabetic wound healing was also characterized by a significant elevation in caspase-3, -8 and -9 activity and a marked reduction in the expression of TGF-β and VEGF, which led to decreased neovascularization and angiogenesis of the injured tissue by impairing EPC mobilization. Interestingly, BV treatment significantly enhanced wound closure in diabetic mice by increasing collagen production and restoring the levels of inflammatory cytokines, free radical, TGF-β and VEGF. Most importantly, BV-treated diabetic mice exhibited mobilized long-lived EPCs by inhibiting caspase activity in the wounded tissue. Our findings reveal the molecular mechanisms underlying improved diabetic wound healing and closure following BV treatment. This article is protected by copyright. All rights reserved.

Schistosomasis is one of the most tropical neglected diseases (NTDs), which have very complex antigenically different life stages. So that studying the effect of each antigen on cellular immune response is required. Three schistosomal antigens were used CAP, SEA and SWAP separately in vivo. Blood parameters and lymphocytes blastogenesis were evaluated. The most changes were reported in WBCs and differential cells with maximum immune response after 33 dpv in CAP and 47 dpv in SEA and SWAP. These changes reflected the defense and cellular immune response for each antigen.

Micronutrients in food have been found to have chemopreventive effects, supporting the conclusions from epidemiologie studies that consumption of fresh fruits and vegetables reduces cancer risk. The present study was carried out to evaluate the role of querctin (Q) and sodium gluconate (GNA) supplementation separately or in combination in ameliorating promotion of colon tumor development by dimethyl-hydrazine (DMH) in mice. Histopathological observation of colons in mice treated with DMH showed goblet cell dysplasia with inlammatory cell iniltration. This pathological inding was associated with signiicant alteration in oxidative stress markers in colon tissues and carcinoembryonic antigen (CEA) levels in plasma. Mice co-treated with GNA and Q showed mild changes of absorptive and goblet cells and inlammatory cell iniltration in lamina properia, with improvement in oxidative stress markers. In conclusion, indings of the present study indicate signiicant roles for reactive oxygen species (ROS) in pathogenesis of DMH-induced colon toxicity and initiation of colon cancer. Also, they suggest that Q, GNA or the combination of both have a positive beneicial effect against DMH induced colonic cancer induction in mice.

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