Resveratrol alleviates cardiac apoptosis following exposure to fenitrothion by modulating the sirtuin1/c-Jun N-terminal kinases/p53 pathway through pro-oxidant and inflammatory response improvements: In vivo and in silico studies.

Fenitrothion (FNT), a commonly used organophosphate, can cause oxidative damage and apoptosis on various organs. However, the underlying mechanisms for FNT-induced cardiotoxicity did not formally report. Here, we have evaluated the possible ameliorative roles of resveratrol (RSV) against FNT-induced cardiac apoptosis in male rats through the sirtuin1 (SIRT1)/c-Jun N-terminal kinase (c-JNK)/p53 pathway concerning pro-oxidant and inflammatory cytokines. Forty-eight male rats were equally grouped into control, RSV (20 mg/kg), 5-FNT (5 mg/kg), 10-FNT (10 mg/kg), 20-FNT (20 mg/kg), 5-FNT-RSV, 10-FNT-RSV, and 20-FNT-RSV where all doses administrated by gavage for four weeks. The present findings demonstrated that RSV markedly diminished the level of hyperlipidemia and elevation in lactate dehydrogenase (LDH), total creatine kinase (CK-T), and troponin T (TnT) levels following FNT intoxication. Furthermore, RSV significantly reduced FNT-induced cardiac oxidative injury by reducing malondialdehyde (MDA) level and improving the levels of glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and acetylcholinesterase (AchE). Also, the levels of interleukin-1ß (IL1ß,), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were significantly attenuated in the co-treated groups. Moreover, RSV alleviated the histopathological changes promoted by FNT and repaired the transcript levels of SIRT1, c-JNK, and caspase-9/3 along with p53 immunoreactivity. In silico study revealed that the free binding energies of RSV complexes with protein and DNA sequences of SIRT1 were lower than docked complexes of FNT. Therefore, RSV reserved myocardial injury-induced apoptosis following exposure to FNT by modulating the SIRT1/c-JNK/p53 pathway through cellular redox status and inflammatory response improvements.

Alpha-mangostin attenuates the apoptotic pathway of abamectin in the fetal rats' brain by targeting pro-oxidant stimulus, catecholaminergic neurotransmitters, and transcriptional regulation of reelin and nestin.

Abamectin, an avermectin member, can induce significant neurodegeneration symptoms in non-target organisms. However, its neurodevelopmental influences in mammals are unclear. Here, we focus on the antiapoptotic action of alpha-mangostin against the developmental neurotoxicity of abamectin with the possible involvement of reelin and nestin mRNA gene expression. Thirty-two pregnant rats were allocated to four groups (8 rats/group); control, alpha-mangostin (20 mg/kg/d), abamectin (0.5 mg/kg), and co-treated group (alpha-mangostin + abamectin). The animals have gavaged their doses during the gestation period. The fetotoxicity and many signs of growth retardation were observed in the abamectin-intoxicated rats. In comparison with the control group, abamectin prompted a significant elevation (p < 0.05) in the levels of malondialdehyde and nitric oxide, along with many symptoms of histopathological changes in the fetal cerebral cortex. However, the glutathione, dopamine, and serotonin concentrations together with the activities of glutathione-S-transferase, catalase, and superoxide dismutase were markedly decreased (p < 0.05) in the abamectin group. Moreover, abamectin remarkably upregulated (p < 0.05) the brain mRNA gene expression of reelin, nestin, and caspase-9 as well as the immunoreactivity of Bax and caspase-3 proteins in the cerebral cortex. It should be noted that alpha-mangostin mitigated the developmental neurotoxicity of abamectin to the normal range by recovering the levels of oxidant/antioxidant biomarkers, catecholamines; and apoptosis-related proteins with the involvement of reelin and nestin genes regulation. Those records revealed that the transcription regulation of reelin and nestin could be involved in the neuroprotective efficacy of alpha-mangostin, especially avermectin's developmental neurotoxicity.

Ginger reserves testicular spermatogenesis and steroidogenesis in difenoconazole-intoxicated rats by conducting oxidative stress, apoptosis and proliferation.

Difenoconazole, a triazole fungicide, can induce reproductive toxicity in aquatic species, but the probable mechanisms of this hazard in mammals are not formally reported. Here, we have examined the possible ameliorative efficiency of the ginger aqueous extract against the reproductive toxicity of difenoconazole in male rats. Thirty-six animals were equally divided into six groups: control, ginger aqueous extract (50 mg/kg), difenoconazole (15 mg/kg), difenoconazole (30 mg/kg) and ginger co-treated with two doses of difenoconazole. Difenoconazole markedly decreased sperm count, motility and normality percentage, together with the Johnson score. Difenoconazole also significantly reduced serum testosterone, luteinizing hormone and follicle-stimulating hormone levels, as well as the activities of testicular steroidogenic acute regulatory protein and 17 ß-hydroxysteroid dehydrogenases. Furthermore, difenoconazole brought a significant decrease in the testicular activity of catalase, but it increased the activity of glutathione peroxidase. Moreover, difenoconazole upregulated the testicular transcripts of Bax and caspase-3, increased Ki-67 immunoreactivity and induced histoarchitecture alterations plus DNA damage. Remarkably, ginger co-treatment preserved sperm toxicity, restored hormone profiles, increased steroidogenic activity and prevented oxidative injury-promoted testicular apoptosis. In conclusion, phenolic acids and flavonoids of ginger can reserve spermatogenesis and steroidogenesis in difenoconazole-intoxicated rats by improving testicular redox status, inhibiting apoptosis and refining proliferation capacity.

Synthesis and hyperglycemic, biochemical and histopathological evaluation of novel sulfonylbiguanide and sulfonylurea derivatives as potent anti-diabetic agents.

New sulfonylbiguanide hydrochloride salts and sulfonylurea derivatives containing two sulfonyl groups were synthesized through the reaction of arylsulfonohydrazides with cyanoguanidine and p-tolylsulfonylisocyanate, respectively. Oral treatment of hyperglycemic rats with the synthesized sulfonylbiguanide derivatives 2 and sulfonylurea derivatives 3 revealed that sulfonylurea derivatives 3a and 3c possessed significant decrease of the elevated glucose in compression with the anti-diabetic standard drugs. Effects of the synthesized sulfonylurea derivatives 3a and 3c on the diabetic properties towards α-amylase, liver function enzyme levels (AST, ALT, ALP, TB and γ-GT), kidney functions (urea and creatinine), lipids profiles (TG, TL, TC and HDL-C) were studied. Also, the effect of sulfonylurea derivatives 3a and 3c as antioxidants (reduced glutathione and lipid peroxide) was evaluated. Histopathological examination of hepatic and pancreatic tissues was investigated. The obtained results suggested that the most potent sulfonylurea derivatives 3a and 3c might be possible used as novel diabetic inhibitor agents.

The Influence of Chicken Egg Lysozyme or Zinc-Bacitracin Antibiotic on the Growth Performance, Antibacterial Capacity, Blood Profiles, and Antioxidative Status of Rabbits: A Comparative Study.

Dietary egg lysozyme has beneficial roles in the growth performance and health conditions of animals. The study was performed using 90 multicolored rabbits in three groups (each replicate with thirty rabbits). In the control group, rabbits were fed a diet without zinc bacitracin (ZnB) or egg lysozyme, while the second and third groups were treated with ZnB and lysozyme additive at 100 mg/kg, respectively. After eight weeks, the final weight and body weight gain (BWG) of rabbits fed dietary egg lysozyme and ZnB additives were meaningfully increased (p < 0.05). Nevertheless, the feed conversion ratio (FCR) was markedly decreased by dietary egg lysozyme and ZnB (p < 0.05). Interestingly, dietary egg lysozyme resulted in higher final weight and BWG and lower FCR than rabbits treated with ZnB (p < 0.05). Rabbits treated with egg lysozyme and ZnB additives had markedly lower populations of Clostridium spp. and Escherichia coli (p < 0.05) compared with the control. However, the counts of Lactobacillus and total bacteria were meaningfully increased in the the intestines of rabbits treated with egg lysozyme and ZnB (p < 0.05). The blood total protein and globulin of rabbits fed dietary egg lysozyme and ZnB additives were meaningfully increased (p < 0.05). Blood creatinine was significantly lowered by dietary egg lysozyme compared with the control and ZnB-treated rabbits (p < 0.05). The levels of blood urea, ALT, and AST were markedly lowered (p < 0.05) by dietary egg lysozyme and ZnB. The gene expressions of superoxide dismutase 1 (SOD1) and glutathione peroxidase (GPX) in the liver of rabbits fed dietary egg lysozyme and ZnB additives were markedly upregulated (p < 0.05) compared with the control. Dietary egg lysozyme resulted in higher expression of SOD1 and GPX genes than rabbits treated with ZnB (p < 0.05). In conclusion, the inclusion of egg lysozyme could replace the inclusion of ZnB in the diets of rabbits.

Quercetin ameliorates the hepatic apoptosis of foetal rats induced by in utero exposure to fenitrothion via the transcriptional regulation of paraoxonase-1 and apoptosis-related genes.

BACKGROUND & PURPOSE: Exposure to organophosphorus during different phases of pregnancy induces many adverse impacts on the developing foetuses due to their immature detoxification system. We have estimated the potential amelioration role of quercetin against hepatic injury-induced apoptosis in rat foetuses following gestational exposure to fenitrothion and probable involvement of paraoxonase-1. METHODS: Forty pregnant rats were allocated into four groups; the first one kept as control, the second intubated with quercetin (100 mg/kg), the third orally administrated fenitrothion (4.62 mg/kg) and the last group received quercetin two hours before fenitrothion intoxication. RESULTS: Fenitrothion significantly elevated the foetal hepatic levels of thiobarbituric acid reactive substances, protein carbonyl, and nitric oxide, but it reduced the enzymatic activities of glutathione-S-transferase, superoxide dismutase, catalase, and acetylcholinesterase. Furthermore, fenitrothion provoked many histopathological changes in the foetal liver and markedly up-regulated the mRNA gene expression of p53, caspase-9 along with elevation in the immunoreactivity of Bax and caspase-3, but it down-regulated the expression level of paraoxonase-1. Remarkably, quercetin co-treatment successfully ameliorated the hepatic oxidative injury and apoptosis prompted by fenitrothion. CONCLUSIONS: Dietary supplements with quercetin can be used to reduce the risk from organophosphorus exposure probably through paraoxonase-1 up-regulation and enhancement of the cellular antioxidant system.

Linseed ameliorates renal apoptosis in rat fetuses induced by single or combined exposure to diesel nanoparticles or fenitrothion by inhibiting transcriptional activation of p21/p53 and caspase-3/9 through pro-oxidant stimulus.

Gestational exposure to environmental pollutants can induce oxidative injury and apoptosis since the fetal organs are sensitively vulnerable to these chemicals. In this work, we have investigated the renal anti-apoptotic efficiency of linseed (LS) against the oxidative stress-mediated upregulation of the fetal apoptosis-related genes following the prenatal intoxication with diesel nanoparticles (DNPs) and/or fenitrothion (FNT). A fifty-six timed-pregnant rats were equally divided to eight groups; control, LS (20% in diet), DNPs (0.5 mg/kg by intratracheal inoculation), FNT (3.76 mg/kg by gavage), DNPs+FNT, LS + DNPs, LS + FNT, and LS + DNPs+FNT. The transmission electron microscope analysis revealed the spherical shape of diesel particles with a homogeneous nanosized range (20-92.3 nm) and the crystallinity was confirmed by electron diffraction microscopy. Administration of DNPs and/or FNT significantly increased fetal renal malondialdehyde, nitric oxide, and glutathione reductase as compared with the control group. However, they declined the level of glutathione together with the activities of glutathione peroxidase, glutathione-S-transferase, superoxide dismutase, and catalase. Furthermore, DNPs and/or FNT elicited many histopathological changes in fetal renal cells, markedly up-regulated apoptosis-related gene expressions (p53, p21 caspase-3, and caspase-9), and evoked DNA breaks as detected by comet assay. Interestingly, LS supplementation significantly ameliorated the disturbances in oxidant/antioxidant biomarkers, downregulated the apoptosis gene expressions, and alleviated DNA damage alongside renal cell architecture. These findings reveal that the antioxidant and anti-apoptotic characteristics of LS are acceptable defender pointers for the renal injury especially during gestational exposure to DNPs and/or FNT.

Effect of feeding wheat middlings and calcium lignosulfonate as pellet binders on pellet quality growth performance and lipid peroxidation in broiler chickens.

Basal diets supplemented with 4 kg Ca-LS/ton of diet. Pellet quality characteristics (per cent fines, the present study was conducted to evaluate the influence of wheat middlings (WM) and calcium lignosulfonate (Ca-LS) as pellet binders on the pellet quality characteristics, growth performance, blood parameters, nutrients digestibilities, lipid peroxidation and muscle fatty acids profile in Egyptian broiler strain. A total of 3,120 broiler chicks at 1-day of age were divided randomly into three experimental treatments with eight replicates (130 each). The first treatment was fed the basal pelleted diets without any additives, the second treatment was fed diets including 50 kg WM/ton of diet and the third treatment was fed per cent pellets, and pellet durability index) were significantly improved in WM and Ca-LS treatments compared with the control. Body weight gain was significantly increased, while feed intake was significantly decreased resulting in improving of feed conversion ratio significantly in WM group in comparison with control and Ca-LS groups (p < .05). Nutrients apparent digestibility (dry matter, crude protein and crude fibre) were significantly improved by inclusion of WM compared with control and Ca-LS. Plasma total cholesterol, and uric acid concentrations were significantly decreased by dietary WM in comparison with control and Ca-LS experimental groups. Furthermore, linoleic, alpha-linolenic and arachidonic acids contents in breast muscle were significantly increased by WM and Ca-LS, while, muscle malondialdehyde concentration was significantly decreased. It could be concluded that inclusion of WM and Ca-LS can improve pellet quality characteristics, and WM (at a level of 50 kg/ton) had positive effects on growth performance, nutrients digestibilities, lipid peroxidation and fatty acids profile in Egyptian broiler strain.

The Influence of Dietary Chicken Egg Lysozyme on the Growth Performance, Blood Health, and Resistance Against Escherichia coli in the Growing Rabbits' Cecum.

The dietary chicken egg lysozyme (LZM) at different concentrations was tested on the growth performance, blood health, and resistance against Escherichia coli of growing rabbits. A total number of 48 rabbits averaged 611.25 g (5 weeks of age) of APRI line-rabbits (Egyptian developed line) were allocated into four treatments (three replicates and each contained four rabbits) of 5-week weaning APRI rabbits. The first group was fed a basal diet without LZM supplementation and served as a control group, whereas the remaining groups of rabbits were fed a basal diet supplemented with LZM at 50, 100, and 200 mg/kg diet, respectively, for 8 weeks. The obtained results revealed that rabbits fed the basal diet supplemented with different concentrations of LZM linearly (P < 0.05) displayed improved growth performance and reduced feed intake and FCR. The best result was for rabbits fed a 200 mg per kg diet supplemented with LZM, followed by a 100 mg per kg diet. The total count of Escherichia coli and Clostridium count was linearly (P < 0.05) decreased by adding LZM at 100 and 200 mg/kg in the diets compared to the control groups. In contrast, total bacterial count and the total count of Lactobacilli had increased considerably by increasing LZM at different levels relative to the control groups. The LZM supplementation linearly (P < 0.05) increased hematological parameters (RBCs, PCV, Hb, and WBCs) together with an increase in lymphocyte count compared to the control group. The total protein and globulin concentrations were significantly (P < 0.05) increased by feeding with LZM. On the other hand, ALT, AST, urea, and creatinine were significantly (P < 0.05) decreased by increasing LZM supplementation. It could be concluded that supplementation of the rabbit's diet with chicken egg LZM was able to improve the growth performance and hematological and serum biochemical parameters compared with the control group. Therefore, LZM is required at the rate of the hobx100-200 mg/kg diet as a potential feed additive and a friendly alternative for antibiotics in rabbit feed.

Hypothermia induced by central injection of sucralose potentially occurs via monoaminergic pathways in the hypothalamus of chicks.

Oral administration of sucralose has been reported to stimulate food intake through inducing hypothalamic neuropeptide Y (NPY) in mice and fruit flies. However, the underlying mechanisms of action of sucralose in hypothermia and NPY and monoamine regulation remain unknown. The aim of the present study was to investigate central effects of sucralose on body temperature, NPY, and monoamine regulation, as well as its peripheral effects, in chicks. In Experiment 1, 5-day-old chicks were centrally injected with 1 µmol of sucralose, other sweeteners (erythritol and glucose), or saline. In Experiment 2, chicks were centrally injected with 0.2, 0.4, and 1.6 µmol of sucralose or saline. In Experiment 3, chicks were centrally injected with 0.8 µmol of sucralose or saline, with a co-injection of 100 µg fusaric acid (FA), an inhibitor of dopamine-ß-hydroxylase, to examine the role dopamine in sucralose induced hypothermia. In Experiment 4, 7-16-day-old chicks were orally administered with 75, 150, and 300 mg/2 ml distilled water or sucralose, daily. We observed that the central injection of sucralose, but not other sweeteners, decreased body temperature (P < .05) in chicks; however, the oral injection did not influence body temperature, food intake, and body weight gain. Central sucralose administration decreased dopamine and serotonin and stimulated dopamine turnover rate in the hypothalamus significantly (P < .05). Notably, sucralose co-injection with FA impeded sucralose-induced hypothermia. Sucralose decreases body temperature potentially via central monoaminergic pathways in the hypothalamus.

Oxidative stress, hemato-immunological, and intestinal morphometry changes induced by ochratoxin A in APRI rabbits and the protective role of probiotics.

This work studied the protective effects of Aspergillus awamori against ochratoxin A (OTA)-induced toxicity in APRI maternal line rabbits. A total number of 48 APRI line weanling rabbits (5 weeks) were divided into 4 groups (12 rabbits each) and fed the basal diet, 30 ppb/kg diet of OTA, 1 g/kg diet of A. awamori, and a mixture of OTA and A. awamori for 8 weeks. OTA reduced the final body weight and weight gain as well as the intestinal villi length and thickness, whereas increased the feed intake and feed conversion ratio. Rabbits fed diets with OTA showed significantly reduced crude protein, lipids, and fibers apparent digestibility coefficients (P < 0.05). The red blood cells and hemoglobin were significantly decreased in the OTA group comparing with the other groups (P < 0.05). The blood total protein and albumin displayed significantly lower levels by OTA than the other groups. In contrast, glucose, aspartate aminotransferase (AST), alkaline phosphatase (ALP), urea, and creatinine levels were significantly increased by OTA (P < 0.05). Phagocytic activity (PA) and phagocytic index (PI) showed significantly (P < 0.05) decreased levels in OTA-contaminated group, while rabbits fed A. awamori significantly showed the highest PA and PI levels (P < 0.05). Dietary A. awamori kept the levels of PA and PI in rabbits fed OTA significantly higher than those fed without A. awamori (P < 0.05) and not significantly different from the control group (P > 0.05). Catalase (CAT) and superoxide dismutase (SOD) displayed significantly lower levels in the OTA group, while malondialdehyde (MDA) was significantly higher than the other groups (P < 0.05). Rabbits fed OTA-contaminated diets displayed significantly lower CAT and SOD and higher MDA than rabbits fed OTA combined with A. awamori (P < 0.05). Our results indicated that dietary A. awamori ameliorated the damage in APRI rabbits fed OTA through alleviation of oxidative stress and immunity.

Modulation of Paraoxonase-1 and Apoptotic Gene Expression Involves in the Cardioprotective Role of Flaxseed Following Gestational Exposure to Diesel Exhaust Particles and/or Fenitrothion Insecticide.

The developmental exposure to a single chemical may elicit apoptosis in the different fetal organs, while the combined effects are restricted. We have examined the protective role of flaxseed (FS) against diesel exhaust particles (DEPs)- and/or fenitrothion (FNT)-induced fetal cardiac oxidative stress and apoptosis. A total of 48 timed pregnant rats were divided into eight groups (n = 6). The first group was saved as the control and the second fed on 20% FS diet. Animals in the third, fourth, and fifth groups were administered with DEPs (2.0 mg/kg), FNT (3.76 mg/kg), and their combination, respectively, while the sixth, seventh, and eighth groups were supplemented with 20% FS through intoxication with DEPs, FNT, and their combination, respectively. Our results revealed that DEPs and/or FNT significantly elevated the level of protein carbonyl and superoxide dismutase activity in the fetal cardiac tissues. However, the catalase activity and total thiol level were decreased; besides the histopathological alterations were remarked. Moreover, DEPs and/or FNT exhibited significant down-regulation in the anti-apoptotic (Bcl-2) and paraoxonase-1 gene expression, and up-regulation in the apoptotic (Bax and caspase-3) gene expression along with DNA fragmentation. Remarkably, FS supplementation significantly ameliorated the fetal cardiac oxidative injury, down-regulated the expression of the apoptotic genes, up-regulated the anti-apoptotic and paraoxonase-1 gene expression, reduced DNA fragmentation, and alleviated the myocardial cell architectures. These findings revealed that FS attenuates DEPs- and/or FNT-induced apoptotic cell death by repairing the disturbance in the anti-apoptotic/pro-apoptotic gene balance toward cell survival in the fetal myocardial cells.

In ovo injection of nano-selenium spheres mitigates the hatchability, histopathology image and immune response of hatched chicks.

In ovo injection of nano-selenium (Se) produced by lactic acid bacteria (LAB-nano-Se) was investigated on the hatchability, immune responses and the histopathological alterations in hatched chicks. The eggs (18 day age) were injected with 0.5 ml of 0.9% NaCl (normal saline, NS), while the control group was kept without injection. In the third, fourth and fifth groups, the eggs were injected with 0.5 ml of NS and LAB-nano-Se at 10, 20 and 30 µg/egg. The results revealed improved growth performance in groups injected with LAB-nano-Se when compared to the control treatment. The highest final weight and weight gain were noticed in 20 µg LAB-nano-Se/egg group (p < .05). The feed conversion ratio was reduced in all treated groups when compared to the control group (p < .05). Groups injected with LAB-nano-Se showed enhanced hatchability of the whole incubated eggs (p < .05). Total lipids and cholesterol levels were decreased significantly in groups treated with LAB-nano-Se at 10 and 20 µg/egg when compared to the non-treated group. At the same time, globulin was increased by LAB-nano-Se in ovo injection. Furthermore, the total antioxidant capacity, catalase, glutathione peroxidase, superoxide dismutase increased in groups treated with LAB-nano-Se at 10 and 20 µg/egg with insignificant (p > .05) differences with those treated with LAB-nano-Se at 30 µg/egg using in ovo injection technique. Also, higher total blood protein and phagocytosis were significantly observed in groups treated with at 10, 20 and 30 µg LAB-nano-Se/egg. The histopathological images of hatched chicks revealed that nano-Se presented normal effects on liver and kidney tissues and restored the parameters as mentioned earlier. To conclude, LAB-nano-Se exhibited beneficial effects in hatched chicks through improving immune and antioxidant activities as well as histopathological effects by using in ovo technique.

A Mixture of Exogenous Emulsifiers Increased the Acceptance of Broilers to Low Energy Diets: Growth Performance, Blood Chemistry, and Fatty Acids Traits.

To investigate the influence of emulsifiers on broilers fed low-energy diets, the birds were distributed into three sets-the control was fed the basal diet, the second group was fed diets 50 kcal/kg less than control, and the third group was fed diets 50 kcal/kg less than control and supplemented with 500 g/ton of emulsifiers. The used mixture of exogenous emulsifiers contains phosphatidyl choline, lysophosphatidyl choline, and polyethylene glycol ricinoleate. Although the feed intake was not meaningfully affected by dietary low-energy level with emulsifier inclusion (P = 0.42), the weight gain and FCR were clearly enhanced (P = 0.005 and P = 0.044, respectively). Protein and lipids utilization were decreased by reducing energy level, but they were increased by emulsifier supplementation (P = 0.022 and P = 0.011, respectively). Liver thiobarbituric acid-reactive substances (TBARs) and muscle palmitic acid concentrations were decreased by reducing the energy level and emulsifier's supplementation (P = 0.014 and P = 0.042, respectively). However, muscle total lipids and α-tocopherol, oleic acid, linoleic acid, and α-linolenic acid were not affected by dietary treatments (P > 0.05). Interestingly, the plasma total cholesterol, HDL-cholesterol, total protein, and globulin were decreased in the low-energy group without emulsifier but they were increased by emulsifier supplementation (P = 0.008, P = 0.005, P = 0.037, and P = 0.005, respectively). It could be concluded that the mixture of emulsifier supplementation to low-energy diets enhanced fat utilization and resulted in positive effects on the growth performance, nutrient utilization, lipid peroxidation, and modified plasma lipid profiles in broilers. Getting such benefits in broilers is a necessity to reduce the feed cost and consequently the price of the product, which will lead to improved welfare of mankind.

Quercetin Attenuates the Oxidative Injury-Mediated Upregulation of Apoptotic Gene Expression and Catecholaminergic Neurotransmitters of the Fetal Rats' Brain Following Prenatal Exposure to Fenitrothion Insecticide.

The association between gestational exposure to organophosphate and neurodevelopmental deficits is an area of particular interest, since the developing brain is sensitively susceptible to this neurotoxic pesticide. Instead, the neuroprotective role of quercetin has been suggested, but its exact protective mechanism against the developmental neurotoxicity of organophosphate did not previously notify. In this study, we have evaluated the anti-apoptotic role of quercetin against the developmental neurotoxicity of fenitrothion. Forty timed pregnant rats (from the 5th to the 19th day) were divided into four groups: control, quercetin (100 mg/kg/day), fenitrothion (2.31 mg/kg/day), and quercetin-fenitrothion co-treated groups where all animals received the corresponding doses by gavage. The embryotoxicity and many symptoms of the fetal growth retardation were recorded in the fenitrothion-intoxicated group. As compared with the control, fenitrothion brought significant (p < 0.05) elevation in the fetal brain dopamine, serotonin, and malondialdehyde levels as well as the activities of superoxide dismutase and catalase. However, fenitrothion decreased the glutathione concentration together with the activities of acetylcholinesterase, glutathione-S-transferase, and glutathione reductase. Moreover, fenitrothion induced some of the histopathological alterations in fetal brain and remarkably (p < 0.05) upregulated the mRNA gene expression of Bax and caspase-3 plus their protein immunoreactivity. It is worth mentioning that quercetin co-treatment alleviated (p Ë‚ 0.05) the fetal growth shortfalls, neurotransmission disturbances, lipid peroxidation, antioxidant disorders, and apoptosis evoked by fenitrothion with frequent repair to the control range. These results revealed that the downregulation of apoptosis-related genes and catecholamines is an acceptable indicator for the neuroprotective efficiency of quercetin especially during gestational exposure to organophosphate.

Synergistic antioxidant effects of resveratrol and curcumin against fipronil-triggered oxidative damage in male albino rats.

Fipronil (FPN), a phenylpyrazole insecticide, has been receiving increased attention owing to its toxicity, which is largely mediated through its effects on antioxidant systems. The present study was undertaken to assess the effects of resveratrol (RSV) and curcumin (CUR) on oxidative damage induced by FPN. Forty mature male Wistar rats were randomized into five groups (n = 8 per group): the first group was the control; the second was administered FPN (10 mg/kg); and the third, fourth, and fifth were co-treated with RSV (10 mg/kg), CUR (200 mg/kg), and their combination, respectively, 2 h prior to FPN administration. All animals were dosed via oral gavage for 4 weeks. FPN significantly (p < 0.05) elevated the sera of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), γ-glutamyl transferase (GGT), urea, creatinine, and cholesterol levels, whereas serum total protein, albumin, and triglyceride levels were significantly (p < 0.05) decreased, compared to those of the control group. Reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were decreased (p < 0.05) in the FPN-treated group compared to those in the control group; however, malondialdehyde (MDA) and nitric oxide (NO) levels were markedly increased (p < 0.05) in the hepatic, renal, and brain tissues. Co-treatment with RSV or CUR alleviated (p Ë‚ 0.05) the increased lipid peroxidation and changes in enzymatic/nonenzymatic antioxidants induced by FPN; all these variables mostly returned to normal levels with the combined of RSV and CUR treatment. In conclusion, RSV and/or CUR relieved and synergistically reversed the FPN-induced tissue oxidative injury, probably by improving the antioxidant defenses via their free radical scavenging and antioxidant characteristics.

Impact of Dietary Organic Mineral Supplementation on Reproductive Performance, Egg Quality Characteristics, Lipid Oxidation, Ovarian Follicular Development, and Immune Response in Laying Hens Under High Ambient Temperature.

The objectives of this study were to investigate the impact of dietary organic mineral mixture (manganese, zinc, and copper) supplementation on reproductive performance, egg quality characteristics, and immune response in laying hens under high ambient temperature. Hens were randomly divided into three treatments: (1) control (basal diet without organic mineral mixture (Mn, Zn, and Cu) supplementation); (2) basal diet + 0.5 g/kg of organic mineral mixture; and (3) basal diet + 1 g/kg of organic mineral mixture from 30 to 38 weeks of age. Hen-day egg production and egg mass were significantly increased by dietary supplementation of 1 g/kg of organic mineral mixture, while feed intake was not affected; therefore, feed conversion ratio (FCR) was significantly improved (P < 0.01). Egg weight, albumen width, shell weight, and shell thickness were significantly increased by the dietary treatments. Serum total cholesterol and glucose were significantly decreased by organic mineral mixture supplementation. Interestingly, yolk contents of total cholesterol and malondialdehyde (MDA) were significantly decreased. Yolk contents of Zn and Cu were significantly increased, while Mn was numerically increased (P > 0.05). Dietary organic mineral mixture supplementation improved the antibody titers against avian influenza H9N1 significantly (P < 0.05) and Newcastle disease virus numerically (P > 0.05) in comparison with the control diet. It might be concluded that the inclusion of organic mineral mixture (Mn, Zn, and Cu) enhanced reproductive performance, shell quality characteristics, plasma profile, yolk mineral concentration, yolk lipid oxidation, and immune response in laying hens under high ambient temperature.

Pterocarpus santalinus ameliorates streptozotocin-induced diabetes mellitus via anti-inflammatory pathways and enhancement of insulin function.

OBJECTIVES: Morbidity and mortality due to diabetes mellitus (DM) result in exorbitant psycho-economical costs, so there is a strong need to create new strategies and drugs for controlling DM. The aim of the current study was to investigate the anti-diabetic effect of the aqueous extract of Pterocarpus santalinus on streptozotocin (STZ)-induced DM as compared to glustin. MATERIALS AND METHODS: Thirty male rats were divided into five groups of six rats each as follows: control; the second group, received the aqueous plant extract (250 mg/kg) orally and daily for three weeks; the third group, was intraperitoneally injected with a single dose of 65 mg/kg of STZ and sacrificed after four weeks; the fourth and fifth groups, were injected with STZ, then after one week these were treated orally with either plant extract or with 3 mg/kg of glustin for three weeks, then sacrificed. RESULTS: HPLC analysis of the plant aqueous extract showed that it contains many polyphenols and flavonoids. Treatment with STZ resulted in significant reductions in body weight, insulin level, and the expression of Fetuin-A and IRS-1. It also caused significant elevations in glucose, HOMA-IR, glycated hemoglobin, urea, and the expression of JNK and SIRT-1. STZ also caused an extensive ß-cell degranulation and decreased cellular density. The aqueous extract of red sandalwood was able to abrogate the deleterious effects caused by STZ and improved the histological architecture of pancreas. CONCLUSION: The aqueous extract of P. santalinus ameliorates diabetes mellitus via anti-inflammatory pathways and enhancement of insulin function.

Synthesis, structural characterization and in vivo anti-diabetic evaluation of some new sulfonylurea derivatives in normal and silicate coated nanoparticle forms as anti-hyperglycemic agents.

Series of new sulfonylurea derivatives (gliclazide analogues) was synthesized and characterized. Thus, p-tolylsulfonylisocyanate was left to react with different amino derivatives under mild conditions to afford the desired sulfonylurea derivatives 1-5. The molecular structure of the compound N-(2,6-Dichlorophenylcarbamoyl)-4-methylbenzenesulfonamide, 1c has been elucidated by single crystal X-ray diffraction. Anti-diabetic properties of the synthesized compounds relative to anti-diabetic drug (gliclazidem MR60) were carried out, where most of the tested compounds showed significant activity for reducing the blood glucose level. The results revealed that compounds 1c and 5 showed better anti-diabetic activities compared with gliclazide. Activity of the most potent derivatives of sulfonylurea compounds namely 1c and 5 were increased using coated nanostructure tetraethyl orthosilicate (TEOS) as a modified release (MR) agent. The effect of the prepared sulfonylurea compounds against the diabetic condition was investigated using specific selected biomarkers as of liver enzyme activities as transaminases (AST, ALT) and alkaline phosphatase (ALP), lipids profiles; total cholesterol (TC), triacylglycerols (TG) and total lipid (TL). The antioxidants, oxidative stress biomarkers and histological examination were also examined and discussed.

Propolis relieves the cardiotoxicity of chlorpyrifos in diabetic rats via alleviations of paraoxonase-1 and xanthine oxidase genes expression.

Pesticides cardiotoxicity in case of diabetic-induced cardiac complications is unidentified. The probable amelioration role of propolis is gauged against the cardiotoxic effects of chlorpyrifos in the diabetic rats through paraoxonase-1 (PON1) and xanthine oxidase (XO) genes dysregulation. Fifty-six male rats were distributed (n = 7) into eight groups. The first one saved as control whereas the 2nd, 3rd, and 4th were kept for propolis aqueous extract (100 mg/kg), diabetes (60 mg/kg streptozotocin) and chlorpyrifos (2.5 mg/kg), respectively. The 5th was diabetes/chlorpyrifos combination, while 6th, 7th, and 8th were intubated with propolis for four weeks after diabetic induction, chlorpyrifos intoxication, and their combination, respectively. The plasma glucose, lipid profiles, cardiac enzymes and interleukin-6 (IL-6) significantly elevated, while insulin decreased in the diabetic and combination groups. Although the cardiac acetylcholinesterase, total thiols, and PON1 significantly reduced after diabetic and/or chlorpyrifos gavage, the protein carbonyl, superoxide dismutase, catalase, and XO significantly elevated. The mRNA genes expression of PON1 and XO have also confirmed the enzymatic activities. Interestingly, propolis significantly restored the hyperglycemia, hypoinsulinemia, hyperlipidemia, IL-6 elevations, and antioxidant defense system disorder. These records revealed that the immunomodulatory, anti-diabetic and antioxidant tasks are fine pointers for the cardiovascular defender of propolis especially during diabetes and/or pesticides exposure.