The massive meat production of broiler chickens make them continuously exposed to potential stressors that stimulate releasing of stress-related hormones like corticosterone (CORT) which is responsible for specific pathways in biological mechanisms and physiological activities. Therefore, this research was conducted to evaluate a wide range of responses related to broiler performance, immune function, plasma biochemistry, related gene expressions and cell death morphology during and after a 7-day course of CORT injection. A total number of 200 one-day-old commercial Cobb broiler chicks were used in this study. From 21 to 28 d of age, broilers were randomly assigned to one of 2 groups with 5 replicates of 20 birds each; the first group received a daily intramuscular injection of 5 mg/kg BW corticosterone dissolved in 0.5 ml ethanol:saline solution (CORT group), while the second group received a daily intramuscular injection of 0.5 ml ethanol:saline only (CONT group). Growth performance, including body weight (BW), daily weight gain (DG), feed intake (FI) and feed conversion ratio (FC), were calculated at 0, 3 and 7 d after the start of the CORT injections. At the same times, blood samples were collected in each group for hematological (TWBC’s and H/L ratio), T- and B-lymphocytes proliferation and plasma biochemical assays (total protein, TP; free triiodothyronine hormone, fT3; aspartate amino transaminase, AST; and alanine amino transaminase, ALT). The liver, thymus, bursa of Fabricius and spleen were dissected and weighed, and the mRNA expression of insulin-like growth factor 1 gene (IGF-1) in liver and cell-death-program gene (caspase-9) in bursa were analyzed for each group and time; while the apoptotic/necrotic cells were morphologically detected in the spleen. From 28 to 35 d of age, broilers were kept for recovery period without CORT injection and the same sampling and parameters were repeated at the end (at 14 d after initiation of the CORT injection). In general, all parameters of broiler performance were negatively affected by the CORT injection. In addition, CORT treatment decreased the plasma concentration of fT3 and the mRNA expression of hepatic IGF-1. A significant increase in liver weight accompanied by an increase in plasma TP, AST and ALT was observed with CORT treatment, indicating an incidence of liver malfunction by CORT. Moreover, the relative weights of thymus, bursa and spleen decreased by the CORT treatment with low counts of TWBC’s and low stimulation of T & B cells while the H/L ratio increased; indicating immunosuppressive effect for CORT treatment. Furthermore, high expression of caspase-9 gene occurred in the bursa of CORT-treated chickens, however, it was associated with a high necrotic vs. low apoptotic cell death pathway in the spleen. Seven days after termination of the CORT treatment in broilers, most of these aspects remained negatively affected by CORT and did not recover to its normal status. The current study provides a comprehensive view of different physiological modulations...

Modern methods of industrial poultry and egg production systems involve stressful practices that stimulate Escherichia coli (E. coli) activity causing endotoxic shock. This investigation was conducted to evaluate the expression of pro-inflammatory cytokines and cell death program genes and DNA damage induced by E. coli in the brain and liver tissues of laying hens. A total of two hundred and ten H&N brown layer hens with 20 week age, were used in this research. First, preliminary experiments were designed (60 hens in total) to establish the optimal exposure dose of E. coli and to determine the nearest time of notable response to be used in the remainder studies of this research. At 35-wk of age, 150 hens were randomly assigned into 2 groups with 3 replicates of 25 birds each; the first group was injected in the brachial wing vein with 107 E. coli colony/hen, while the second group was injected with saline and served as a control. The body temperature and plasma corticosterone concentration were measured 3 hr after injection. Specimens of liver and brain were obtained from each group and the gene expression of p38 mitogen-activated protein kinase, interlukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), Bax, and caspase-3 genes were measured by quantitative real-time PCR. DNA damage in the brain and liver tissues were also measured by comet assay. Hens treated with E. coli showed significant (P<0.05) increase of body temperature and plasma corticosterone (42.6°C and 14.5 ng/ml, respectively) compared to the control group (41.1°C and 5.5 ng/ml, respectively). Additional remarkable over-inflammation gene expression of p38, IL-1β and TNF-α.genes were also detected in the brain (2.2-fold, 2.0-fold and 3.3-fold, respectively) and the liver (2.1-fold, 1.9-fold and 3.0-fold, respectively) tissues of the infected chickens. It is also important to note that hens injected with E. coli showed an increase in DNA damage in the brain and liver cells (P<0.05). These results were synchronized with activating cell death program since our data showed significant high expression of Bax gene by 2.8- and 2.7-fold and caspase-3 gene by 2.5- and 2.7-fold in the brain and liver tissues of infected chickens, respectively (P<0.05). In conclusion, the current study indicates that E. coli injection induces inflammatory physiological response and triggers cell death program in the brain and liver. Our results provide more understanding to endotoxic shock by E. coli in chickens at cellular level. Further studies are required to confirm if such responses are destructive or protective to set the means through which a chicken mounts a successful defense against avian pathogenic E. coli.

Aim:To study the efficacy of Na-butyrate encapsulated in palm fat on performance of broiler chickens experimentally infected with necrotic enteritis (NE) with the determination of its protective effect against the changes in the gene expression profiles and deoxyribonucleic acid (DNA) fragmentation.Materials and Methods:A total of 800 one-day-old male Arbor Acres Plus broiler chickens were randomly allocated into four groups for 5 weeks. Na-butyrate was supplemented at dosages of 1 kg/ton for starter diet, 0.5 kg/ton for grower diet, and 0.25 kg/ton for finisher diet (presence or absence). Birds of groups 1 and 2 were inoculated by crop gavages with 4×108 CFU/ml/bird of Clostridium perfringens in phosphate buffered saline for 4 successive days, from 14 to 17 days of age to produce NE.Results:Addition of Na-butyrate, encapsulated in palm fat, to ration of experimentally infected broilers with NE resulted in increased final body weight, at 35 days of age, reduced total feed consumption, improved feed conversion ratio, reduced cumulative mortality, and increased production number. There were increased intestinal diameter, intestinal length, and significantly increased the weight of bursa of Fabricius(BF) with higher hemagglutination inhibition titers against Newcastle disease (ND) vaccination versus untreated infected and untreated negative control birds. The results showed increased expression levels of alpha-toxin and glyceraldehyde-3-phosphate dehydrogenase in the bursa tissues of broilers infected with C. perfringens. However, the expression levels of these genes in broilers treated with Na-butyrate were similar to the non-infected control group. Supplementation of broilers with Na-butyrate increased the expression level of insulin-like growth factor-1 (IGF-1) and decreased the DNA fragmentation induced by C. perfringens.Conclusion:Na-butyrate significantly improved chicken broiler body weights, increased relative weights of BF, increased antibody titers against ND vaccination, numerically lowered mortality due to C. perfringens infection, increased the expression level of IGF-1, and decreased the DNA fragmentation induced by C. perfringens. Obtained results point out the effectiveness of Na-butyrate encapsulated in palm fat in improving the production performance variables, immune response, and intestinal morphology in experimentally induced NE as well as in non-infected chicken broilers.

A laboratory-scale bioremediation unit was designed, built and tested for the bio-removal of several Direct textile dyes. Four experiments were carried out to assess the efficiency of the bioremediation unit using Aspergillus niger fungal strain. Three commonly used Direct dyes and textile dyes mixture (simulated effluent: Direct brown, Direct violet, Direct green) were tested in this study. The strain of A. niger was efficient in the removal of the three Direct dyes. The decolorization percentages of the dyes after 24 h of incubation were 56.2, 51.7, and 95.4% for Direct brown, Direct green, Direct violet dyes, respectively. The percentages increased up to 79.4, 86.4, and 96.7% after 72 h of incubation for the same dyes, respectively. The results also showed that the fungal strain reduced the chemical oxygen demand values of simulated dye effluents from 165 to 564 mg/l with most of the dyes. The assessment of bioremediation products on biomodel was conducted using a fresh water fish. The liver and brain of Nile tilapia were tested to evaluate the expression of genes coding for several proteins related to stress such as metallothioneins (MTs), cytochrome P450 (CYP450), and heat shock proteins (HSPs). To assess the alterations in the gene expression, ten animals from each group were killed after 4 weeks of treatment. The results revealed significant increases in the brain and hepatic mRNA levels of all stress protein genes MT, CYP450, Hsp70a, b, and Hsp47 in the fish groups treated with industrial Direct violet, green, and brown dye water. Exposure of tilapia to bioremediation products after treatment with A. niger fungi reduced the over-expression of the stress protein genes in the brain and liver tissues.

The genotoxicity of the azo dye 'Direct Violet' and the removal of this dye by Aspergillus niger strain at different conditions have been investigated in male rats. Two genotoxicity techniques, namely bone marrow micronucleus assay and RAPD fingerprinting pattern, were used in this study for the direct dye and its removal by the fungal strain. Sixty male rats were divided into six treatment groups including a control group and other groups which were exposed for 2 or 8 weeks to Direct Violet dye, Direct Violet dye treated with A. niger at pH 2 or pH 9 or without agitation and acrylamide (30 mg/kg b.w.). A potent dose-dependent response was observed following oral gavage of the dye up to 1000 mg kg(-1), after which significant toxicity to the erythroid compartment was observed. Acrylamide and Direct Violet treatments increased the number of micronucleated polychromatic erythrocytes (MnPCEs) with respect to the controls. This increase was statistically significant in the two time intervals (2 and 8 weeks treatment, P < 0.0001). Fungi treatments at pH 2 and without agitation were able to reduce the number of MnPCEs induced by Direct Violet administration in all duration groups. Fungi treatment at pH 9 was only able to inhibit the genotoxicity of Direct Violet after 8 weeks treatment. The RAPD fingerprinting pattern indicated that most DNA of the samples treated with dye alone or acrylamide revealed polymorphic bands including the appearance and disappearance of the bands, which did not appear in the DNA samples of normal or fungi protected rats. The implications of these findings for the health and safety of occupationally exposed workers are discussed.