Blood hematology and biochemical of four laying hen strains exposed to acute heat stress.

This study is aimed at defining physiological responses to heat stress (HS) in four different lines to better understand the underlying mechanisms of various responses in these genotypes when exposed to heat for a short period. At the age of 30 weeks, 176 laying hens (44 each from the Fayoumi, Golden Sabahia, White Leghorn, and Lohman Brown) were allotted to 2 groups (thermoneutral temperature (26.0 ± 1 °C) and HS (35 ± 1 °C) with relative humidity 55 ± 5% for 6 h/day). Blood samples were collected after 6 h of heat. According to the findings of this study, acute HS increased the concentration of LH in hens by 20.2% while decreasing the concentration of FSH by 4.24. Genotype was found to have a significant effect on blood hematology and most blood biochemical. Significant differences were found between heat stress and genotype in most of the blood parameters. Golden sabahia laying hens had significantly higher WBC, IgY, and LH levels than other groups under HS. The findings of the current study suggested that Lohman Brown was less tolerant to acute HS than another genotype.

Cellular antioxidant enzyme activity and biomarkers for oxidative stress are affected by heat stress.

Heat stress (HS) causes oxidative stress and cellular changes in an attempt to detoxify the harmful effects of reactive oxygen species (ROS). However, how ROS affect different organs in chickens under acute and chronic HS is relatively unknown. We investigated the cellular enzyme activity and biomarker changes in the liver and Pectoralis (P) major muscle in broiler chickens subjected to both acute and chronic HS. Forty-eight broiler chickens at 14 days old were randomly assigned to either 25 °C (control) or 35 °C (heat-stressed) for 12 days. Five birds per treatment at 1 and 12 days post-HS were euthanized, and the liver and P. major muscle were sampled. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), glutathione reductase (GR), glutathione S-transferase (GST) activity as well as 8-hydroxy-2'-deoxyguanosine (8-OHdG), advanced glycation end product (AGE), malondialdehyde (MDA), and protein carbonyl (PCO) were analyzed as biomarkers for DNA, carbohydrate, lipid, and protein oxidation, respectively. The SOD, CAT, and GSH-GPx activity levels in the liver and the P. major muscle changed under HS; however, some of the changes were tissue-specific or dependent on the duration of the HS. There were increased liver 8-OHdG during chronic HS and also increased liver AGE levels during both acute and chronic HS indicating significant carbohydrate and DNA oxidations. In the P. major muscle, we observed significant increases in lipid peroxidation and protein oxidation which may reflect that this tissue is less resilient to oxidative damage under heat stress. We show that heat stress caused tissue-specific changes to levels of oxidation biomarkers in chicken.

Expression of genes that encode cellular oxidant/antioxidant systems are affected by heat stress.

Heat stress causes critical molecular dysfunction that affects productivity in chickens. Thus, the purpose of this study was to evaluate the effect of heat stress (HS) on the expression of select genes in the oxidation/antioxidation machinery in the liver of chickens. Chickens at 14 days of age were randomly assigned to two treatment groups and kept under either a constant normal temperature (25 °C) or high temperature (35 °C) in individual cages for 12 days. mRNA expression of Nrf2, oxidants NADPH(NOX): [NOX1, NOX2, NOX3, NOX4, NOX5 and DUOX2], and antioxidants [SOD1, CAT, GR, GPx1, NQO1] in the liver were analyzed at 1 and 12 days post-HS. We show that, HS changes the mRNA expression of oxidants thereby increasing cellular reactive oxygen species (ROS). Additionally, persistent HS up-regulates SOD which converts superoxides to hydrogen peroxide. We further demonstrated the dynamic relationship between catalase, GSH peroxidase (GPx) and NADPH under both acute and chronic heat stress. The pentose phosphate pathway could be important under HS since it generates NADPH which serves as a cofactor for GPx. Also, methionine, a precursor of cysteine has been shown to have reducing properties and thereby makes for an alternative fuel for redox processes. Genes in the ROS and antioxidant generation pathways may provide insight into nutritional intervention strategies, especially the use of methionine and/or cysteine when birds are suffering from heat stress.

Effect of heat stress on protein utilization and nutrient transporters in meat-type chickens.

The aim of this study was to investigate the effect of heat stress (HS) on digestibility of protein and fat and the expression of nutrient transporters in broilers. Forty-eight male Cobb500 chicks were used in this study. At day 14, birds were randomly divided into two groups and kept under either constant normal temperature (25 °C) or high temperature (35 °C) in individual cages. Five birds per treatment at 1 and 12 days post-treatment were euthanized, and Pectoralis major (P. major) and ileum were sampled for gene expression analysis. At day 33, ileal contents were collected and used for digestibility analysis. The total consumption and retention of protein and fat were significantly lower in the HS group compared to the control group. Meanwhile, the retention of crude protein per BWG was significantly higher in the HS group compared to the control group. In P. major and ileum tissues at day 1, transporters FATP1 and SGLT1 were down-regulated in the HS group. Meanwhile, FABP1 and PepT1 were down-regulated only in the ileum of the HS group. The converse was shown in P. major. The nutrient transporter FABP1 at day 12 post-HS was down-regulated in the P. major and ileum, but GLUT1 and PepT2 were down-regulated only in the ileum, and PepT1 was down-regulated only in the P. major compared with the control group. These changes in nutrient transporters suggest that high ambient temperature might change the ileum and P. major lipids, glucose, and oligopeptide transporters.

Molecular and Cellular Responses of DNA Methylation and Thioredoxin System to Heat Stress in Meat-Type Chickens.

Heat stress (HS) causes molecular dysfunction that adversely affects chicken performance and increases mortality. The responses of chickens to HS are extremely complex. Thus, the aim of this study was to evaluate the influence of acute and chronic exposure to HS on the expression of thioredoxin-peroxiredoxin system genes and DNA methylation in chickens. Chickens at 14 d of age were divided into two groups and reared under either constant normal temperature (25 °C) or high temperature (35 °C) in individual cages for 12 days. Five birds per group at one and 12 days post-HS were euthanized and livers were sampled for gene expression. The liver and Pectoralis major muscle were sampled for cellular analysis. mRNA expression of thioredoxin and peroxiredoxins (Prdx) 1, 3, and 4 in the liver were down-regulated at 12 days post-HS compared to controls. The liver activity of thioredoxin reductase (TXNRD) and levels of peroxiredoxin1 (Prdx1) at 12 days post-HS were significantly decreased. The results reveal that there was a significant decrease in DNA methylation at 12 days post HS in liver tissues. In conclusion, pathway of thioredoxin system under HS may provide clues to nutritional strategies to mitigate the effect of HS in meat-type chicken.

Impact of Fennel Essential Oil as an Antibiotic Alternative in Rabbit Diet on Antioxidant Enzymes Levels, Growth Performance, and Meat Quality.

In the current study, fennel essential oil was used as an antibiotic alternative compared to gentamycin for enhancing the expression of apoptosis genes and antioxidant enzymes in weaned rabbits as well as meat quality and growth performance. The gene expression of the cell lymphoma 2 (BAX and BCL2), caspase3 (CASP3), and glutathione peroxidase (GPX1) were estimated in the liver tissue using qRT-PCR. A total of 45 Moshtohor weaned male rabbits aged four weeks were randomly allocated to control, T1, and T2 treatment groups; each consisted of 15 weaned male rabbits with five replicates. Rabbits in the T1 and T2 groups were orally supplied with 1 mL fennel oil and 1 mL gentamycin, respectively. Weaned rabbits under different treatments showed increased body weight (BW) at 8 and 12 weeks of age and average daily gain (ADG) at 4-8 and 4-12 weeks of age compared to the control group. Compared to the controls, the weaned rabbits supplemented with fennel oil and gentamycin had lower total cholesterol, triglyceride, and MDA. In addition, villus length, mRNA of BAX, BCL2, Casp3, and GPX were increased in the different treatments compared to the control. Furthermore, the meat of these rabbits was less tender, had a lower aerobic plate count (APC), pH, and was brighter and redder in color than the control. Under the conditions of the present study, the supplementation of weaned Moshtohor rabbits with fennel oil as a natural alternative for gentamycin enhanced feed conversion and daily gain through enhancing villus length and mucus thickness. Additionally, fennel essential oil reduces oxidative stress by increasing the antioxidant enzymes.

Modulation of Heat-Shock Proteins Mediates Chicken Cell Survival against Thermal Stress.

Heat stress is one of the most challenging environmental stresses affecting domestic animal production, particularly commercial poultry, subsequently causing severe yearly economic losses. Heat stress, a major source of oxidative stress, stimulates mitochondrial oxidative stress and cell dysfunction, leading to cell damage and apoptosis. Cell survival under stress conditions needs urgent response mechanisms and the consequent effective reinitiation of cell functions following stress mitigation. Exposure of cells to heat-stress conditions induces molecules that are ready for mediating cell death and survival signals, and for supporting the cell's tolerance and/or recovery from damage. Heat-shock proteins (HSPs) confer cell protection against heat stress via different mechanisms, including developing thermotolerance, modulating apoptotic and antiapoptotic signaling pathways, and regulating cellular redox conditions. These functions mainly depend on the capacity of HSPs to work as molecular chaperones and to inhibit the aggregation of non-native and misfolded proteins. This review sheds light on the key factors in heat-shock responses for protection against cell damage induced by heat stress in chicken.