Search

Galactooligosaccharides (GOS) delivered in ovo improve intestinal health of broiler chickens. This study aimed to demonstrate the impact of in ovo stimulation with GOS prebiotic on day 12 of egg incubation on performance and welfare traits in broiler chickens. The incubating eggs were divided into 3 groups, based on the substance injected in ovo: 3.5 mg of GOS dissolved in 0.2 mL physiological saline (GOS), 0.2 mL physiological saline (S), or uninjected controls (C). Constant heat stress (HS) was induced on days 32 to 42 post-hatch by increasing environmental temperature to 30°C. Thermoneutral (TN) animals were kept at 25°C. The performance (body weight [BW], daily feed intake [DFI], daily weight gain [DWG], and feed conversion rate [FCR]) were measured and mortality was scored for starter (days 0 to 13), grower (days 14 to 27), and finisher (days 28 to 42) feeding phases. Rectal temperature was scored on days 32 to 42. Food-pad dermatitis (FPD) was scored post-mortem (day 42). GOS increased (P < 0.01) BW on day 42 (2.892 kg in GOS vs. 2.758 kg in C). Heat stress significantly reduced (P < 0.01) final BW (2.516 kg in TN vs. 3.110 kg in HS). During finisher phase, DFI was significantly higher in GOS vs. C (173.2 g vs. 165.7 g; P < 0.05). FCR calculated for the entire rearing period (days 0 to 42) ranged from 1.701 in C to 1.653 in GOS (P < 0.05). GOS improved FCR in HS animals during finisher phase (P < 0.05). Rectal temperature of GOS chickens under HS reached 42.5°C 1 day earlier than C and S (P < 0.05), which suggests that those birds recovered earlier from the high environmental temperature. Heat stress increased (P < 0.05) mortality about 5 times compared to TN during finisher phase (from 1.59% in TN to 7.69% in HS). GOS decreased FPD in TN conditions by 20% (no lesions in 81% in GOS vs. 60% in C). GOS delivered in ovo mitigated negative effects of HS on performance and welfare in broiler chickens.

Reactive Oxygen Species (ROS) are essential cellular messengers required for cellular homeostasis and regulate the lifespan of several animal species. The main site of ROS production is the mitochondrion, and within it, respiratory complex I (CI) is the main ROS generator. ROS produced by CI trigger several physiological responses that are essential for the survival of neurons, cardiomyocytes and macrophages. Here, we show that CI produces ROS when electrons flow in either the forward (Forward Electron Transport, FET) or reverse direction (Reverse Electron Transport, RET). We demonstrate that ROS production via RET (ROS-RET) is activated under thermal stress conditions and that interruption of ROS-RET production, through ectopic expression of the alternative oxidase AOX, attenuates the activation of pro-survival pathways in response to stress. Accordingly, we find that both suppressing ROS-RET signalling or decreasing levels of mitochondrial H2O2 by overexpressing mitochondrial catalase (mtCAT), reduces survival dramatically in flies under stress. Our results uncover a specific ROS signalling pathway where hydrogen peroxide (H2O2) generated by CI via RET is required to activate adaptive mechanisms, maximising survival under stress conditions., Graphical abstract Image 1, Highlights • Heat stress induces ROS generation through the activation of Reverse electron transport (ROS-RET). • Suppressing ROS-RET attenuates the transcriptional stress response reducing survival under stress. • Mitochondrial catalase reduces survival under stress, identifying H2O2 as the main ROS signalling molecule.