Table 1.

The main findings summarized from previous literature are related to the effects of heat stress on lipid and protein peroxidations, reactive oxygen species, redox balance and mitochondria function in broilers.

Item	HS condition	Main findings	References
Lipid peroxidation	Broiler kept at control (23°C) and HS group (38°C); RH 70%, for 7 d	•Significantly increased in hepatic MDA compared to the control group.	Tan et al. (2010)
	Broiler exposed to (36°C  ± 2°C; 8 h/d lasted for 7-14 d.	•Broiler exposed to HS exhibited higher values of MDA in breast muscle compared to the control group.	Lu et al. (2017)
	Acute HS (34°C ± 1°C, 24 h)	•The values of MDA were significantly increased by 37.3%, 12.5%, and 40% in serum and both tissues of the liver and ileum of broiler after exposure to HS, respectively.	Ouyang et al. (2022)
	Embryo chicken exposed to HS conditions (39.5°C for 6 h)	•HS conditions enhanced the MDA levels in the hepatocytes of chicken embryo.	Zhang et al. (2022)
	Broiler exposed to 34°C ± 1°C for 8 h/d	•The levels of MDA were significantly increased by 20%.•Superior levels of MDA and hydrogen peroxide were also observed in the serum of HS group.	Deng et al. (2023)
	Broiler exposed to HS (34°C)	•Broiler exposed to HS had higher levels of MDA than the treated group (rutin 0.5 g/kg feed).•The levels of MDA were significantly increased by 20% in the hepatic broiler's control group after exposure to HS (35°C ± 2°C).	Chen et al. (2023b)
	Broiler exposed to cyclic HS (34°C for 8 h and 24°C for 16 h)	•High-temperature conditions (cyclic HS) increased (P < 0.05) hepatic MDA values in broilers.	Bai et al. (2023)
Protein oxidation	Broiler exposed to HS (38°C; RH 70%)	•Elevation in hepatic protein carbonyl was noticed in the HS group.•An increase in the protein carbonyl of hepatic tissues after exposure to HS.	Saracila et al. (2023), Tan et al. (2010)
	Chicken embryo hepatocytes (39.5°C heat stress for 6 h)	•HS conditions significantly increased the protein carbonyl levels in chicken embryo hepatocytes.	Zhang et al. (2015), Zhang et al. (2022)
ROS	Broilers exposed to high temperature (34°C ± 1°C for 8 h and 22°C ± 1°C for the remaining time) for 20 d	•Acute HS instigated a marked ROS release.•Broilers exposed to high temperatures significantly elevated ROS in the hepatocytes.	Zhang et al. (2018a), Zhang et al. (2018b)
	HS (7 d, 32°C)	•Compared to the control group, there were significantly higher values of ROS in broiler breast muscle exposed to HS.	Lu et al. (2017)
	Broiler exposed to HS (36°C  ± 2°C; 8 h/d lasted for 1 or 2 wk)	•HS induced superior values of ROS than the control group (25°C  ± 2°C; 24 h/d) in broilers.	Wang et al. (2019)
	HS (39.5°C for 6 h)	•HS conditions enhanced the ROS and 8-OHdG (DNA marker damage) levels in chicken embryo hepatocytes.	Zhang et al. (2022)
Mitochondria redox balance	Broiler chickens (34°C for 8 h)	•Mitochondrial GSH levels were reduced significantly in the livers of heat-stressed broilers.•HS diminished the antioxidant reactions through the NF-E2-related factor 2 (Nrf2) signaling pathway.•HS inhibited the gene expression of Prx3, TrxR2, and Trx2, which are related to redox balance in mitochondria.	Zhang et al. (2018a), Zhang (2018b)
	Acute HS (34°C ± 1°C, 24 h)	•HS diminished the activities of GSH-Px, CAT, SOD, and TAC in hepatic and ileum tissues of stressed broilers.•Acute HS exposure resulted in elevated expression of GPx1 and Nrf2 in the ileum of the small intestine and HO-1, NQO1, and Nrf2 in the hepatic tissues compared with the control group.	Ouyang et al. (2022)
	HS (34°C)	•Stressed broiler had inferior SOD, GPx, and TAC levels than the treated group (rutin 0.5 g/kg feed).	Chen et al. (2023a)
	HS 35°C ± 2°C	•Stressed broiler had inferior hepatic antioxidant indices such SOD (↓33.3%), and GPx (↓38.46%), as compared with the control group (23°C ± 2°C).•HS induced (34°C ± 1°C for 8 h/d) intestinal barrier dysfunction and antioxidant capacity in broilers.	Ding et al. (2023)
	Heat stress conditions (39.5°C HS for 6 h)	•Chicken exposed to high temperature showed inferior SOD, TAC, GSH-Px, CuZn-SOD, and CAT activities.	Zhang et al. (2022)
Mitochondrial activity	–	•Stressed broilers experienced significant ATP levels reductions, complexes I and III activities, relative MMP (mitochondrial membrane potential), and swelling.	Liao et al. (2022)
	Acute heat stress	•Upregulated the mitochondrial membrane potential (increased the acceleration of energy consumption and activated mitochondria to produce more energy).•Acute heat stress caused an upregulation in the broilers’ mitochondrial membrane potential due to increased energy consumption and mitochondrial activation, resulting in increased energy production.	Uyanga et al. (2022)