Transport Stress Induced Cardiac NO-NOS Disorder Is Mitigated by Activating Nrf2/HO-1/NQO1 Antioxidant Defense Response in Newly Hatched Chicks

Abstract

With the development of the intensive poultry industry, the health problems of chickens caused by transportation have attracted more and more attention. Transport stress reduces performance, immune function, and meat quality in chicks, which has become one of the most important factors that endanger the development of the poultry industry. Currently, studies on the effects of transport stress have mainly focused on the performance of livestock and poultry to be slaughtered. However, the effects of transport stress on heart damage and oxidative stress in newborn chicks have not been reported. In this study, we selected newborn chicks as the object. This study was intended to explore the effects of transport stress on the heart damage of newly hatched chicks. The findings suggested that transport stress could cause oxidative stress in the hearts of newly hatched chicks by increasing the levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and decreasing the contents of Total antioxidant capacity (T-AOC), and the activities of antioxidant enzymes (SOD), together with increasing the activities of antioxidant enzymes (Catalase (CAT) and Glutathione S-transferase (GST)). Transport stress disrupted the balance between oxidation and antioxidant systems. The Nrf2 signaling pathway was activated by transport stress and triggered the transcription of antioxidant signaling. In short, transport stress-induced nitric oxide (NO)—nitric oxide synthases (NOS) system metabolic disorders and cardiac oxidative stress are mitigated by activating the nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/NAD(P)H quinone oxidoreductase-1 (NQO1) antioxidant defense response in newly hatched chicks.

Inhibition of mtDNA-PRRs pathway-mediated sterile inflammation by astragalus polysaccharide protects against transport stress-induced cardiac injury in chicks

“…Damaged mature cardiomyocytes, as the postmitotic cells, are unable to self-recover, which means that cardiac tissue is irreversible. Moreover, according to previous studies, TS can cause heart damage in chicks, as evidenced by the obvious vacuolar degeneration and necrosis of cardiomyocytes after TS lasting 8 h ( Sun et al, 2018 ; Xu et al, 2022 ). However, how TS induces cardiac injury in chicks is not yet fully understood.…”

“…It has been well documented that TS can cause weight loss, immune disorders, and metabolic dysfunction in animals ( Li et al, 2017 ). Of note, chicks often experience a higher heart rate or even sudden death during or after transportation, which is considered to be related to heart damage caused by TS ( Li et al, 2017 ; Chen et al, 2022a ; Xu et al, 2022 ). A previous study in chicks indicated that TS evoked cardiac damage and notably reduced body weight via inducing nitric oxide and arresting the heat shock response ( Li et al, 2017 ).…”

“…Oxidative stress is widely described as an imbalance between ROS production and endogenous antioxidant defense mechanisms. Evidence has consistently demonstrated that TS can evoke oxidative stress in chicks via promoting free radical production and lipid peroxidation, together with reducing the activity of antioxidant enzymes (such as GSH and SOD2) ( Ge et al, 2017 ; Xu et al, 2022 ). Our results are consistent with these reports that TS overtly depressed the levels of the antioxidant enzymes GSH, GPX, GST and SOD2 and augmented the content of the lipid peroxidation product MDA.…”

“…For instance, a scientific study proved that TS-caused cerebrum oxidative stress cannot be completely mitigated by its own nuclear factor-erythroid 2-related factor 2 ( Nrf2 )-mediated antioxidant defense system ( Ge et al, 2017 ). Likewise, a previous study also showed that TS destroys the balance between oxidation and antioxidant systems in the chick heart, as reflected by the increased malondialdehyde ( MDA ) and the reduced total antioxidant capacity ( T-AOC ) ( Xu et al, 2022 ). These findings further validate that oxidative stress-mediated sterile inflammation plays a key role in TS-induced cardiac injury.…”

Effect of transport stress on apoptosis and autophagy in goat lung cells

“…Heat stress has been shown to cause morphological damage to the lungs, trachea and bronchi, and oxidative stress after a certain length of transportation has been shown to trigger signi cant changes in the expression of apoptosis-related genes Bcl-2 and Bax, as well as autophagy-related genes LC3B, PINK1 and Parkin [ 7,26]. Similarly, during transportation, animals are subjected to counter-organismic disturbances such as environmentally harmful chemicals, bumps and occlusions, and temperature and humidity discomfort, which can trigger a series of events at the cellular and molecular level, such as the elicitation of malondialdehyde (MDA), reactive oxygen species (ROS), nitric oxide, DNA/RNA oxidative stress damage products (DNA/RNA OSDP), and heat shock proteins 27, 70, 90 ( HPS27, 70, 90) and other indicators of oxidative stress and heat stress climbed, which ultimately induced in ammation, apoptosis and autophagy in goats after causing them to be subjected to oxidative stress and heat stress [27][28][29][30]. The lungs are the gateway for gas exchange, and their normal activity and linkage to the immune system facilitates the repair of infections and damage caused by transportation stress [31].…”