Dietary squalene supplementation alleviates diquat-induced oxidative stress and liver damage of broiler chickens

Abstract

The aim of this study was to explore the protective effects of squalene supplementation on growth performance, oxidative status, and liver function of diquat-challenged broilers. One hundred forty-four 1-day-old male Ross 308 broiler chicks were allocated to 3 groups, and each group consisted of 6 replicates of 8 birds each. The three groups were as follows: 1) nonchallenged broilers fed with a basal diet (control group), 2) diquat-challenged broilers fed a basal diet, and 3) diquat-challenged broilers fed with a basal diet supplemented with 1.0 g/kg of squalene. Broilers were intraperitoneally injected with 20 mg/mL of diquat solution at a dosage of 1 mL/kg of BW or an equivalent amount of saline at 20 d. Compared with the control group, weight gain and BW change rate during 24 h after injection were decreased by diquat challenge ( P < 0.05), and the diquat-induced compromised growth performance was improved by squalene supplementation ( P < 0.05). Diquat administration reduced plasma superoxide dismutase activity and increased malondialdehyde accumulation and glutathione peroxidase activity in both plasma and the liver ( P < 0.05). In contrast, plasma glutathione peroxidase activity in diquat-challenged broilers was reduced by squalene supplementation ( P < 0.05). The hepatic glutathione level was reduced by diquat administration ( P < 0.05), whereas its level in plasma and the liver of diquat-challenged broilers was increased by squalene supplementation ( P < 0.05). The relative liver weight of broilers was increased by diquat challenge ( P < 0.05), with its value being intermediate in the squalene-supplemented group ( P > 0.05). The plasma aminotransferase activities and total bilirubin concentration were increased by diquat challenge ( P < 0.05), which were reduced by squalene supplementation ( P < 0.05). The mRNA abundance of hepatic nuclear factor erythroid 2–related factor 2 ( P < 0.05) was upregulated by diquat treatment, regardless of squalene supplementation. The mRNA abundance of hepatic glutathione peroxidase 1 and B-cell lymphoma/leukemia 2–associated X protein was upregulated by diquat challenge ( P < 0.05), which was reversed by squalene administration ( P < 0.05). Squalene increased NAD(P)H quinone dehydrogenase 1 mRNA abundance and decreased caspase 3 mRNA abundance in the liver of diquat-challenged broilers ( P < 0.05). The results suggested that squalene can increase weight gain, improve oxidative status, and alleviate liver injury in diquat-challenged broilers.

Effects of dietary supplementation with itaconic acid on the growth performance, nutrient digestibility, slaughter variables, blood biochemical parameters, and intestinal morphology of broiler chickens

“…The pursuit of a rapid growth rate and intensive feeding in modern broilers make them particularly vulnerable to oxidative stress arising from various sources such as diseases, high temperatures, and exposure to toxic substances from water and feed ( Chen et al, 2021a ). The oxidative stress results in inferior growth, disruption of cellular antioxidant defenses, compromised health status, and lower product quality in broiler chickens ( Abdel-Monerm et al, 2021 ; Chen et al, 2021b ). The enzymes SOD and CAT are important antioxidant defenses of the host ( Chen et al, 2021c ).…”

Vitamin D3 Protects Mice from Diquat‐Induced Oxidative Stress through the NF‐κB/Nrf2/HO‐1 Signaling Pathway

“…As a consequence, superfluous reactive oxygen species could be eliminated timely and the induction of cell apoptosis could be largely avoided. The liver and kidney are essential organs ensuring the synthesis of the active form of VitD 3 [44], and the diquat challenge could cause serious damage to these two organs [13,16,45]. In this study, we decided to add the active form of VitD 3 directly.…”

“…As a consequence, the inflammatory status will aggravate both the intestine and the whole circulatory system. The ROS leaked from the intestine may transfer to other parenchymal organs such as the liver, kidney, and spleen through blood, which could attack these organs and result in dysfunction [13]. Diquat (DQ), as an oxidant, is an ideal inducer to establish animal models of oxidative stress and has been widely used in different animals to duplicate the oxidative damage models successfully [14][15][16].…”

Effects of Acute Diquat Poisoning on Liver Mitochondrial Apoptosis and Autophagy in Ducks

“…These results indicate that DQ can affect glucose metabolism in the liver and reduce weight gain ( 57 ). It can also increase the accumulation of glutathione peroxidase (GPX) activity and MDA in the plasma and liver; increase the activity of AST, alanine aminotransferase, and T-Bil concentrations; and increase the relative liver weight, indicating that DQ causes liver damage ( 10 ). DQ increases Ca efflux due to the weakened ATP-dependent Ca chelation of liver microsomes ( 58 ).…”

“…DQ can induce increased oxidative stress to produce a large number of superoxides and can alter different liver functional activities such as metabolism, detoxification, and immune response resulting in the production of a large number of ROS in the liver ( 9 ). The liver toxicity leads to hepatocyte degeneration, inflammation, mitochondrial dysfunction, and even apoptosis ( 10 , 11 ). Oxidative stress can reduce glutathione (GSH) in the liver and can enhance the production of ROS to promote the activation of pro-apoptotic factors such as p53 and Bax leading to apoptosis ( 12 ).…”