Involvement of mitochondrial pathway in environmental metal pollutant lead-induced apoptosis of chicken liver: perspectives from oxidative stress and energy metabolism

Abstract

This study aimed to investigate the possible mechanisms of environmental metal pollutant lead (Pb)-induced apoptosis in chicken. Forty 8-day-old healthy chickens were randomly assigned to two groups (n = 20/group) after raising standard commercial diet and drinking water for 1 week: including control group and Pb group ((CHCOO)Pb 350 mg/L of drinking water); the chickens were given euthanasia and collected livers at 90 days. A significant increase of apoptosis rate were found in Pb group and Pb induced obvious ultrastructural changes of chicken liver. The mRNA levels of glycometabolism key enzymes were significantly lower in Pb group than those in controls. Higher levels of malondialdehyde (MDA) and nitric oxide (NO) were observed in Pb group; the activities of antioxidant enzymes and ATPases were significantly lower in Pb group than those in controls, while the inducible nitric oxide synthase (iNOS) activity was on the contrary. The mRNA and protein levels of pro-apoptotic genes were all lower in Pb group than those in controls. Altogether, Pb-induced mitochondrial swelling and nuclear chromatin condensation, oxidative stress, energy metabolism disorder, thereby lead to apoptosis via mitochondrial pathway in chicken liver, suggesting that Pb-induced mitochondrial pathway apoptosis plays an important role in the mechanisms of Pb cytotoxicity to chicken liver.

Proper cold stimulation starting at an earlier age can enhance immunity and improve adaptability to cold stress in broilers

“…NO is one kind of important messenger molecule, and its overproduction can induce the occurrence of oxidative stress (Chi et al, 2017 ). iNOS can aggravate intestinal tissue damage by producing NO which induced oxidative stress (Barocelli et al, 2006 ).…”

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

“…It has been reported that reactive oxygen species (ROS)‐scavenging ability plays an important role in the intestinal inflammation and NF‐κB signal activation caused by Se deficiency (Khan, Samson, & Grover, 2017), and Se deficiency of the duodenal mucosa of chickens could activate NF‐κB pathway signaling by increasing ROS levels (J. Wang et al, 2018). The expression of key cytokines and chemokines is also mediated by the activation of the NF‐κB pathway, including TNF‐α and IL‐6, and inflammatory enzymes, such as COX‐2 and iNOS (Chi et al, 2017). Moreover, the changes in GPX1 expression were related to NF‐κB and COX‐2 activation (Lei, Cheng, & Mcclung, 2007).…”

Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen

“…The activities of Na + -K + -ATPase, Ca 2+ - Mg 2+ -ATPase, Ca 2+ -ATPase, and Mg 2+ -ATPase were determined using the appropriate assay kits (Nanjing Jiancheng Bioengineering Institute, China) and were measured as previously described [31].…”