SelW protects against H₂O₂-induced liver injury in chickens via inhibiting inflammation and apoptosis

Abstract

Selenium (Se) is recognized as a necessary trace mineral in animal diets. Se deficiency induces a number of diseases and injuries in chickens including liver damage, which is related to oxidative stress.

Selenium-Dependent Antioxidant Enzymes: Actions and Properties of Selenoproteins

“…Results revealed that after cell exposure to H 2 O 2 , levels of caspase-3, p53, Bak, Bax, prostaglandin E synthase (PTGEs, COX-2, TNF-α, NF-κB and iNOS were reduced in the selenoprotein W overexpressed cells but increased in the selenoprotein W knockdown cells in comparison to the H 2 O 2 -only treatment group. Levels of Bax, Bak, p53, COX-2, PTGEs, TNF-α, iNOS and NF-κB in the liver of Se-deficient chickens were highly increased compared to the control group [ 188 ]. Next, positive correlation has been reported in GPX1-4, DIO1, DIO3, selenoprotein S, selenoprotein N, selenoprotein T, selenoprotein W, selenoprotein 15, selenoprotein H, selenoprotein U and selenoprotein I with selenoprotein K, whereas selenoprotein P and DIO2 presented negative correlation with selenoprotein K. The above study was demonstrated by silencing selenoprotein K in chickens myoblasts [ 189 ].…”

Gut microbiota contribution to selenium deficiency‐induced gut–liver inflammation

“…This may also explain the findings of a prior study that Se deficiency caused liver inflammation in mice but did not cause liver inflammation in Se gene knockout liver cells. 6 Here, we found that Se deficiency decreased the relative abundance of L. reuteri. L. reuteri was found to have a protective role in animals against Se deficiencyinduced liver inflammation, improving intestinal barrier function and attenuating liver injury.…”

“…Se supplementation, which increases the diversity of the gut microbiota, may be beneficial in preventing colon cancer 18 . In this and prior studies, Se deficiency has been shown to cause liver injury, complications with nitric oxide, oxidative stress, and inflammation 41–43 ; however, it is unclear whether the shifts in intestinal flora associated with Se deficiency are responsible for the observed changes involved in intestinal and liver injury.…”

“…By contrast, biosynthesis and the activity of key antioxidant selenoproteins, such as glutathione peroxidase 1 (GPX1) and thioredoxin reductase (TXNRD), are suppressed in dietary Se deficiency, resulting in oxidative stress and inflammation associated with elevated glucose and glutamine catabolism, as well as decreased lipid accumulation. 4 Our study and others have shown that Se deficiency induces liver inflammation and necrosis [5][6][7] and decreases the ability of the liver to eliminate toxic substances, which causes liver damage that is often characterized by hepatomegaly or liver atrophy, leaves a rough surface of red and yellow liver cells, and leads to fatty degeneration, cytoplasm disappearance, and diffuse cellular debris. 8 Additionally, it leads to a significant accumulation of reactive oxygen species (ROS), enhanced endoplasmic reticulum stress, abnormally elevated heat shock protein (HSP) expression, and activation of the receptor-interacting protein kinase 1 (RIPK1)-RIPK3 complex.…”

Identification of novel N-acetylcysteine derivatives for the treatment of hepatocellular injury

“…As a small molecule, NAC has been elucidated to interact with numerous meta-bolic pathways including, but not limited to, regulation of the cell cycle and apoptosis, carcinogenesis and tumor progression, mutagenesis, gene expression and signal transduction, immune modulation, cytoskeleton organization and trafficking and mitochondrial functions. [8][9][10] The molecular mechanisms of NAC are complex which makes it have many metabolic pathways. The insignificant route under physiological conditions of NAC is serving as a precursor of cysteine for GSH synthesis which can help in the detoxification of reactive metabolites and scavenging of free radicals.…”