scholarly journals Vitamin E Supplementation Enhances Lipid Oxidative Stability via Increasing Vitamin E Retention, Rather Than Gene Expression of MAPK-Nrf2 Signaling Pathway in Muscles of Broilers

Foods ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2555
Author(s):  
Lei Xu ◽  
Jing Wang ◽  
Haijun Zhang ◽  
Shugeng Wu ◽  
Hongyuan Yue ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vitamin E ◽  
Oxidative Stability ◽  
Signaling Pathway ◽  
Dietary Vitamin ◽  
Related Factor ◽  
Thiobarbituric Acid Reactive Substance ◽  
Thigh Muscles ◽  
Nrf2 Signaling Pathway ◽  
Vitamin E Supplementation

Dietary vitamin E (VE) supplementation is a method to produce VE-enriched meat and improve meat lipid oxidative stability. We aimed to study the effect of the VE supplementation duration on meat lipid oxidative stability, VE retention, and antioxidant enzymes’ activity, and explore its relationship with the mitogen-activated protein kinases (MAPK)-nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway in broilers slaughtered after electrical stunning. A total of 240 male 18-day-old Arbor Acres Plus broilers were distributed to four treatments, with six replicates in each treatment, and ten broilers per replicate. Broilers were fed with a basal diet (no supplementation of VE) or VE diet (200 IU/kg VE, DL-α- tocopherol) for one (W1), two (W2), or three (W3) weeks before electrical stunning (130 mA, 60 Hz, for 1s) and slaughter. The VE retention was positively and linearly affected (p < 0.01) by the VE feeding duration at one to three weeks before slaughter, and negatively (all p < 0.01) related to the thiobarbituric acid reactive substance (TBARS) content in both breast and thigh muscles at d 0, d 2, and d 6 postmortem. The VE retention was negatively (p < 0.05) related to the gene expression of c-Jun N-terminal kinases 1 (JNK1) and 2 (JNK2), Nrf2 in breast muscles, and JNK1 and p38 MAPK in thigh muscles. In conclusion, dietary vitamin E supplementation at 200 IU/kg for three weeks before electrical stunning and slaughter improved lipid oxidative stability via increasing VE retention, rather than the regulation by gene expression of the MAPK-Nrf2 signaling pathway in skeletal muscles of broilers.

Improved oxidative stability of veal lipids and cholesterol through dietary vitamin E supplementation

Meat Science ◽  
1993 ◽  
Vol 35 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Nicki J. Engeseth ◽  
J. Ian Gray ◽  
Alden M. Booren ◽  
Ali Asghar
Keyword(s):  
Vitamin E ◽  
Oxidative Stability ◽  
Dietary Vitamin ◽  
Vitamin E Supplementation

scholarly journals Quercetin Protects against Lipopolysaccharide-Induced Intestinal Oxidative Stress in Broiler Chickens through Activation of Nrf2 Pathway

Molecules ◽  
2020 ◽  
Vol 25 (5) ◽  
pp. 1053 ◽  
Author(s):  
Lei Sun ◽  
Gaoqing Xu ◽  
Yangyunyi Dong ◽  
Meng Li ◽  
Lianyu Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Superoxide Dismutase ◽  
Signaling Pathway ◽  
Broiler Chickens ◽  
Mapk Pathway ◽  
Basal Diet ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nrf2 Signaling Pathway

We investigated the potential ability of quercetin to protect against lipopolysaccharide (LPS)-induced intestinal oxidative stress in broiler chickens and the potential role of the Nrf2 (nuclear factor erythroid 2-related factor 2) signaling pathway. One-day-old broiler chickens (n = 240) were randomized into four groups: saline-challenged broiler chickens fed a basal diet (Con), LPS-challenged broiler chickens on a basal diet (LPS), and LPS-treated broiler chickens on a basal diet containing either 200 or 500 mg/kg of quercetin (Que200+LPS or Que500+LPS). Quercetin (200 mg/kg) significantly alleviated LPS-induced decreased duodenal, jejunal, and illeal villus height and increased the crypt depth in these regions. Quercetin significantly inhibited LPS-induced jejunal oxidative stress, including downregulated reactive oxygen species (ROS), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, and it upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. Quercetin relieved LPS-induced jejunal mitochondria damage and upregulated mitochondrial DNA copy number-related gene expression, including cytochrome c oxidase subunit 1 (COX1), ATP synthase F0 subunit 6 (ATP6), and NADH dehydrogenase subunit 1 (ND1). Quercetin attenuated the LPS-induced inhibition of Nrf2 activation, translocation, and downstream gene expression, including heme oxygenase-1 (HO-1), NAD (P) H dehydrogenase quinone 1 (NQO1), and manganese superoxide dismutase (SOD2). Additionally, quercetin attenuated the LPS-inhibition of c-Jun N-terminal kinase (JNK), Extracellular Regulated protein Kinases (ERK), and p38MAPK (p38) phosphorylation in the MAPK pathway. Thus, quercetin attenuated LPS-induced oxidative stress in the intestines of broiler chickens via the MAPK/Nrf2 signaling pathway.

Effect of forage type and supplemental dietary vitamin E on milk oxidative stability

1991 ◽  
Vol 71 (4) ◽  
pp. 1181-1186 ◽  
Author(s):  
J. W. G. Nicholson ◽  
Anne-Marie St-Laurent
Keyword(s):  
Vitamin E ◽  
Oxidative Stability ◽  
Corn Silage ◽  
Dietary Vitamin ◽  
Plasma Vitamin ◽  
Forage Type ◽  
Alfalfa Silage ◽  
Plasma Vitamin E ◽  
Spontaneous Oxidation ◽  
Vitamin E Supplementation

Twelve Holstein cows in each of two replicates were used to determine the effect of forage type and vitamin E supplementation on the oxidative stability of milk. Alfalfa or corn silage was fed ad libitum as the sole roughage, with a concentrate to milk ratio of 1:2.5. Half the cows on each forage were fed 7000 IU d−1 of dL-α-tocopherol acetate top-dressed on the concentrate in two feedings per day over a 4-wk period. Cows consuming the alfalfa silage had higher (P < 0.05) plasma vitamin E content, but there were no differences in milk vitamin E or flavor due to forage type. Supplementing the diets with vitamin E resulted in higher (P < 0.01) vitamin E content of plasma and milk and improved milk oxidative stability. There was an interaction (P = 0.03) between forage type and vitamin E supplementation for oxidative flavor score in week 2. Supplementing the corn silage diet with 7000 IU d−1 of vitamin E resulted in almost complete elimination of oxidized flavor in milk within 1 wk of starting supplementation. However, supplementing the alfalfa silage diet had no effect on flavor over the first 3 wk of feeding. It is apparent that the vitamin E content of milk is not the sole determinant of its oxidative stability. Key words: Spontaneous oxidation, flavor, milk, vitamin E, alfalfa, corn silage, cow

scholarly journals Nrf2 Activation Attenuates Acrylamide-Induced Neuropathy in Mice

2021 ◽  
Vol 22 (11) ◽  
pp. 5995
Author(s):  
Chand Basha Davuljigari ◽  
Frederick Adams Ekuban ◽  
Cai Zong ◽  
Alzahraa A. M. Fergany ◽  
Kota Morikawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Messenger Rna ◽  
Hepatic Necrosis ◽  
Related Factor ◽  
Necrosis Factor Alpha ◽  
Adult Mice ◽  
Nrf2 Signaling Pathway ◽  
Antioxidant Proteins ◽  
Oxide Synthase

Acrylamide is a well characterized neurotoxicant known to cause neuropathy and encephalopathy in humans and experimental animals. To investigate the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in acrylamide-induced neuropathy, male C57Bl/6JJcl adult mice were exposed to acrylamide at 0, 200 or 300 ppm in drinking water and co-administered with subcutaneous injections of sulforaphane, a known activator of the Nrf2 signaling pathway at 0 or 25 mg/kg body weight daily for 4 weeks. Assessments for neurotoxicity, hepatotoxicity, oxidative stress as well as messenger RNA-expression analysis for Nrf2-antioxidant and pro-inflammatory cytokine genes were conducted. Relative to mice exposed only to acrylamide, co-administration of sulforaphane protected against acrylamide-induced neurotoxic effects such as increase in landing foot spread or decrease in density of noradrenergic axons as well as hepatic necrosis and hemorrhage. Moreover, co-administration of sulforaphane enhanced acrylamide-induced mRNA upregulation of Nrf2 and its downstream antioxidant proteins and suppressed acrylamide-induced mRNA upregulation of tumor necrosis factor alpha (TNF-α) and inducible nitric oxide synthase (iNOS) in the cerebral cortex. The results demonstrate that activation of the Nrf2 signaling pathway by co-treatment of sulforaphane provides protection against acrylamide-induced neurotoxicity through suppression of oxidative stress and inflammation. Nrf2 remains an important target for the strategic prevention of acrylamide-induced neurotoxicity.

scholarly journals Sulforaphane induces colorectal cancer cell proliferation through Nrf2 activation in a p53-dependent manner

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Yunjeong Gwon ◽  
Jisun Oh ◽  
Jong-Sang Kim
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Related Factor ◽  
Mild Stress ◽  
Dependent Manner ◽  
Cancer Cell Proliferation ◽  
Nrf2 Signaling Pathway ◽  
Dose Dependent

AbstractSulforaphane is a well-known phytochemical that stimulates nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant cellular response. In this study, we found that sulforaphane promoted cell proliferation in HCT116 human colon cancer cells expressing a normal p53 gene in a dose-dependent but biphasic manner. Since p53 has been reported to contribute to cell survival by regulating various metabolic pathways to adapt to mild stress, we further examined cellular responses in both p53-wild-type (WT) and p53-knockout (KO) HCT116 cells exposed to sulforaphane in vitro and in vivo. Results demonstrated that sulforaphane treatment activated Nrf2-mediated antioxidant enzymes in both p53-WT and p53-KO cells, decreased apoptotic protein expression in WT cells but increased in KO cells in a dose-dependent manner, and increased the expression of a mitochondrial biogenesis marker PGC1α in WT cells but decreased in KO cells. Moreover, a low dose of sulforaphane promoted tumor growth, upregulated the Nrf2 signaling pathway, and decreased apoptotic cell death in p53-WT HCT116 xenografts compared to that in p53-KO HCT116 xenografts in BALB/c nude mice. These findings suggest that sulforaphane can influence colon cancer cell proliferation and mitochondrial function through a crosstalk between the Nrf2 signaling pathway and p53 axis.

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