1096 DL-methionine increases glutathione concentration and alleviates inflammatory responses in primary bovine hepatocytes

2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 525-525
Author(s):  
Q. Zhang ◽  
D. N. Luchini ◽  
H. M. White
2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 111-112
Author(s):  
Andrew Magnuson ◽  
Guanchen Liu ◽  
Tao Sun ◽  
Samar Tolba ◽  
Rose Whelan ◽  
...  

Abstract We determined if 30% extra supplemental DL-methionine affected oxidative and inflammatory responses of broilers stocked at a high density. A total of 560 day-old male Cornish cockerel chicks were divided into 4 groups: 2 stocking densities (2.9 and 3.8 kg/ft2) and 2 methionine supplementations (grower: 2.90 or 3.77 g/kg and finisher: 2.60 or 3.38 g/kg). Chicks were fed the same corn-soy starter diet and then respective experimental diets (grower: 6.4 g SAA/kg, finisher: 5.9 g SAA/kg, n = 10 pens/treatment). Blood and tissues (3 chicks/pen) were sampled at the end of each period. Data were analyzed by two-way ANOVA. The high density elevated (P < 0.05) glutathione concentration in the plasma, breast, and thigh of growers, but decreased (P < 0.05) it in the liver of growers and thigh of finishers. The high methionine elevated (P < 0.05) glutathione concentration in the thigh at both ages. There were interactions (P < 0.05) between dietary methionine and stocking density on activities of antioxidant enzymes including GST in 2 or more tissues at both ages and GPX and SOD in the thigh of growers. Hepatic expression of inflammation-related gene IL-6 was decreased (P < 0.05) by the high density, while heat shock protein genes HSP70 and HSP90 were decreased (P < 0.05) by the high methionine. Expression of stress-related genes TNFα and JNK was decreased (P < 0.05) by a combined high methionine and density treatment. The high methionine decreased (P < 0.05) finisher thigh and breast malondialdehyde concentrations and grower plasma glucose concentrations. Neither the density nor the methionine supplementation affected concentrations of plasma ferric reducing ability, serum amyloid A, and corticosterone or hepatic protein carbonyl. In conclusion, the high stocking density showed bilateral effects on the redox and inflammatory responses of broilers. Supplemental extra methionine modulated some of those effects.


2001 ◽  
Vol 86 (11) ◽  
pp. 1257-1263 ◽  
Author(s):  
Attilio Bondanza ◽  
Angelo Manfredi ◽  
Valérie Zimmermann ◽  
Matteo Iannacone ◽  
Angela Tincani ◽  
...  

SummaryScavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets. In contrast to other particulate substrates, the phagocytosis of platelets does not incite pro-inflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets. Furthermore, we verified whether antibodies against the β2 Glycoprotein I (β2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets. In agreement with the uneventful nature of the clearance of platelets in vivo, phagocytosing macrophages did not release IL-1β, TNF-α or IL-10. β2GPI bound to activated platelets and was required for their recognition by anti-ββ2GPI antibodies. DCs internalised platelets opsonised by anti-ββ2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-α and IL-1β by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-1β0. We conclude that anti-ββ2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.


1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.


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