Differential protection by nitroxides and hydroxylamines to radiation-induced and metal ion-catalyzed oxidative damage

2002 ◽  
Vol 1573 (2) ◽  
pp. 109-120 ◽  
Author(s):  
Sandhya Xavier ◽  
Ken-ichi Yamada ◽  
Ayelet M Samuni ◽  
Amram Samuni ◽  
William DeGraff ◽  
...  
Lipids ◽  
2013 ◽  
Vol 48 (10) ◽  
pp. 977-987 ◽  
Author(s):  
R. C. S. Barcelos ◽  
H. J. Segat ◽  
D. M. Benvegnú ◽  
F. Trevizol ◽  
K. Roversi ◽  
...  

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 59-59
Author(s):  
Marie-France Palin ◽  
Jérôme Lapointe ◽  
Claude Gariépy ◽  
Danièle Beaudry ◽  
Claudia Kalbe

Abstract Carnosine (β-alanyl-L-histidine) is a molecule naturally and exclusively present in muscle food with the highest concentrations found in skeletal muscles and brain of the animal. Among its numerous biochemical properties, carnosine has antioxidant activity which include metal ion chelation and free radical scavenging. We have recently reported that high muscle carnosine content in pig is associated with better meat quality. Moreover, supplementing pigs with β-alanine reduced oxidative damage to Longissimus muscle (LM) lipids and proteins. Among previously reported antioxidant activities, carnosine was found to limit the production of reactive oxygen species (ROS) and increase antioxidant enzyme activities. However, these studies were mainly conducted in rodents and cell lines and mechanisms in play remain to be characterized. To determine the effect of carnosine in preventing oxidative damage and characterize the mechanisms in play, we have undertaken experiments using the progeny (myoblasts) of satellite cells isolated from the LM of newborn piglets. Cells were treated with carnosine (0, 10, 25 and 50 mM) for 48 h and were then either collected immediately or treated with H2O2 (0.3 mM, 1 h) to induce an oxidative stress. Our results showed that carnosine prevents oxidative stress through the reduction of total intracellular ROS and by modulating the antioxidant system in myoblasts.Carnosine increased the mRNA abundance of NEF2L2, a transcription factor activated by oxidative stress, and several of its downstream regulated antioxidant genes. Western blot analyses further suggest that the protective effect of carnosine on H2O2-induced oxidative stress is mediated through the p38 MAPK intracellular pathway. Finally, the addition of carnosine to H2O2-treated myoblasts increased the basal cellular oxygen consumption rate (OCR), the ATP-linked OCR and proton leaks, thus suggesting an effect of carnosine on mitochondrial functions. Taken together, these findings demonstrate the important role of carnosine in preventing oxidative damage in porcine muscle cells.


Open Biology ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 180249 ◽  
Author(s):  
Anita Krisko ◽  
Miroslav Radman

Ageing is considered as a snowballing phenotype of the accumulation of damaged dysfunctional or toxic proteins and silent mutations (polymorphisms) that sensitize relevant proteins to oxidative damage as inborn predispositions to age-related diseases. Ageing is not a disease, but it causes (or shares common cause with) age-related diseases as suggested by similar slopes of age-related increase in the incidence of diseases and death. Studies of robust and more standard species revealed that dysfunctional oxidatively damaged proteins are the root cause of radiation-induced morbidity and mortality. Oxidized proteins accumulate with age and cause reversible ageing-like phenotypes with some irreversible consequences (e.g. mutations). Here, we observe in yeast that aggregation rate of damaged proteins follows the Gompertz law of mortality and review arguments for a causal relationship between oxidative protein damage, ageing and disease. Aerobes evolved proteomes remarkably resistant to oxidative damage, but imperfectly folded proteins become sensitive to oxidation. We show that α-synuclein mutations that predispose to early-onset Parkinson's disease bestow an increased intrinsic sensitivity of α-synuclein to in vitro oxidation. Considering how initially silent protein polymorphism becomes phenotypic while causing age-related diseases and how protein damage leads to genome alterations inspires a vision of predictive diagnostic, prognostic, prevention and treatment of degenerative diseases.


2005 ◽  
Vol 57 (1) ◽  
pp. 135-143 ◽  
Author(s):  
Harish Chandra Goel ◽  
Damodar Gupta ◽  
Shobha Gupta ◽  
A. P. Garg ◽  
Madhu Bala

2010 ◽  
Vol 86 (9) ◽  
pp. 719-731 ◽  
Author(s):  
Lori Rastogi ◽  
Shaikh Feroz ◽  
Badri Narain Pandey ◽  
Arti Jagtap ◽  
Kaushala Prasad Mishra

1981 ◽  
Vol 19 (7) ◽  
pp. 1803-1809 ◽  
Author(s):  
Masayuki Kato ◽  
Hiroyuki Nishide ◽  
Eishun Tsuchida ◽  
Takashi Sasaki
Keyword(s):  

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