Evidence that 3-hydroxy-3-methylglutaric acid promotes lipid and protein oxidative damage and reduces the nonenzymatic antioxidant defenses in rat cerebral cortex

2008 ◽  
Vol 86 (3) ◽  
pp. 683-693 ◽  
Author(s):  
Guilhian Leipnitz ◽  
Bianca Seminotti ◽  
Josué Haubrich ◽  
Manuela B. Dalcin ◽  
Karina B. Dalcin ◽  
...  
2010 ◽  
Vol 25 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Carolina Didonet Pederzolli ◽  
Caroline Paula Mescka ◽  
Bernardo Remuzzi Zandoná ◽  
Daniella de Moura Coelho ◽  
Ângela Malysz Sgaravatti ◽  
...  

2003 ◽  
Vol 37 (4) ◽  
pp. 367-372 ◽  
Author(s):  
Koji Onodera ◽  
Nao-Omi Omoi ◽  
Koji Fukui ◽  
Takahiro Hayasaka ◽  
Tadashi Shinkai ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3181
Author(s):  
Ewa Żebrowska ◽  
Adrian Chabowski ◽  
Anna Zalewska ◽  
Mateusz Maciejczyk

Despite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of an HSD on the activity of prooxidative enzymes, enzymatic and non-enzymatic antioxidants, and protein oxidative damage in the brain structures regulating energy metabolism (hypothalamus) and cognitive functions (cerebral cortex). Male Wistar rats were randomly divided into two groups (n = 10)—control diet (CD) and high-sugar diet (HSD)—for 8 weeks. We showed a decrease in glutathione peroxidase and superoxide dismutase activity and an increase in catalase activity in the hypothalamus of HSD rats compared to controls. The activity of xanthine oxidase and NADPH oxidase and the contents of oxidation (protein carbonyls), glycoxidation (dityrosine, kynurenine and N-formylkynurenine) and protein glycation products (advanced glycation end products and Amadori products) were significantly higher only in the hypothalamus of the study group. The HSD was also responsible for the disruption of antioxidant systems and oxidative damage to blood proteins, but we did not show any correlation between systemic redox homeostasis and the brain levels. In summary, HSD is responsible for disorders of enzymatic antioxidant defenses only at the central (plasma/serum) and hypothalamic levels but does not affect the cerebral cortex. The hypothalamus is much more sensitive to oxidative damage caused by an HSD than the cerebral cortex.


Life Sciences ◽  
2010 ◽  
Vol 87 (9-10) ◽  
pp. 275-280 ◽  
Author(s):  
Guilhian Leipnitz ◽  
Alexandre U. Amaral ◽  
Ângela Zanatta ◽  
Bianca Seminotti ◽  
Carolina G. Fernandes ◽  
...  

2013 ◽  
Vol 133 (8) ◽  
pp. 1493-1500 ◽  
Author(s):  
Ryuji Kano ◽  
Kenichi Usami ◽  
Takahiro Noda ◽  
Tomoyo I. Shiramatsu ◽  
Ryohei Kanzaki ◽  
...  

Author(s):  
Sergiy I. Savosko ◽  
Juriy B. Chaikovsky ◽  
Nelly Kh. Pogorela ◽  
Alexandr N. Makarenko

1971 ◽  
Vol 246 (1) ◽  
pp. 62-68 ◽  
Author(s):  
John P. Perkins ◽  
Marilyn M. Moore

1994 ◽  
Vol 269 (24) ◽  
pp. 16780-16784
Author(s):  
N. Brose ◽  
G.W. Huntley ◽  
Y. Stern-Bach ◽  
G. Sharma ◽  
J.H. Morrison ◽  
...  

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