Protective role of sulforaphane against oxidative stress mediated mitochondrial dysfunction induced by benzo(a)pyrene in female Swiss albino mice

2011 ◽  
Vol 24 (1) ◽  
pp. 110-117 ◽  
Author(s):  
D. Kalpana Deepa Priya ◽  
R. Gayathri ◽  
G.R. Gunassekaran ◽  
D. Sakthisekaran
2014 ◽  
Vol 89 (4) ◽  
pp. 545-556 ◽  
Author(s):  
Giovanni Quarato ◽  
Rosella Scrima ◽  
Maria Ripoli ◽  
Francesca Agriesti ◽  
Darius Moradpour ◽  
...  

2014 ◽  
Vol 4 (4) ◽  
pp. 535-541 ◽  
Author(s):  
R. Venugopal ◽  
V. Mahesh ◽  
G. Ekambaram ◽  
A. Aadithya ◽  
D. Sakthisekaran

2017 ◽  
Vol 96 ◽  
pp. 685-694 ◽  
Author(s):  
Pushpa Rani Guvvala ◽  
Janivara Parameswaraiah Ravindra ◽  
Chukkath Vijayan Rajani ◽  
Muniandy Sivaram ◽  
Sellappan Selvaraju

2016 ◽  
Vol 4 (12) ◽  
pp. 2826-2856 ◽  
Author(s):  
C.L. Jonwal ◽  
◽  
Rashmi Sisodia ◽  
V.K. Saxena ◽  
Archana Sharma ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Sergio A. Rosales-Corral ◽  
Gabriela Lopez-Armas ◽  
Jose Cruz-Ramos ◽  
Valery G. Melnikov ◽  
Dun-Xian Tan ◽  
...  

Alzheimer pathogenesis involves mitochondrial dysfunction, which is closely related to amyloid-ß(Aß) generation, abnormal tau phosphorylation, oxidative stress, and apoptosis. Alterations in membranal components, including cholesterol and fatty acids, their characteristics, disposition, and distribution along the membranes, have been studied as evidence of cell membrane alterations in AD brain. The majority of these studies have been focused on the cytoplasmic membrane; meanwhile the mitochondrial membranes have been less explored. In this work, we studied lipids and mitochondrial membranesin vivo, following intracerebral injection of fibrillar amyloid-ß(Aß). The purpose was to determine how Aßmay be responsible for beginning of a vicious cycle where oxidative stress and alterations in cholesterol, lipids and fatty acids, feed back on each other to cause mitochondrial dysfunction. We observed changes in mitochondrial membrane lipids, and fatty acids, following intracerebral injection of fibrillar Aßin aged Wistar rats. Melatonin, a well-known antioxidant and neuroimmunomodulator indoleamine, reversed some of these alterations and protected mitochondrial membranes from obvious damage. Additionally, melatonin increased the levels of linolenic and n-3 eicosapentaenoic acid, in the same site where amyloidßwas injected, favoring an endogenous anti-inflammatory pathway.


2016 ◽  
Vol 69 (3) ◽  
pp. 236-243 ◽  
Author(s):  
Mohammad Hossein Asghari ◽  
Mohammad Abdollahi ◽  
Marcos Roberto de Oliveira ◽  
Seyed Mohammad Nabavi

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