Lipid peroxidation, mitochondrial dysfunction and neurochemical and behavioural deficits in different neurotoxic models: Protective role of S-allylcysteine

2008 ◽  
Vol 42 (10) ◽  
pp. 892-902 ◽  
Author(s):  
Esperanza Garcia ◽  
Daniel Limon ◽  
Veronica Perez-De La Cruz ◽  
Magda Giordano ◽  
Mauricio Diaz-Muñoz ◽  
...  
2012 ◽  
Vol 302 (7) ◽  
pp. H1394-H1409 ◽  
Author(s):  
Ashlee N. Higdon ◽  
Gloria A. Benavides ◽  
Balu K. Chacko ◽  
Xiaosen Ouyang ◽  
Michelle S. Johnson ◽  
...  

The hemolysis of red blood cells and muscle damage results in the release of the heme proteins myoglobin, hemoglobin, and free heme into the vasculature. The mechanisms of heme toxicity are not clear but may involve lipid peroxidation, which we hypothesized would result in mitochondrial damage in endothelial cells. To test this, we used bovine aortic endothelial cells (BAEC) in culture and exposed them to hemin. Hemin led to mitochondrial dysfunction, activation of autophagy, mitophagy, and, at high concentrations, apoptosis. To detect whether hemin induced lipid peroxidation and damaged proteins, we used derivatives of arachidonic acid tagged with biotin or Bodipy (Bt-AA, BD-AA). We found that in cells treated with hemin, Bt-AA was oxidized and formed adducts with proteins, which were inhibited by α-tocopherol. Hemin-dependent mitochondrial dysfunction was also attenuated by α-tocopherol. Protein thiol modification and carbonyl formation occurred on exposure and was not inhibited by α-tocopherol. Supporting a protective role of autophagy, the inhibitor 3-methyladenine potentiated cell death. These data demonstrate that hemin mediates cytotoxicity through a mechanism which involves protein modification by oxidized lipids and other oxidants, decreased respiratory capacity, and a protective role for the autophagic process. Attenuation of lipid peroxidation may be able to preserve mitochondrial function in the endothelium and protect cells from heme-dependent toxicity.


2009 ◽  
Vol 30 (11) ◽  
pp. 1205-1214 ◽  
Author(s):  
Zafer Türkmen ◽  
Kültiğin Çavuşoğlu ◽  
Kürşat Çavuşoğlu ◽  
Kürşad Yapar ◽  
Emine Yalçin

2007 ◽  
Vol 77 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Chaturvedi ◽  
George ◽  
Machacha

The methanol extract of Raphanus sativus root extract showed a protective effect on paracetamol-induced hepatotoxicity in a dose-dependent manner. Degree of lipid peroxidation caused by paracetamol was measured in terms of thiobarbituric acid reactive substances (TBARS) and protection was measured in reference to serum glutamate oxaloacetate transaminase (SGOT), serum glutamate aspartate transaminase (SGPT), and blood and hepatic levels of antioxidants like glutathione and catalase. Administration of extract along with paracetamol showed significant protection. Levels of TBARS were found to be low, activities of SGOT and SGPT were low, while hepatic glutathione levels were significantly higher in experimental rats that received the mixture of paracetamol and the extract as compared to rats that received paracetamol only. Activities of catalase were also high in all experimental groups. Thus this study indicates the involvement of Raphanus sativus root extract with antioxidants like glutathione and catalase in rendering protection against paracetamol-induced lipid peroxidation and hepatotoxicity.


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