The protective effects of melanoidins in adriamycin-induced oxidative stress in isolated rat hepatocytes

2004 ◽  
Vol 84 (13) ◽  
pp. 1701-1707 ◽  
Author(s):  
V Valls-Bellés ◽  
MC Torres ◽  
P Muñiz ◽  
L Boix ◽  
ML González-Sanjose ◽  
...  
2015 ◽  
Vol 06 (06) ◽  
pp. 799-803 ◽  
Author(s):  
Magdalena Spasova Kondeva-Burdina ◽  
Viktor Bratkov ◽  
Rumyana Lubomirova Simeonova ◽  
Vessela Bisserova Vitcheva ◽  
Ilina Nikolaeva Krasteva ◽  
...  

2014 ◽  
Vol 65 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Sara Nafisi ◽  
Reza Heidari ◽  
Mohammad Ghaffarzadeh ◽  
Mojtaba Ziaee ◽  
Hossein Hamzeiy ◽  
...  

AbstractAcetaminophen (N-acetyl para amino phenol, APAP) is a widely used antipyretic and analgesic drug responsible for various drug-induced liver injuries. This study evaluated APAP-induced toxicity in isolated rat hepatocytes alongside the protective effects of silafibrate and N-acetyl cysteine (NAC). Hepatocytes were isolated from male Sprague-Dawley rats by collagenase enzyme perfusion via the portal vein. This technique is based on liver perfusion with collagenase after removing calcium ions (Ca2+) with a chelator. Cells were treated with different concentrations of APAP, silafibrate, and NAC. Cell death, reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial depolarisation were measured as toxicity markers. ROS formation and lipid peroxidation occurred after APAP administration to rat hepatocytes. APAP caused mitochondrial depolarisation in isolated cells. Administration of silafibrate (200 μmol L-1) and/or NAC (200 μmol L-1) reduced the ROS formation, lipid peroxidation, and mitochondrial depolarisation caused by APAP. Cytotoxicity induced by APAP in rat hepatocytes was mediated by oxidative stress. In addition, APAP seemed to target cellular mitochondria during hepatocyte damage. The protective properties of silafibrate and/or NAC against APAP‑induced hepatic injury may have involved the induction of antioxidant enzymes, protection against oxidative stress and inflammatory responses, and alteration in cellular glutathione content.


2015 ◽  
Vol 31 (8) ◽  
pp. 979-985 ◽  
Author(s):  
Mir-Jamal Hosseini ◽  
Jafar Shahraki ◽  
Saman Tafreshian ◽  
Ahmad Salimi ◽  
Mohammad Kamalinejad ◽  
...  

2011 ◽  
Vol 18 (4) ◽  
pp. 279-285 ◽  
Author(s):  
Osama S. El-Tawil ◽  
Ali H. Abou-Hadeed ◽  
Mohamed F. EL-Bab ◽  
Abeir A. Shalaby

2010 ◽  
Vol 30 (3) ◽  
pp. 173-181 ◽  
Author(s):  
Jalal Pourahmad ◽  
Fatemeh Shaki ◽  
Farahnaz Tanbakosazan ◽  
Ruhollah Ghalandari ◽  
Hossein Ali Ettehadi ◽  
...  

Previous reports suggested that certain carbohydrate polymers, such as β-(1→3)-D-glucan, may possess free radical scavenging activity. The present study examined the free radical scavenging activity of a carbohydrate polymer, β-(1→3)-D-glucan against oxidative stress induced by depleted uranium in isolated rat hepatocytes. Addition of U (VI) (uranyl acetate) to isolated rat hepatocytes results in reactive oxygen species (ROS) formation, rapid glutathione depletion, mitochondrial membrane potential collapse and lysosomal membrane rupture before hepatocyte lysis occurred. Our results showed that quite similar to silymarin, which is a known antioxidant and radical scavenger, tiny concentration of β-glucan (138 nM) very successfully protected the hepatocytes against cell lysis and all oxidative stress cytotoxicity endpoints caused by depleted uranium including ROS formation, glutathione depletion, decreased mitochondrial membrane potential, lysosomal membrane rupture and caspase 3 activity increase. In conclusion, our results confirmed the antioxidant and radical scavenging activity of β-(1→3)-D-glucan and suggested this compound and silymarin as possible drug candidates for prophylaxis and treatment against depleted uranium toxic effects.


2013 ◽  
Vol 64 (2) ◽  
pp. 201-210 ◽  
Author(s):  
Reza Heidari ◽  
Hossein Babaei ◽  
Mohammad Ali Eghbal

Isoniazid is one of the most commonly used drugs to treat tuberculosis. Its administration is associated with a high incidence of hepatotoxicity. The aim of this study was to establish the protective effects of taurine against cytotoxicity induced by isoniazid and its suspected toxic metabolite hydrazine in isolated rat hepatocytes by measuring reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial depolarisation, reduced glutathione (GSH), and oxidised glutathione (GSSG). Isoniazid caused no significant ROS formation in normal hepatocytes, but in glutathione-depleted cells it was considerable. Hydrazine caused ROS formation and lipid peroxidation in both intact and glutathione-depleted cells. Both isoniazid and hydrazine caused mitochondrial membrane depolarisation. Hydrazine lowered cellular GSH reserve and increased GSSG. Taurine (200 μmol L-1) and N-acetylcysteine (200 μmol L-1) effectively countered the toxic effects of isoniazid and/or hydrazine by decreasing ROS formation, lipid peroxidation, and mitochondrial damage. Taurine prevented depletion of GSH and lowered GSSG levels in hydrazine-treated cells. This study suggests that the protective effects of taurine against isoniazid and its intermediary metabolite hydrazine cytotoxicity in rat hepatocytes could be attributed to antioxidative action.


2005 ◽  
Vol 38 (7) ◽  
pp. 867-873 ◽  
Author(s):  
Tom S. Chan ◽  
Nandita Shangari ◽  
John X. Wilson ◽  
Helen Chan ◽  
Roger F. Butterworth ◽  
...  

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