scholarly journals Catalase Takes Part in Rat Liver Mitochondria Oxidative Stress Defense

2007 ◽  
Vol 282 (33) ◽  
pp. 24407-24415 ◽  
Author(s):  
Mauro Salvi ◽  
Valentina Battaglia ◽  
Anna Maria Brunati ◽  
Nicoletta La Rocca ◽  
Elena Tibaldi ◽  
...  
2003 ◽  
Vol 17 (15) ◽  
pp. 2194-2201 ◽  
Author(s):  
Lorenz Schild ◽  
Thomas Reinheckel ◽  
Michael Reiser ◽  
Thomas F. W. Horn ◽  
Gerald Wolf ◽  
...  

2006 ◽  
Vol 8 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Pilar Caro ◽  
José Gómez ◽  
Alberto Sanz ◽  
Manel Portero-Otín ◽  
Reinald Pamplona ◽  
...  

Author(s):  
Mona Pourjafar ◽  
Sara Malih ◽  
Akram Ranjbar

: In recent years, the applications of nanoparticles have received a great attention due to their industrial and biomedical applications, while their beneficial effects suffer from controversial results at clinical stages. In the current study, cytotoxicity of cerium oxide (CeNP) nanoparticles (100 nm) were evaluated using mitochondria derived from wistar rat's liver. Isolated mitochondria from rat’s liver were divided into 7 groups including group 1 as control and group 2 to 7 as treatment group with different doses of CeNP (5, 10, 50, 100, 250 and 500mg/ml, respectively), for 24,48 and 72 hours. After exposure, oxidative stress biomarkers such as total ‎antioxidant capacity (TAC), lipid peroxidation (LPO), total thiol groups (TTG), catalase activity (CAT) and mitochondrial viability, were determined in isolated rat liver mitochondria. Results have shown that CeNPs increase TAC, TTG, CAT, LPO and viability of mitochondria in various exposure times and confirm antioxidant properties of CeNPs in mithocondria while mitochondria is a main source for the generation of reactive oxygen species (ROS).


Mitochondrion ◽  
2006 ◽  
Vol 6 (4) ◽  
pp. 176-185 ◽  
Author(s):  
Maria A.S. Fernandes ◽  
José B.A. Custódio ◽  
Maria S. Santos ◽  
António J.M. Moreno ◽  
Joaquim A.F. Vicente

2013 ◽  
Vol 30 (2) ◽  
pp. 232-241 ◽  
Author(s):  
M R Eskandari ◽  
Vida Mashayekhi ◽  
Majid Aslani ◽  
Mir-Jamal Hosseini

2015 ◽  
Vol 46 (8) ◽  
pp. 597-603 ◽  
Author(s):  
Heena Tabassum ◽  
Mohammad Waseem ◽  
Suhel Parvez ◽  
M. Irfan Qureshi

Author(s):  
Mousumi Dutta ◽  
Goutam Paul

Objective: The probable toxic effects of bisphenol A (BPA) on different physiological functions have been reported in animal models. The role of BPA in mitochondrial oxidative stress has not been reported till date. The present study is aimed to elucidate dose- and time-dependent oxidative stress generation by BPA, respectively, in rat liver mitochondria in ex vivo model. Methods: The incubation mixture of BPA-treated groups containing mitochondria, 50 mM potassium phosphate buffer (pH 7.4), and different concentrations of BPA (20–160 μM/ml) (dissolved in 12% DMSO) in a final volume of 1.0 ml was incubated at 37°C in incubator for different time durations (30 min–2 h). Whereas, the incubation mixture of control group contained DMSO (12%), mitochondria and 50 mM potassium phosphatebuffer (pH 7.4).’ will be replaced by ‘Whereas, the incubation mixture of control group contained the same constituents except BPA. Result: We have observed significant decrease in mitochondrial intactness incubated with BPA in dose- and time-dependent manner under bright field and confocal microscopic study compared to control. Further, we have observed a decrease in mitochondrial reduced glutathione (GSH) content and increase in lipid peroxidation and protein carbonylation levels in dose- and time-dependent manner in BPA-exposed mitochondria. We have found a significant increase in the activity of Mn-superoxide dismutase and decrease in the activities of GSH peroxidase, GSH reductase, pyruvate dehydrogenase, and other three enzymes of Kreb’s cycle dose and time dependently in BPA-exposed mitochondria. The results indicate that exposure to BPA leads to decrease in intactness of mitochondria and increase in oxidative stress in mitochondria isolated from rat liver in a dose- and time-dependent manner. Conclusion: It can be concluded that the incubation of mitochondria isolated from rat liver with BPA, caused oxidative stress-mediated damages in mitochondria in both dose- and time-dependent manners.


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