Dimethoate-induced oxidative stress in human erythrocytes and the protective effect of Vitamins C and E in vitro

2011 ◽  
Vol 26 (3) ◽  
pp. 287-291 ◽  
Author(s):  
Fatma Ben Abdallah ◽  
Bochra Gargouri ◽  
Hafedh Bejaoui ◽  
Saloua Lassoued ◽  
Leila Ammar-Keskes
2010 ◽  
Vol 30 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Izabela Sadowska-Woda ◽  
Barbara Sychta ◽  
Marta Rachel ◽  
Edyta Bieszczad-Bedrejczuk

2010 ◽  
Vol 196 ◽  
pp. S81
Author(s):  
F. Ben Abdallah ◽  
B. Gargouri ◽  
S. Lassoued ◽  
L. Ammar-Keskes

2010 ◽  
Vol 24 (2) ◽  
pp. 460-464 ◽  
Author(s):  
Izabela Sadowska-Woda ◽  
Diana Popowicz ◽  
Agata Karowicz-Bilińska

2020 ◽  
Vol 55 (9) ◽  
pp. 1103-1114
Author(s):  
Pei‐Pei Zhang ◽  
Jing‐Jing Wang ◽  
Chong‐Yang Li ◽  
Hai‐sheng Hao ◽  
Hao‐Yu Wang ◽  
...  

2009 ◽  
Vol 28 (10) ◽  
pp. 611-617 ◽  
Author(s):  
Betul Catalgol ◽  
Gül Özhan ◽  
Buket Alpertunga

Acrylamide (AA), a widely used industrial chemical, is shown to be neurotoxic, mutagenic and carcinogenic. This study was carried out to investigate the effects of different doses of AA on lipid peroxidation (LPO), haemolysis, methaemoglobin (MetHb) and antioxidant system in human erythrocytes in vitro. Erythrocyte solutions were incubated with 0.10, 0.25, 0.50 and 1.00 mM of AA at 37°C for 1 hour. At the end of the incubation, malondialdehyde (MDA), an end product of LPO, was determined by liquid chromatography (LC) while total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes and the rates of haemolysis and MetHb were determined by spectrophotometric methods. All of the studied concentrations of AA increased MetHb formation and SOD activity, and induced MDA formation and haemolysis due to the destruction of erythrocyte cell membrane. AA caused a decrease in the activities of GSH-Px, CAT and GSH levels. However, these effects of AA were seen only at higher concentrations than AA intake estimated for populations in many countries. We suggest that LPO process may not be involved in the toxic effects of AA in low concentrations, although the present results showed that the studied concentrations of AA exert deteriorating effects on antioxidant enzyme activities, LPO process and haemolysis.


2021 ◽  

Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play a role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential role of miR-187 in cardiac I/R injury and its underlying mechanisms. miR-187 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor to confirm the function of miR-187 in H/R. DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with DYRK2 inhibitor. A myocardium I/R mouse model was established. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.


2016 ◽  
Vol 48 ◽  
pp. 253-264 ◽  
Author(s):  
Pamela Soledad Bustos ◽  
Romina Deza-Ponzio ◽  
Paulina Laura Páez ◽  
Ines Albesa ◽  
José Luis Cabrera ◽  
...  

2021 ◽  
Author(s):  
Yajun Chen ◽  
Lei Wang ◽  
Tianjia Liu ◽  
Zhidong Qiu ◽  
Ye Qiu ◽  
...  

We investigated the protective effect of PGP against DOX-induced cardiotoxicity in vitro and in vivo. PGP increases H9C2 cell viability and inhibits apoptosis, alleviating DOX-induced myocardial oxidative stress-related cardiotoxicity.


Author(s):  
Rosalia Crupi ◽  
Ernesto Palma ◽  
Rosalba Siracusa ◽  
Roberta Fusco ◽  
Enrico Gugliandolo ◽  
...  

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