Antioxidant enzyme activities and oxidative stress in affective disorders

2004 ◽  
Vol 19 (2) ◽  
pp. 89-95 ◽  
Author(s):  
M. Erkan Ozcan ◽  
Mukaddes Gulec ◽  
Elif Ozerol ◽  
Ruhcan Polat ◽  
Omer Akyol
1994 ◽  
Vol 120 (6) ◽  
pp. 374-377 ◽  
Author(s):  
K. Punnonen ◽  
M. Ahotupa ◽  
K. Asaishi ◽  
M. Hy�ty ◽  
R. Kudo ◽  
...  

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e21042-e21042
Author(s):  
Gabriel de Souza Macedo ◽  
Juliana Giacomazzi ◽  
Cristina Netto ◽  
Leonardo Motta ◽  
Fábio Klamt ◽  
...  

e21042 Background: Germline mutations in the TP53 gene are the underlying genetic defect of Li-Fraumeni Syndrome (LFS) and its variant, Li-Fraumeni-like (LFL) Syndrome, autosomal dominant disorders characterized by predisposition to multiple early-onset cancers. More recently, p53 is emerging as an important player in redox metabolism and important enzymes involved in defenses against oxidative stress have shown to be regulated by p53, including glutathione peroxidase 1 (GPX1) and mitochondrial superoxide dismutase 2 (SOD2). The aim of the present study was to investigate the redox profile parameters in blood of p.R337H mutation carriers and non-carriers individuals. Methods: A total of 34 individuals were included in the study and they were divided in two groups: mutation carriers (n=17) and non-carriers (n=17). Antioxidant enzyme activities (SOD, CAT, GPx) and oxidative stress parameters (Protein carbonyl content, Sulfhydryl content and TBARS) were measured in plasma, erythrocytes, leukocytes and serum. Results: Erythrocyte SOD and GPx activities, two first-line players in enzimatic antioxidant defense, differed significantly between mutation carriers and non-carriers, with an increased activity in the latter (p>0,05). Plasma Carbonyl content, an indicative of protein damage related to ROS overgeneration, was also increased in carriers (p=0,015). There was no significant difference between groups in all other parameters evaluated. Conclusions: Our findings suggest that TP53 p.R337H mutation carriers present different antioxidant enzyme activities and oxidative stress parameters when compared to non-carriers.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Nazatul Shima Nayan ◽  
Muhammad Aiman Mohd Yazid ◽  
Kamachisree Nallappan ◽  
Amirul Asyiq Amran ◽  
Nur Syuhaidah Zaidi ◽  
...  

Autism has been associated with a low antioxidant defense mechanism, while honey has been known for decades for its antioxidant and healing properties. Determination of stingless bee honey (KH) effects on antioxidant enzyme activities and oxidative damage in Autism Lymphoblastoid Cell Line (ALCL) was performed. ALCL and its normal sibling pair (NALCL) were cultured in RPMI-1640 medium at 37°C and 5% CO2. ALCL was treated with 400 μg/mL KH (24 h), and oxidative stress marker, malondialdehyde (MDA), and antioxidant enzyme activities (catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)) were measured via enzyme-linked immunosorbent assay (ELISA), while deoxyribonucleic acid (DNA) damage was determined via comet assay. Low SOD activity ( p < 0.05 ) and high MDA level ( p < 0.05 ) were observed in ALCL compared to NALCL. Higher grade (Grades 2 and 3) of DNA damage was highly observed ( p < 0.05 ) in ALCL compared to NALCL, whereas lower grade (Grades 0 and 1) DNA damage was highly detected ( p < 0.05 ) in NALCL compared to ALCL. KH treatment caused a significant increase in SOD and GPx activities ( p < 0.05 ) in ALCL compared to untreated ALCL. Correspondingly, KH treatment reduced the Grade 2 DNA damage ( p < 0.05 ) in ALCL compared to untreated ALCL. CAT activity showed no significant difference between all three groups, while the MDA level showed no significant difference between treated and untreated ALCL. In conclusion, KH treatment significantly reduced the oxidative stress in ALCL by increasing the SOD and GPx antioxidant enzyme activities, while reducing the DNA damage.


2019 ◽  
Vol 70 (1) ◽  
pp. 18-29 ◽  
Author(s):  
Pinar Erkekoglu ◽  
Ming-Wei Chao ◽  
Chia-Yi Tseng ◽  
Bevin P. Engelward ◽  
Ozge Kose ◽  
...  

AbstractExposure to alkyl anilines may lead to bladder cancer, which is the second most frequent cancer of the urogenital tract. 3,5-dimethylaniline is highly used in industry. Studies on its primary metabolite 3,5-dimethylaminophenol (3,5-DMAP) showed that this compound causes oxidative stress, changes antioxidant enzyme activities, and leads to death of different mammalian cells. However, there is no in vitro study to show the direct effects of 3,5-DMAP on human bladder and urothelial cells. Selenocompounds are suggested to decrease oxidative stress caused by some chemicals, and selenium supplementation was shown to reduce the risk of bladder cancer. The main aim of this study was to investigate whether selenocompounds organic selenomethionine (SM, 10 µmol/L) or inorganic sodium selenite (SS, 30 nmol/L) could reduce oxidative stress, DNA damage, and apoptosis in UROtsa cells exposed to 3,5-DMAP. 3,5-DMAP caused a dose-dependent increase in intracellular generation of reactive oxygen species, and its dose of 50 µmol/L caused lipid peroxidation, protein oxidation, and changes in antioxidant enzyme activities in different cellular fractions. The comet assay also showed single-strand DNA breaks induced by the 3,5-DMAP dose of 50 µmol/L, but no changes in double-strand DNA breaks. Apoptosis was also triggered. Both selenocompounds provided partial protection against the cellular toxicity of 3,5-DMAP. Low selenium status along with exposure to alkyl anilines can be a major factor in the development of bladder cancer. More mechanistic studies are needed to specify the role of selenium in bladder cancer.


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