Redox imbalance in peripheral blood of type 1 myotonic dystrophy patients
2016
Аутори:
Nikolić-Kokić, AleksandraMarinković, Dragan
Perić, Stojan
Stević, Zorica
Spasić, Mihajlo
Blagojević, Duško
Rakočević Stojanović, Vidosava
Тип документа:
Чланак у часопису (Објављена верзија)
,
© Taylor & Francis 2016
Метаподаци
Приказ свих података о документуАпстракт:
Objectives: The aim of our study was to determine if redox imbalance caused by the activities of antioxidant
enzymes existed in erythrocytes of type 1 myotonic dystrophy (DM1) patients.
Methods: The activities of erythrocyte superoxide dismutase, catalase, glutathione peroxidase, and
glutathione reductase were measured in 30 DM1 patients and 15 healthy controls (HCs). The obtained
values were correlated with the Muscular Impairment Rating Scale (MIRS) score and creatine kinase (CK).
Results: Superoxide dismutase and catalase activities were lower in DM1 patients compared to HCs. A
positive correlation was found between disease duration and MIRS score as well as with glutathione
reductase activity. In DM1 patients, there were positive correlations between catalase, glutathione
peroxidase, and glutathione reductase activities. After sub-dividing DM1 patients according to CK levels,
superoxide dismutase activity was still statistically different from HCs. However, catalase activity was
significantly lower only in DM1 patients with increased CK.
Discussion: Undesirable alterations in antioxidant enzyme activities during DM1 disease progression may
result in conditions favoring oxidative stress and changes in metabolism which together could contribute
to muscle wasting.
Кључне речи:
Catalase; Erythrocytes; Glutathione reductase; Glutatione peroxidase; Type 1 myotonic dystrophy; Superoxide dismutaseИзвор:
Redox Report, 2016, 21, 5, 232-237Финансирање / пројекти:
- Испитивање молекуларно-генетских, патохистолошких и биохемијских карактеристика неуромишићних болести (RS-MESTD-Basic Research (BR or ON)-175083)
- Молекуларни механизми редокс сигналинга у хомеостази, адаптацији и патологији (RS-MESTD-Basic Research (BR or ON)-173014)
DOI: 10.1080/13510002.2015.1107311
ISSN: 1351-0002
PubMed: 26817806