Abstract
Desynchronosis may be the cause of many diseases. Oxidative stress plays an important role in the pathogenesis of various diseases. The present study investigates the effect of constant light on biomarkers of oxidative stress and content of glial intermediate filaments protein in the brains of old rats. We found that desynchronosis led to development of oxidative stress in the hippocampus, cerebral cortex and cerebellum of old rats. Prolonged continuous lighting led to an increase in the content of TBA-reactive products in all studied regions of the brains of old rats. This indicates an activation of lipid peroxidation and oxidative stress. Significant changes in the content of TBA-reactive products were found in the departments responsible for the functions of the higher nervous activity, particularly in the hippocampus and cerebral cortex. The level of restored glutathione in all three regions of the brain decreased in the group of rats kept under constant illumination in comparison with the control group. The results of the indicators of locomotor and orienting-investigative activity of the animals in the "open field" test revealled changes in the indices for desynchronosis. This showed a reduction in locomotor activity, inhibition of exploratory activity and development of emotional stress. In the brains of old rats kept under constant illumination a significant increase in the content of glial fibrillary protein (GFAP) was shown. There was a significant increase in the intensity of the polypeptide zone 49 kDa in the filamentous and soluble fraction of the cerebellum and hippocampus. This fact indicates that desynchronosis activates fibrillogenesis in glial cells. At the same time, there is degradation of polypeptides GFAP with Mr in the field of 46 kDa. Melatonin is a universal adaptogen that regulates the function of many body systems. The amount of melatonin which is synthesized depends on the illumination mode. Violation of the global mode reduces the amount of melatonin and leads to the development of desynchronosis, which may be the cause of many diseases. The administration of melatonin helped reverse the changes – raising the level of restored glutathione and preventing the growth of the content of peroxidation products and indices of "open field" test, and also decreasing the degradation of GFAP and the amount of protein. The results indicate the protective effect of melatonin, showing reductions in glial reactivity and in the level of oxidative stress in the brains of old rats subject to desynchronosis.
Highlights
The present study investigates the effect of constant light on biomarkers of oxidative stress and content of glial intermediate filaments protein in the brains of old rats
We found that desynchronosis led to development of oxidative stress in the hippocampus, cerebral cortex and cerebellum of old rats
In the brains of old rats kept under constant illumination a significant increase in the content of glial fibrillary protein (GFAP) was shown
Summary
Експерименти проводили на 40 старих щурах лінії Вістар (18–22 місяці) масою 260–340 г (за класифікацією Западнюка), яких утримували у стандартних умовах віварію. Щури контрольної групи (n = 10) щодня одержували ін’єкцію фізіологічного розчину, їх утримували за постійної температури (24 oС) та контрольованої довжини світлового дня (12 год/12 год освітлення/темрява). Щури інтактної групи (n = 10) щодня одержували ін’єкцію мелатоніну (10 мг/кг), їх утримували за постійної температури (24 oС) та контрольованої довжини світлового дня (12 год/12 год освітлення/темрява). Дві експериментальні групи тварин (третя та четверта) утримували за постійного освітлення 250 люкс протягом 10 діб. Тварин усіх груп декапітували через 10 діб після початку експерименту. Супернатант, що отримували після другого центрифугування (S2), містив нерозчинні білки проміжних філаментів. Визначення поліпептидного складу гліальних філаментів проводили за допомогою імуноблотингу з використанням поліклональної моноспецифічної антисироватки у розведенні 1 : 1 500. Проводили за допомогою комп’ютерної обробки сканованих результатів імуноблотингу. Вміст глутатіону у зразках головного мозку визначали за допомогою методу, запропонованого Sedlak (1968). У таблиці наведено середньоарифметичні значення та їх стандартні похибки (SE)
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