Abstract
Redox-dependent mechanisms of brain neuroprotection of rats with experimental diabetes mellitus
Highlights
Diabetes mellitus (DM) is one of the most common diseases with a steady tendency to increase, "a non-infectious epidemic of the 21st century" [1]
Animals were kept in the conditions of 12-hour daily regime (8: 00–20: 00 light and 20: 00–8: 00 – dark time of day), natural light, at room temperature (19– 24 °C), relative humidity (50–65 %) in standard plastic cages of 3–4 animals
We studied the changes in the functioning of the electron transport chain (ETL) of the mitochondria, the rate of superoxide radicals (SR) generation, the activity of the neuronal NO synthase, the concentration of lactoferrin, "free iron", methemoglobin (MetHb), and the level of 8oxoguanin in rat brain tissue cells
Summary
Diabetes mellitus (DM) is one of the most common diseases with a steady tendency to increase, "a non-infectious epidemic of the 21st century" [1]. We studied the changes in the functioning of the electron transport chain (ETL) of the mitochondria, the rate of SR generation, the activity of the neuronal NO synthase (nNOS), the concentration of lactoferrin, "free iron", methemoglobin (MetHb), and the level of 8oxoguanin in rat brain tissue cells. The damaging effect of DM 1 on ETL on the mitochondria of rat brain cells was manifested by the increase in the level of complexes of NO-FeS proteins (Fig. 3, a) to 0.097±0.007 c.u., when compared with the control group – 0.05±0.02 (p
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