A pandemic expansion of diabetes mellitus (DM) observed nowadays across the globe is increasingly acknowledged as a disaster by all peoples of the world. Statistical analysis indicates an annual increase in prevalence of DM in Russian Federation that had reached 3 779 423 registered patients by 01.01.2013. Besides the humanitarian aspects, DM poses severe economic challenges for this country ? challenges that stem both from high mortality and growing disability rate due to limb loss, decrease in visual acuity and need for hemodialysis, plaguing many DM patients. Aim. To produce an epidemiological evaluation based on the dynamics of prevalence of diabetic retinopathy in the Russian Federation ? nationwide and in individual regions ? across the last 13 years. Materials and Methods. Current survey included patients from various regions of the Russian Federation that were examined during epidemiological missions conducted by the federal Endocrinology Research Centre (2000?2009), as well as National Programmes ?Health? (2007) and ?Diabetes ? Learn In Advance? (2012?2013). Results. In the Russian Federation registered more than 630,000 patients with different stages of diabetic retinopathy. The prevalence of diabetic retinopathy among adults (18 years and older) with type 1 diabetes is 35.25%, while in type 2 diabetes - 16.67%. On average, this means that almost one in five patients (17.63%) with diabetes have certain eye problems. Conclusion. In summary, our data indicate a dramatic growth in the rate of diabetic ocular complications, with a particular increase in proliferative diabetic retinopathy, complicated cataract and neovascular glaucoma. These findings call for an even closer attention to early diagnostics, adequate management and, above everything else, timely prevention of ocular pathologies in patients with DM.
Changes in NADH fluorescence in brain mitochondria of rats exposed to hypercapnic hypoxia were studied. The status of the succinate oxidation system determines the level and kinetic characteristics of pyridine nucleotide reduction. The kinetic characteristics of energy production are more susceptible to hypoxia than changes in NADH level. Key Words: brain mitochondria; NADH; hypoxia; transamination; succinate oxidationThe state of the energy production system is evaluated by the characteristics suggested by B. Chance [5]. We consider that such an approach provides insufficient intbrmation about the system in general and does not allow a comparison between the contribution of the fast and slow metabolic cluster [1,2] to the maintenance of energy homeostasis. We investigated the level of NADH fluorescence in brain mitochondria (MC) of rats exposed to hypercapnic hypoxia. Special attention was paid to the relationship between the rate of reduction of pyridine nucleotide (PN) oxidized with ADP and the oxidation substrate and functional state of the organism. MATERIALS AND METHODSMale Wistar rats aged 2 months (200-250 g) from Rassvet Breeding Center (Tomsk) were used. During 2-week acclimatization and the experiment the rats were kept in standard plastic cages (no more than 15 per cage) at 20-25~ humidity no more than 50%, outflow/inflow 8:10 air exchange, and day-night light regimen. Hypercapnic hypoxia was modeled by placing the animal tot 2 h into a sealed 5-liter vessel. The brain MC oxidation system was evaluated fluorimically by the level of PN reduction (PNR) on a Hitachi [7]. The oxidation substrates were succinic acid (0.5 raM), malate-glutamate mixture (3 mM each), their combination with SDH inhibitor malonate (2 raM) or aminotransferase inhibitor aminooxyacetic acid (0.5 raM). PNR was studied during oxidation of endogenous substrates (arbitrary metabolic state 2), denoted as the "silent" status 2 (2S), and the PNR was consequently denoted as F2s (Fig. 1). PNR changes were studied after addition of 50 ~tM ADP to the medium (transition from the 2S metabolic status to active phosphorylation 2AP and then to a resting status 2R, i.e., the F2s---~F2Ap-~F2R transitions were examined).Effects of oxidation substrate (transition from 2R to 4S, i.e. F2R--~Fgs) and of subsequent addition of ADP during utilization of exogenous substrates (metabolic states 4S, 3, 4R, i.e., Fes--~F3--~Fek transformations) were examined. The time of 2S to 2R transition (Tr2) and 4S to 4R transition (Tr3) and the rate of transition from 2AP to 2R metabolic state and from 3 to 4R (V 2 and V 3, respectively) were studied. The results were processed by paired Wilcoxon--Mann--Whitney's test. RESULTSThe results provide a new interpretation of changes in PNR in MC during transition from one metabolic stale to another. Due to a better preservation of the MC structure [4], we demonstrated stability of PNR and
Posthypoxic encephalopathy is characterized by inhibition of the succinate oxidase stage in cerebral energy production. When administered to rats exposed to hypoxia, Bergeniae crassifolia extract reduced mortality and restricted the inhibition of rapid metabolic cluster reactions Key Words: Bergenia crassifolia extract; posthypoxic encephalopathy," brain mitochondria; NADHThis study analyzes the role of rapid and slow metabolic clusters [2,3] in the maintenance of brain energy homeostasis by measuring the level of NADH fluorescence in rat brain mitochondria during posthypoxic encephalopathy (PHE) and its correction with extract from Bergenia crassifolia leaves. Previous screening revealed high cerebroprotective activity of this preparation in hypoxia [4,5]. The present study used an original approach to the assessment of energy production based on the analysis of kinetic characteristics of pyridine nucleotide reduction (PNR) during phosphorylation of exogenous ADP [4]. MATERIALS AND METHODSThe study was carried out on 2-month-old male Wistar rats weighing 180-200 g (Laboratory of Experimental Biomedical Modeling, Tomsk Research Center).Piracetam (400 mg/kg) and extract of Bergenia crassifolia leaves (300 mg/kg) were suspended in water and administered intragastrically for 5 days starting from day 14 after hypoxia. Hypoxia was modeled in a hermetically sealed 5-liter jar until the start of agony (3.5-4.0 h), after which the jar was open, and the aniLaboratory of Molecular Pharmacology, Institute of Pharmacology, Tomsk Research Center. Siberian Division of the Russian Academy of Medical Sciences mal was returned to its home cage. After the 19th hypoxia session the rats were decapitated under ether anesthesia.Isolated brains were homogenized in an ice-cold medium containing: 1.2• ~ M KC1, 2x10 3 M K2CO3, l0 -2 M HEPES, 2x10 -4 M EDTA (pH=7.2), 2x10-3 M KH2PO 4 (pH=7.2 at 26~ was added during incubation. The functional state of the energy production system was evaluated by the level of reduced pyridine nucleotides [9].The data were analyzed statistically using paired Wilcoxon--Mann--Whitney test. RESULTSIn the experimental animals, the time of NAD reduction after the addition of ADP to cerebral mitochondria oxidizing an endogenous substrate was 2.65-fold prolonged and the rate of transition from 2AP to 2R metabolic state was 2.8 times lower compared to the control (Table 1 ). During oxidation of exogenous succinate, the time of NAD reduction was 2.3-fold prolonged and the rate of transition from metabolic state 3 to 4R was 2.5 times lower than the corresponding control values. During oxidation of NAD-dependent substrates, Tr 3 increased 1.95-fold and V 3 decreased 2.9-fold. These changes indicate that hypoxic injury causes pronounced negative shifts in the brain energy metabolism [ 1 ].
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