The results of comparative studies of the long-term ef ect (dynamics) of polymetallic dust containing 0.6% copper in the shops of Balkhash mining and metallurgical combine on the liver of rats are presented. These data on the action of dust with a predominant copper content of 0.6% give reason to assert that in the liver for 30 days there were changes in the structure, which were ref ected by metabolic rearrangements and are characterized as a failure of adaptation. The phenomena of hepatitis also took place on day 90, but these changes led to a decrease in the rate of metabolic processes. Microscopic examination showed that long-term exposure to polymetallic dust with a copper concentration of 0.6% in the body leads to signif cant changes in the liver reactive character, followed by transformation into hepatitis portal type. There is an accumulation of copper in the cytoplasm of hepatocytes; on day 90, the number of dust particles in rat hepatocytes increases by 2.25 times compared to 30 days of the experiment. T is can be explained by the inhibition of the phagocytic function of liver macrophages and ways to eliminate dust from the body. The lat er, in turn, leads to functional and metabolic damage to the structural component of the organ. It should be noted that an important role in the neutralization and removal of copper from the cell belongs to lysosomes. T ere is an assumption that copper damages lysosomal membranes and stimulates the release of enzymes from lysosomes due to a decrease in the number of mitochondria in the cell or inhibition of their enzymes. Thus, the ef ects of polymetallic dust with a copper concentration of 0.6% in the body in the early stages leads to changes in the liver, in the form of reactive hepatitis with subsequent transformation into portal-type hepatitis. The use of alimentary corrections slows down the development of post-necrotic f brosis in the liver, and there was a signif cant decrease in the volume fraction of f brotic liver tissue.
BACKGROUND: The diabetogenic effect of alloxan is known is determined by ability to stimulate lipid peroxydation processes in B-cells of the pancreas. AIM: to investigate of the possible antidiabetic action of long time prolonged of Iodine-Selenium concentrate action in rats with alloxan diabetes. METHODS: Reproduction of experimental alloxan diabetes was carried out in rats by a single intravenous injection of alloxan 35-43 mg / kg body weight. The “iodine-selenium” concentrate was administered per os through a tube at the rate of 1.25 ml / 100 g of the concentrate. In experimental animals with mild and heavy diabetes mellitus, the level of glucose in the blood was assessed, products of LPO-AOD; the state of the histostructure of the pancreas and of insulin content in B cells were studied using of aldehyde fuchsin and diethylpseudoisocyanine methods. RESULTS: Long time prolonged administration of the “iodine-selenium” concentrate (60 days) to animals with mild experimental diabetes mellitus is accompanied by a significant decrease in blood glucose levels by 1.89 times compared to the control (p ˂ 0.05) and of LPO within normal values as by increase of the level of glutathione peroxidase (GPO) by 2.23 times compared with the initial (p˂ 0.01), by prevention of the development of histological changes in pancreatic islets and a slight decrease of insulin content in B-cells. Under similar experimental conditions in animals with severe alloxan diabetes, the level of glycemia significantly decreased from 20.23 ± 2.15 mmol / l to 12.39 ± 1.52 mmol / l as of the level of diene conjugates of erythrocytes and plasma, as decrease of ketodienes, MDA of plasma and in erythrocytes and primary lipid peroxidation products, while remaining elevated, despite an increase in GPO by 50.0% compared with control (p˂0.05) in the presence of histological changes in the pancreatic islets as in experimental diabetes. CONCLUSION: The antidiabetic effect of the “iodine-selenium” concentrate in rats with mild alloxan diabetes on the level of glycemia, LPO - AOD and state of the histostructure of the pancreas and the content of deposited insulin in pancreatic B-cells, is probably due to antioxidant effect of selenium to stimulate activity of glutathione blocking lipid peroxide and hydrogen peroxide in alloxan diabetes mellitus.
BACKGROUND: It is known that an increased intake of copper (Cu) has an adverse effect, and above all leads to the defeat of parenchymal organs, including liver tissue. AIM: This study the morphological changes in the hepatic tissue at the impact of polymetallic Cu dust. METHODS: An experimental study was carried out on the outbred white male rats. Dust was injected once intratracheally at a dose of 50 mg. For dynamic observation, the animals were killed in 1, 3, and 6 months with the control group using instant decapitation. The Balkhash industrial polymetallic dust with a predominant Cu content (Cu-0.6%) was used for the study. Morphological changes were assessed using histological and morphometric methods. RESULTS: Morphometric examination of liver tissue at 30 days showed Vv necrosis increasing in 320 times in Group 2 (p < 0.001), Vv infiltrates – in 121 times (p < 0.001), Vv dystrophic altered hepatocytes – in 19.91 times (p < 0.001), Vv dual-core cells – in 23 times (p < 0.01), and Vv fibrosis – in 2.82 times (p < 0.001) in comparison with Group 1. Vv portal tracts are not reliably changed. In 90 days, there were also the following morphometric parameters increasing in comparison with the control group: Vv necrosis – in 522 times (p < 0.001), Vv infiltrates – in 395 times (p < 0.001), Vv dystrophic altered hepatocytes – in 26.7 times (p < 0.001), Vv dual-core cells – in 314 times (p < 0.01), and Vv fibrosis – in 13.27 times (p < 0.001). On the 180 day of the experiment, there was the increasing of Vv infiltrates in 421 times (p < 0.001), Vv dystrophic altered hepatocytes – in 34.09 times (p < 0.001), Vv dual-core cells – in 411 times (p < 0.001), and Vv fibrosis – in 54.09 times (p < 0.001) CONCLUSION: The impact of polymetallic dust with 0.6% Cu concentration at the early stages leads to the changes in the liver in the form of reactive hepatitis with the following transformation into portal-type hepatitis.
BACKGROUND: The issues of the pathogenetic relationship of thyroid-adrenal disorders in diabetes mellitus (DM) remain relevant, despite certain advances in the study of the pathogenesis and the clinic of DM. These issues are especially actual in the case of a combination of DM with ischemic heart disease (IHD) and obesity. AIM: The aim was to reveal the pathogenetic mechanisms of the relationship between metabolic and morphofunctional thyroid-adrenal disorders in DM and obesity. METHODS: The study included 395 patients with type 1 and 2 diabetes. The diagnosis of DM was verified in accordance with International Programs and was based on WHO criteria. The glycemic level of patients was determined using a One Touch® basic glucometer (Johnson&Johnson, USA). The degree of carbohydrate metabolism compensation was assessed by the level of glycated hemoglobin (HbA1c), determined using a laboratory analyzer DCA-2000 MT (BAYER, Germany). The concentration of C-peptide in the blood serum was determined by the method of immunoluminometric analysis “Immunotech” (Czech Republic). Caro and HOMA-IR indices were calculated to identify and assess the insulin resistance (IR). The indices of hormone metabolism were determined by ELISA using DSL kits (USA) with subsequent measurement of optical density on a Spectra Classic reader from Tecan (Austria): Corticotropic hormone, adrenaline, noradrenaline, cortisol, free hydrocortisone; 17-ketosteroids, 17-oxycorticosteroids, glucogone, insulin, somatotropic hormone (STH); thyroid-stimulating hormone (TSH); thyroxine (T4); and thyroxine (T3). Instrumental-functional and radiation research methods. Ultrasound examination of the adrenal glands, thyroid gland, lungs, liver, and kidneys was performed in all patients. Morphological changes were assessed using histological and morphometric methods. RESULTS: Disorders of carbohydrate metabolism in diabetic patients were revealed by increased glycemic parameters – in 2.14 times, immunoreactive insulin (IRI) – in 2.8 times, HbA1c – in 1.85 times, and HOMA – in 5.3 times compared with the control group. The following indicators were significantly higher in patients with combination of DM, IHD, and obesity: Glycemia – in 2.29 times (p < 0.05), IRI – in 3.81 times, HbA1c – in 2.01 times, and HOMA – in 7.76 times compared with Co and CIHD groups. An increase in the content of pyruvate and lactate and the ratio in the DM2o and DM2IHDo groups indicate an acceleration of glycolysis and the degree of pyridine nucleotides reduction, as well as excessive lipolysis and progression of tissue hypoxia. Thus, the rate of glucose oxidation in patients of DM2o subgroup is reduced in 3.02 times, in patients of DM2IHDo subgroup (p < 0.05) – in 3.18 times compared with Co group. Computed tomography (CT) revealed an increase in the volume of adipose tissue in relation to muscle and bone tissue in patients of DM2o and DM2IHDo subgroups. Abdominal obesity type is expressed in these patients. An increase of glucose promotes its conversion into triglycerides (TG) of adipose tissue under the condition of hyperinsulinemia. Lipogenesis in the body of patients with DM and coronary heart disease increases, and obesity develops. The increase of cortisol and TSH (p < 0.01) levels was observed in patients of DM2o, DM2IHDo groups compared with the control groups. In patients of DM1 group, the parameters of norepinephrine were increased in 2.23 times, TSH (p < 0.01) – in 3.15 times, and the content of STH was reduced in 3.76 times and the content of cortisol – in 1.5 times significantly (p < 0.01) compared to C1 group. Ultrasound and CT with contrast revealed diffuse adrenal hyperplasia, signs of a decrease in the size of the thyroid gland with a medium-grained structure, areas of its cystic degeneration in the form of hypoechoic zones with a medium-grained echo structure. Thus, the expressed atrophic processes in the lobes of the thyroid gland were observed in 27 (15.4%) patients of DM2 group and in 13 (13%) patients of DM2CHDo group. Analysis of spectral characteristics during Doppler ultrasonography of the thyroid gland vessels made it possible to determine low peak systolic blood flow velocities in CIHD group. Pathomorphological examination of the adrenal glands on electronograms recorded that the porosity of the walls of the sinusoidal capillaries increased primarily within the bundle zone of the cortex. Corticocytes of the fascicular and reticular zones underwent degenerative and necrotic changes. Along with this, some of the epithelial cells contained the usual number of light and an increased number of dark fat droplets. The study of the sectional material revealed signs of suppression of the function of the thyroid gland, dystrophic changes in the cells increased, which contributed to a decrease in the functional capabilities of the follicular epithelium, destruction of individual thyrocytes, and substitutional sclerosis with an increase in the exchange surface area in the blood-tissue barriers. CONCLUSION: The main pathogenetic mechanism of suppression of the structural and functional state of the adrenal and thyroid glands is due to dystrophic changes in the microvasculature. With the addition of ischemic heart disease, the oppression of their functions of the glands develops, which leads to destruction, an increase in vascularization, porosity of the capillary walls, and tissue hardening. There is a further aggravation of hormonal and metabolic disorders in patients with DM with coronary heart disease. It is confirmed by a significant increase in the lactate/pyruvate index and the index of IR. The volume of adipose tissue in relation to muscle and bone tissue on CT was significantly higher (p < 0.05) compared to the control groups. The predominance of the abdominal type of fat deposition is expressed.
BACKGROUND: There are a large number of works devoted to the study of the state of the bronchopulmonary system in diabetes mellitus in the literature in the last 20 years. However, these studies are often conflicting. Some researchers identify a deterioration in the function of external respiration and a connection with metabolic changes and complications of the disease, others associate it with vascular pathology. There are a number of reports of increased pulmonary ventilation in diabetes. AIM: To assess the structural and functional state of the lungs in patients with diabetes mellitus and in combination with coronary heart disease and obesity. METHODS: 395 patients with type 1 and type 2 diabetes mellitus were under observation. The diagnosis of diabetes mellitus was verified in accordance with International Programs and was based on WHO criteria. The glycemic level of patients was determined using a One Touch® basic glucometer (Johnson&Johnson, USA). The degree of carbohydrate metabolism compensation was assessed by the level of glycated hemoglobin (HbA1c), determined using a laboratory analyzer DCA-2000 MT (BAYER, Germany). The concentration of C-peptide in the blood serum was determined by the method of immunoluminometric analysis "Immunotech" (Czech Republic). Caro and HOMA-IR indices were calculated to identify and assess the insulin resistance (IR). The indices of hormone metabolism were determined by ELISA using DSL kits (USA) with subsequent measurement of optical density on a Spectra Classic reader from Tecan (Austria): corticotropic hormone (CTG), adrenaline, noradrenaline, cortisol, free hydrocortisone; 17-ketosteroids, 17-oxycorticosteroids, glucogone, insulin, somatotropic hormone (STH); thyroid stimulating hormone (TSH); thyroxine (T4); thyroxine (T3). Instrumental-functional and radiation research methods: X-ray methods for lungs examining, computer spirography, fibrobronchoscopy of the bronchi was performed in all patients. Morphological changes were assessed using histological and morphometric methods. RESULTS: Pathogenetic mechanisms of the bronchopulmonary system disorders in patients with type 1 diabetes mellitus are associated with a decrease in the function of external respiration due to the volumetric air flow rates of the predominantly central airways and an increase in bronchial resistance. Alveolar hypoventilation of a restrictive type with impaired diffusion of gases through the alveolar-capillary membrane was detected in patients with type 2 diabetes mellitus. Restrictive and obstructive type disorders with impaired ventilation-perfusion ratios and pulmonary blood flow are formed in patients with type 2 diabetes mellitus combined with coronary artery disease and obesity. CONCLUSION: A decrease in the function of external respiration due to the central respiratory tract and an increase in bronchial resistance were noted in 38.4% of patients with type 1 diabetes mellitus. Restrictive alveolar hypoventilation was registered in 23.3% of patients with type 2 diabetes mellitus, catarrhal endobronchitis – in 21.31% of patients with type 2 diabetes mellitus. Damage and fibrosis of the alveolar tissue, damage to the endothelium and disorganization of the connective tissue of the lungs were characteristic of microscopic examination of the ultrastructure of the lungs in patients with diabetes mellitus.
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