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A significant increase when perforated ulcers relative volume fraction of the lymphatic vessels is their main difference from the uncomplicated and bleeding ulcers.
Discussion
Analysis of the research showed, that by microscopic counting of morphological structures ulcerative substrate can predict the development of peptic ulcer perforation. To this end, all patients with ulcer history should undergo medical examinations with biopsy of the ulcer for morphological analysis. By increasing the volume fraction of "unstructured" zones in the submucosa, without Paneth cell mitosis and suggested the possible perforation of the ulcer.
Our studies have shown that the perforated ulcers (such as perforated and ulcer with high risk of perforation) major morphological differences are: 1) an increase in the relative volume fraction of cell-free "structureless" zones; 2) an increase in the relative volume fraction of the lymphatic vessels, and 3) a decrease in the number of Paneth cells, followed by a decrease in the number of mitotic figures. These morphological features can serve as predictors of objective possibility of perforation of gastroduodenal ulcers.
Analyzing the literature, the following facts were found. For example, Elisabete Kawakani examined biopsy for neutrophils and HP infection [9]. However, the white blood cells showed only
the degree of inflammation around the ulcer process, predicting perforation or any complications was not possible. A pathogen of ulcer disease is now possible to diagnose even with the help of numerous non-invasive methods.
American Society of Gastroenterology reports that the giant ulcer KDP are more prone to perforation, bleeding and penetration than small ulcers, 65 % and 12 %, respectively [8]. However, there is no information about a possible ulcer perforation.
Also in the medical journal of Hong Kong noted that the perforation (92 % of cases) is more common than bleeding (55 %) and stenosis (45 %) in patients with Helicobacter pylori positive ulcers [6].
In Japan, the granulocytes were found in periulcerative zone, which contained a large number of matrix-metalloprotein-ase-1 (MMP-1) [7]. Increasing these cells also play a role in ulcer perforation of the stomach and duodenum.
However, the literature is still no consensus on the methodology of forecasting of perforation of gastroduodenal ulcers.
Conclusion
The main morphological risk factors of perforation are the increase in the relative volume fraction of cell-free "structureless" zones; increase in the relative volume fraction of the lymphatic vessels and reducing the number of Paneth cells, followed by a decrease in the number of mitotic figures.
References:
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Kasymova Gulmira Gafurovna, Scientific Research Institute of Hematology and Blood Transfusion
E-mail: evovision@bk.ru
Peroxidation of lipids and activity of enzymes of antioxidant protection in microsomal fraction of the liver and kidneys of rats with leucosis
Аbstract: In dynamics of experimental leucosis intensification of the POL (peroxidation of lipids) in microsomal fraction of the liver appears earlier and is more expressed, whereas in kidneys it develops slowly, becoming more active at final terms of experiment. It develops together with activity of antioxidant protection enzymes which progressively decrease in microsomal fraction of the liver, whereas in kidneys that inhibits only during sharp progressing of tumor process. Thus Compensatory capacity ofAOP (antioxidant protection) of microsomal fraction of the liver is sharply oppressed, defining early failure (decompensation), and in kidneys its failure noted after 7 months and aggravated by progressing of pathological process.
Keywords: antioxidant protection, tumor, pathological process.
Leucosis are one of actual problems of hematology due to rate of at persons younger 60 years, and among elderly — the rate high prevalence and high lethality. Optimization of its treatment was 10-12 %. However the lethality remains high due to develop-allowed increasing survival rate of patients. Results of treatment ment of septicinfectious, thrombo-haemorrhagic complications and ofacute myeloblast leucosis (OML) showed 35-50 % 5-year survival development of poly-organ insufficiency. In process of development
Peroxidation of lipids and activity of enzymes of antioxidant protection in microsomal fraction of the liver.
of leucosis of the cellsbecome able to grow out of hemopoietic organs: in skin, kidneys, a liver, brain membranes [1; 2]. It is caused by sharp change of immunological properties of an organism, affection ofhomeostasis, suppression of work of detoxication system organs, violation of the central and peripheral haemodynamics, causing thus development ofhypoxemia. The hypoxemia, leucosis infiltration and toxic effect of cytostaticsleads to affection of the main detoxication organs: liver and kidneys [2; 3]. Cytochrome P-450 dependent mo-nooxygenaze system (MOS) which provides biotransformation of endogen and exogenhydrophobic compoundsis responsible for these processes. Intensification of the POL (peroxidation of lipids) which promotes destruction of membranes of smooth of endoplasmic reticulum in the conditions of a hypoxemia can be one of the mechanisms in decrease of activity of membrane-boundenzymes in rats with leucosis [12; 20]. For clarification of the matter we investigated level malonic dialdehyde (MDA) and activity of AOP (antioxidant protection) enzymesmicrosomal fraction of the liver and kidneys in dynamics of an experimental benzene leucosis.
Material and research methods
For this purpose we have selected and upgraded the benzene model of leucosis which was reproduced on 157 adult malerats by subcutaneousinjection of 40 % oil solution of benzene
(0.01ml/100 g. of weight of a body) during whole period of the experiment [18]. The general mortality rate was 40.1 %. Development of leucosis was determined every month until 8th month from the beginning of experiment based on indicators of peripheral blood and bone marrow [2]. By the end of 6-month 50 % of animals developed leucosis, rate of leucosis increased to 77.4 % in 7 months and to 86.4 % in 8 months. In the mentioned periods the animals with signs of chronic leucosis wereslaughtered under a raush-anesthesia observing the rules of the European Convention on Protection of Vertebrate Animals (Strasbourg, 1986). Mitochondrial fraction of the liver and kidneys were extracted using method of a differential centrifugation. Intensity of peroxidation of lipids estimated by level malonic dialdehyde (MDA) [1], and also activity of antioxidant protection superoxyddismutaze (SOD) [13] and a catalase [10]. The obtained data processed by statistics method using software STATISTICA 5. Confidence interval level was at P < 0.05.
Results and their discussion
The conducted researches showed that level of malonicdialde-hyde (MDA) in microsomal fraction of the liver of rats withleuco-sis increasesto 1.72, 1.75 and 2.04 (P < 0.01) times in process of progressing leucozogeneze (table 1).
Table 1. - Indicators of peroxidation of lipids and activity of enzymes of antioxidant protection in microsomal fraction of the liver of rats with leucosis, M ± m, n = 6-7
Groups and research terms Content of malonic dialdehyde (MDA), nmole/mg. protein Activity of Enzymes
SOD, rel. un./min*mg. protein Catalaze, mkmole ^ О2/min*mg. protein
Intact 0.244 ± 0.011 0.178 ± 0.012 0.219 ± 0.011
Leucosis, after: 6 months 0.419 ± 0.017 0.118 ± 0.003 0.172 ± 0.009
P < 0.001 < 0.01 < 0.05
7 months 0.427 ± 0.011 0.091 ± 0.002 0.151 ± 0.008
P < 0.001 < 0.001 < 0.01
8 months 0.498 ± 0.024 0.078 ± 0.004 0.121 ± 0.008
P < 0.001 < 0.001 < 0.001
Table 2. - Indicators of peroxidation of lipids and activity of enzymes of antioxidant protection in microsomal fraction of the liver of rats with leucosis, M ± m, n = 6-7
Groups and research terms Content of malonicdialdehyde (MDA), nmole/mg. protein Activity of Enzymes
SOD, rel. un./min*mg. protein Catalaze, mkmol Н О2/min*mg. protein
Intact 0.167 ± 0.013 0.178 ± 0.011 0.121 ± 0.011
Leucosis, after: 6 months 0.198 ± 0.014 0.159 ± 0.013 0.117 ± 0.009
P > 0.05 > 0.05 > 0.05
7 months 0.242 ± 0.011 0.129 ± 0.009 0.075 ± 0.002
P < 0.001 < 0.001 < 0.01
8 months 0.298 ± 0.014 0.101 ± 0.007 0.062 ± 0.008
P < 0.001 < 0.001 < 0.001
Activity of SOD enzymes and a catalase progressively decreases: in 6 months — to 1.51 (P < 0.01) and 1.27 (P < 0.05) times, in 7 months — in 1.96 (P < 0.001) and 1.45 (P < 0.05) times, in 8 months — to 2.28 (P < 0.001) and 1.81 (P < 0.001) times, according to enzymes. Dynamics of decrease in a ratio of the sum of activity of SOD enzymes and catalase to the contents malonicdial-dehyde (MDA) can serve as confirmation of development of theim-balance in POL-AOP system. So, if this indicator in intact rats was 1.63 rel. un. in rats with leucosis after 6, 7 and 8 months it progressively decreased to 0.69, 0.58 and 0.4 rel. un., according to terms.
The analysis ofprocesses of POL/AOP in microsomal fraction of kidneys of rats with leucosis showed activizationlipo- peroxidation: level malonicdialdehyde (MDA) increases 1.45 and 1.78 times,
activity of SOD and a catalase decrease 1.39 (P < 0.05) and 1.61 (P < 0.01) time — in 7 months, 1.76 (P < 0.01) and 1.95 (P < 0.001) times — after 8 months from the beginning of experiment (table 2). It leads todesrease of ratio of (SOD + catalase)/MDA to 1.4, 0.84 and 0.55 rel. un., according to terms after 6, 7 and 8 months, at norm of 1.79 rel. un.
At the same time, we observed some distinctions in processes the POL of microsomal fraction of the liver and kidneys of rats with leucosis. Intensification of the POL (peroxidation of lipids) in microsomal fraction of the liver appears earlier and in subsequent terms its increase declines. At the same time in kidneys processes of a hyperlipoperoxidation begin later (after 7 months) and they are intensified in process of progressing of pathological process
pointing later involvement of kidneysin pathological process. In the liver decrease in activity of SOD is more expressed, whereas in kidneys — activity of catalase.
Apparently from the provided data, compensatory capacity of AOP (antioxidant protection) of microsomal fraction of the liver is slightly higher, than in kidneys. Compensatorycapacity ofAOP in kidneys after 6 months from the beginning of experience remain high whereas in the liver they are sharply oppressed, defining early failure (decompensation), causing a destruction of membranes and decrease in activity of microsomal oxidation enzymes of xe-nobiotics. This decompensation is even more oppressed further. In our opinion, it is connected with early involvement of the liverin pathological process. In kidneys failure of compensatory capacity of AOP is noted after 7 months and it is aggravated in process of progressing of pathological process. The results obtained by us coincide with dynamics of change of enzymes of microsomal oxidation in kidneys and confirms later involvement of kidneysin pathological process.
Activizationof processes of free radical oxidation leads to destructive changes in bio membranes. Phospholipidsof the mem-braneswhich contain polynon-saturated fatty acidsare exposed to oxidation in the first instancedue to high solubility of molecular oxygen in a lipid phase. In membranes endoplasmic reticulum the contents phosphothidilcholin decreases, occurs selective modification of arachidon, docosahexaenoic and linoleic acids of
phosphothidiletonolamine, concentration of more polar lipids increases, asymmetry of a membrane, change of its properties amplifies. In these conditions functioning of the membrane-bounded enzymes, in particular cytochrome P450 dependentmonooxigenas-esof the liver and kidneys of experimental animals is affected. The data obtained by us coincide with data from literary which shows the intensification POL, decrease activity glutathione peroxidase, level of sulfhydryl groups, retinol and alpha-tocopherol in patients with hemoblastosis [14; 15; 17]. The labialization of membranes observed in these conditions promoted release of toxic products of a metabolism from tumors, mutilated functional activity of cells of the owner [17] and developed of endogenic toxicosis.
Refering to obtained data we can conclude:
1. The intensification of the POL (peroxidation of lipids) in microsomal fraction of the liver appears earlier and is more expressed, whereas in kidneys it develops slowly, becoming more active at final terms of experiment.
2. In dynamics of an experimental leucosis activity of catalas-eenzymes and especially SOD, progressively decrease in microsomal fraction of the liver, whereas in kidneys that inhibits only during sharp progressing of tumor process.
3. Compensatory capacity of AOP (antioxidant protection) of microsomal fraction of the liver is sharply oppressed, defining early failure (decompensation), and in kidneys its failure noted after 7 months and aggravated by progressing ofpathological process.
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