Activated Braf induces esophageal dilation and gastric epithelial hyperplasia in mice.

Germline mutations in BRAF are a major cause of cardio-facio-cutaneous (CFC) syndrome, which is characterized by heart defects, characteristic craniofacial dysmorphology and dermatologic abnormalities. Patients with CFC syndrome also commonly show gastrointestinal dysfunction, including feeding and swallowing difficulties and gastroesophageal reflux. We have previously found that knock-in mice expressing a Braf Q241R mutation exhibit CFC syndrome-related phenotypes, such as growth retardation, craniofacial dysmorphisms, congenital heart defects and learning deficits. However, it remains unclear whether BrafQ241R/+ mice exhibit gastrointestinal dysfunction. Here, we report that BrafQ241R/+ mice have neonatal feeding difficulties and esophageal dilation. The esophagus tissues from BrafQ241R/+ mice displayed incomplete replacement of smooth muscle with skeletal muscle and decreased contraction. Furthermore, the BrafQ241R/+ mice showed hyperkeratosis and a thickened muscle layer in the forestomach. Treatment with MEK inhibitors ameliorated the growth retardation, esophageal dilation, hyperkeratosis and thickened muscle layer in the forestomach in BrafQ241R/+ mice. The esophageal dilation with aberrant skeletal-smooth muscle boundary in BrafQ241R/+ mice were recovered after treatment with the histone H3K27 demethylase inhibitor GSK-J4. Our results provide clues to elucidate the pathogenesis and possible treatment of gastrointestinal dysfunction and failure to thrive in patients with CFC syndrome.

Acrylonitrile-induced gastric toxicity in rats: the role of xanthine oxidase.

BACKGROUND: Acrylonitrile (ACN) is an extensively produced aliphatic nitrile. The gastrointestinal tract is an important target organ for ACN toxicity. The objective of the present study was to investigate the role of xanthine oxidase (XO) in ACN-induced gastric toxicity in rats. MATERIAL/METHODS: We assessed the effect of ACN on oxidative stress parameters as xanthine oxidase (XO) and total xanthine dehydrogenase (XD)/ XO activity, superoxide anion (O(2)(.-)) production, reduced glutathione (GSH) levels and lipid peroxidation in gastric tissues. RESULTS: A single oral dose of ACN (25 mg/kg) caused a significant enhancement in XO activity. ACN also caused a significant depletion of GSH levels, enhanced O(2)(.-) production and increased lipid peroxidation in the time-course experiment. In the dose-response experiment, ACN accelerated the conversion of XD to XO, with a significant depletion of gastric GSH in a dose-related manner. A strong negative correlation existed between the levels of GSH and the percentage enhancement in XO activity (r =-0.997). (O(2)(.-)) production and malondialdehyde (MDA) formation were significantly elevated in a dose-related manner. Pretreatment with allopurinol (50 mg/kg) significantly protected against ACN-induced rise in XO activity, depletion of GSH, and elevated production of (O(2)(.-)). However, pretreatment with diethyl maleate (DEM; 100 mg/kg) significantly aggravated the ACN-induced GSH depletion and rise in XO activity. Furthermore, DEM significantly enhanced (O(2)(.-)) and MDA production. CONCLUSIONS: The present study indicates that enhancement of XO activity could be implicated in ACN-induced gastric damage in rats.

[Clinical and morphological characteristics and some mechanisms of portal gastroduodenopathy in liver cirrhosis].

We have found out the clinical presentations and peculiarities of endoscopic and morphologic view of pathologies of mucous membrane of gastroduodenal zone caused by liver cirrhosis. We have examined 74 patients with liver cirrhosis of viral and nonviral etiology using the clinical, endoscopic, morphologic and immunohistochemical methods.We have found that during liver cirrhosis morphometric rates of epithelial cells of mucous coat of stomach that produce somatostatin and endothelin-1 decrease and morphometric rates of epithelial cells that produce nitrogen oxide synthase increase. We have also found out that during liver cirrhosis proliferate activity decrease and apoptosis of epithelial cell of mucous coat of stomach increase.

Evaluation of HIF-1α and iNOS in ischemia/reperfusion gastric model: bioimpedance, histological and immunohistochemical analyses.

Gastrointestinal ischemia/reperfusion (I/R) generates pathological alterations that could lead to death. Early ischemic damage markers could be used to guide therapy and improve outcomes. AIM: To relate hypoxia-inducible factor 1α (HIF-1α) activation and inducible nitric oxide synthase (iNOS) expression to gastric impedance changes due to I/R damage. METHODS: Experimental animals were randomly distributed into 3 groups: control, ischemia (30 min) and I/R (60 min). Gastric ischemia was generated by celiac artery clamping for 30 min, and then blood flow was restored for 60 min. Impedance spectra and biopsies of the glandular portion were obtained for histological and immunohistochemical analyses. Immunodetection of both HIF-1α and iNOS was performed. RESULTS: Under ischemia and I/R conditions, there was an increase (p<0.05) in the impedance parameters. Histologically, under ischemic conditions, edema and necrosis were observed in epithelium and significant vascular congestion. In I/R condition, alterations of the glandular and luminal integrity were found, which generated areas of epithelial erosion. Immunohistochemical analysis of HIF-1α revealed an increase (p<0.01) in the number of immunoreactive cells in the ischemia (35.7±13.9) and I/R (119.9±18.8) conditions compared to the control (0.8±1.2). Immunodetection of iNOS showed an increase (p<0.01) in the number of cells expressing iNOS under the ischemia (5.4±2.9) and I/R conditions (27.4±11.3) was observed compared to the control (0.4±0.8). CONCLUSION: Early changes in impedance in response to I/R is related to histopathological changes, the nuclear stabilization and translocation of HIF-1α as well as expression of iNOS.

The CAT-262 C>T, MnSOD Ala16Val, GPX1 Pro198Leu Polymorphisms Related to Oxidative Stress and the Presence of Gastric Lesions.

BACKGROUND AND AIMS: The increased oxidative stress plays an important role in gastro-duodenal ulcers and gastric cancer occurrence. We investigated the association between the genetic polymorphisms of genes encoding the antioxidative enzymes CAT, GPX and SOD and the occurrence of gastric lesions, considering also the environmental risk factors such as H. pylori infection, drug exposure, smoking and alcohol consumption. METHODS: We included 373 patients who underwent endoscopy for symptoms, anemia or bleeding investigation. A complete set of demographical, clinical and pathological data was recorded. All patients were successfully genotyped. RESULTS: In the multivariate logistic regression model, the patients having Pro/Pro genotype of GPX1 gene polymorphism had more severe gastric lesions as compared with patients with the Leu/Pro or Leu/Leu genotype (OR= 1.89, 95%CI: 0.99-3.57, p=0.051). The GPX1 Pro198Leu and the MnSOD Ala16Val gene polymorphism could be independent risk factors for reactive gastropathy changes, as shown by their association very close to statistical significance (p=0.059 and p=0.054, respectively). Consumption of anticoagulants was a significant independent predictor (p=0.023, OR:0.43 95%CI:0.21-0.89) for the absence of active gastritis, while low-dose aspirin consumption was a risk factor for active gastritis in biopsy samples (p=0.025, OR:1.71, 95%CI:1.07-2.74). CONCLUSION: The variant genotype of GPX1Pro198Leu was associated with an increased risk for reactive gastropathy changes in gastric biopsies and with less severe endoscopic lesions, while MnSODAla16Val variant genotype (Val/Val or Val/Ala) seems to be related to the reactive gastropathy. However, none of them were associated with inflammatory or premalignant gastric lesions.

Insulin restores neuronal nitric oxide synthase expression and function that is lost in diabetic gastropathy.

Gastrointestinal dysfunction is common in diabetic patients. In genetic (nonobese diabetic) and toxin-elicited (streptozotocin) models of diabetes in mice, we demonstrate defects in gastric emptying and nonadrenergic, noncholinergic relaxation of pyloric muscle, which resemble defects in mice harboring a deletion of the neuronal nitric oxide synthase gene (nNOS). The diabetic mice manifest pronounced reduction in pyloric nNOS protein and mRNA. The decline of nNOS in diabetic mice does not result from loss of myenteric neurons. nNOS expression and pyloric function are restored to normal levels by insulin treatment. Thus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS. In diabetic animals, delayed gastric emptying can be reversed with a phosphodiesterase inhibitor, sildenafil. These findings have implications for novel therapeutic approaches and may clarify the etiology of diabetic gastropathy.

Gastric graft-versus-host disease revisited: does proton pump inhibitor therapy affect endoscopic gastric biopsy interpretation?

Accurate diagnosis of gastrointestinal graft-versus-host disease (GvHD) is important, as it contributes significantly to postallogeneic stem cell transplant (SCT) morbidity and mortality. To test the hypothesis that proton pump inhibitor (PPI) therapy may interfere with histologic evaluation of gastric GvHD by inducing apoptosis, we evaluated epithelial apoptotic body counts in antral and fundic biopsies from SCT recipients and control patients, both taking and not taking PPIs at the time of endoscopic biopsy. Hematoxylin and eosin-stained slides of gastric biopsies from 130 patients (75 allogeneic SCT with GvHD on clinical and histologic grounds, and a comparison group of 55 age- and sex-matched nontransplant patients with histologically normal gastric biopsies) were reviewed. The groups were further stratified into patients taking (PPI+) and not taking PPIs (PPI-) at the time of biopsy. Apoptotic bodies (AB)/10 (400 x) high power fields (HPF) were quantified for each case. Mean apoptotic body counts were then calculated for each case group. Seventy antral cases (31 control and 39 transplant) were also evaluated via gastrin immunohistochemistry, and the mean number of gastrin positive cells/400 x HPF calculated. In the PPI- groups, apoptosis was increased in biopsies from transplant patients, compared with controls, both in antral and fundic mucosa. In PPI+ patients, there was significantly more apoptosis in the gastric body in transplant patients than in controls. However, comparing antral biopsies from control and transplant PPI+ patients, there was no significant difference in AB quantitation. More apoptosis was seen in antral biopsies from PPI+ control patients when compared with PPI- control patients (P = 0.009). Mean numbers of gastrin positive cells/400 x HPF were increased in both control and transplant patients taking PPIs (85 and 58, respectively) compared with samples from those patients not taking PPIs (48 and 51, respectively). PPI therapy is associated with increased apoptosis in antral biopsies and may interfere with the evaluation of GvHD in biopsies from this site. A similar increase in apoptosis was not seen in fundic biopsies; biopsy of the gastric fundus rather than antrum may be preferable for the diagnosis of upper gastrointestinal GvHD.

Histochemical and histopathological study of the gastric mucosa in the portal hypertensive gastropathy.

It has been studied "in situ" the action of NADH2-cytochrome C reductase, an aerobe oxidative enzyme, in comparison to lactate dehydrogenase, a glycolitic enzyme in the gastric mucosa and with portal hypertensive gastropathy (PHG) accompanied by morpho-pathological observations. In the normal gastric mucosa, the aerobe oxidative metabolism is predominant over the anaerobe one in all types of cells, but in different intensities (medium in the surface epithelium and low in the vascular endothelium, weak, medium, intense and very intense in fibroblasts and in secretory cells of fundic glands and macrophages). In the portal hypertensive gastropathy, this type of metabolism decreases and the anaerobe metabolism increases, tending to equal the first, especially in the glandular cells. The oxidative activity decreases in the surface epithelium and in the vascular endothelium, increases in cells of the inflammatory infiltrate and in fibroblasts and mast cells.

Effect of different organic acids (citric, malic and ascorbic) on intragastric urease activity.

BACKGROUND: The mechanism of citric acid-enhanced Helicobacter pylori urease activity remains unclear. AIM: To compare ascorbic, citric and malic acid given at the same concentration and pH on intragastric urease activity. METHODS: Volunteers received 40 mg of famotidine the evening prior to breath testing. After an overnight fast volunteers were randomized to receive 100 mL of water or 100 mm citric, malic, or ascorbic acid, pH 2.3 containing 75 mg of 13C-urea. At 15 min a second 100 mL solution of one of the test solutions was taken without added urea. RESULTS: Twelve volunteers were studied (eight men, four women, age 19-57, median 50.7) in a randomized-crossover study. The mean breath test result at 30 min with ascorbic (17.5 +/- 5), malic (25.8 +/- 5) and citric acid (29.5 +/- 5) were all significantly greater than with water (9.5 +/- 3). Citric and malic acid were similar (P = 0.699) and significantly greater than ascorbic acid (P < 0.02). When the ascorbic acid was followed by citric acid, the result was similar to that with citrate alone (25.8 +/- 4) and greater than with ascorbic then ascorbic (P = 0.026). CONCLUSIONS: Enhancement of H. pylori urease activity is not strictly a function of the pH. We propose the effect is related to differential effects of the availability of nickel, which is required for urease activity. Citric acid and malic acid were essentially equivalent such that malic acid could substitute for citric acid in the UBT; ascorbic acid would be a poor choice.

Cytochrome P4502E1 (CYP2E1) genetic polymorphism in a case-control study of gastric cancer and liver disease.

Cytochrome P4502E1 (CYP2E1) activates carcinogenic N-nitrosamines, benzene, urethane and other low molecular weight compounds. This enzyme is also inducible by ethanol, and metabolizes alcohol. A restriction fragment length polymorphism (RFLP) using the Rsa I restriction enzyme has been identified in the CYP2E1 transcription regulatory region; recent studies suggest that this polymorphism may affect gene expression. We investigated the frequency of the Rsa I RFLP in a Japanese population in relation to gastric cancer and liver disease susceptibility. The frequency of this polymorphism was determined in 150 gastric cancer, 16 hepatocellular cancer, 48 liver cirrhosis and 203 benign gastric disease (controls) patients. This preliminary study shows no association of the specific genotype with gastric cancer in all subjects (odds ratio = 1.04, 95% CI = 0.74-3.08 for the heterozygote and 0.57, 95% CI = 0.22-1.50 for the homozygous rare allele, respectively). To further confirm this lack of association, an age and gender matched case-control study should be performed. Separately, there was no association of the Rsa I RFLP with hepatocellular carcinoma (p = 0.911), but there was a suggested difference between the non-viral associated liver cirrhosis patients and control patients. Thus, this polymorphism may be related to ethanol metabolism and consequential liver diseases in a Japanese population.

PAR-2: structure, function and relevance to human diseases of the gastric mucosa.

PAR-2 (protease-activated receptor 2), a G-protein-coupled receptor activated by certain serine proteases such as trypsin and tryptase, is now considered a physiologically important molecule and also a novel target for drug development. PAR-2 is widely distributed in the mammalian body, especially throughout the alimentary system. PAR-2 plays various roles in the alimentary, circulatory, respiratory and neuronal systems. In the gastric mucosa, PAR-2 modulates multiple functions and exerts mucosal cytoprotection mainly by activating sensory neurons. Thus, PAR-2 would appear to be a therapeutic target for treatment of gastric mucosal injury. Agonists and/or antagonists for PAR-2 might also be applicable to the clinical treatment of patients with inflammatory diseases in other organs.

O6-alkyltransferase activity in normal and abnormal gastric mucosa.

The activity of the DNA repair enzyme O6-alkyltransferase has been studied in a series of stomachs with abnormal gastric mucosa and the activities found compared with those in normal stomachs. Enzyme activities found in stomachs with the macroscopic abnormalities of gastric ulcer, duodenal ulcer or gastric cancer were not significantly different from normal. In those stomachs where there was histological evidence of chronic atrophic gastritis or intestinal metaplasia however enzyme activities (mean 398 fmole/mg) were significantly higher than normal (mean activity 228 fmole/mg activity P < 0.001). We speculate that the conditions which stimulate these histological changes also give rise to induction of O6-alkyltransferase.

Gastroprotection by pentoxyfilline against stress-induced gastric damage. Role of lipid peroxidation, antioxidizing enzymes and proinflammatory cytokines.

Impairment of blood perfusion in gastric mucosa results in the formation of erosions and ulcers. Nitric oxide (NO), produced via activity of NO-synthase (NOS), appears to be a one of major factors, involved in the regulation of the gastric blood flow (GBF). Inhibition of this enzyme by N-nitro-L-arginine (L-NNA) results in local decrease of NO production, reduces GBF and impairs gastric mucosal integrity, the effects that can be reversed by the pretreatment with L-arginine, the NOS substrate. However, little information is available regarding the contribution of reactive oxygen species (ROS)-induced lipid peroxidation and NO to the mechanism of gastric mucosal integrity. Therefore, the aim of our present study was to determine the action of pentoxyfilline (PTX), an inhibitor of tumor necrosis factor alpha (TNFalpha) with or without NOS inhibition by L-NNA administration in rats with water immersion and restraint stress (WRS)-induced gastric lesions. Experiments were carried out on 100 male Wistar rats. The gastric blood flow (GBF) was measured using laser Doppler flowmeter. The area of gastric lesions was determined by planimetry and the levels of proinflammatory cytokines (IL-1beta and TNFalpha) were measured by ELISA. Colorimetric assays were employed to determine gastric mucosal levels of lipid peroxidation products, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) and antioxidant enzymes including superoxide dismutase (SOD) activity, as well as tissue concentration of reduced glutathione (GSH). Administration of PTX significantly attenuated the gastric lesions, induced by 3.5 h of WRS and this was accompanied by the rise in the GBF and a significant decrease in plasma proinflammatory cytokines (IL-1beta and TNFalpha) levels, as well as the reduction of lipid peroxidation. Exposure of rats to WRS suppressed the SOD and GSH activities and these effects were reversed by PTX. The protective and hyperemic effects of PTX, as well as an increase in mucosal SOD activity and GSH concentration were counteracted by pretreatment with L-NNA, but restored by the pretreatment with L-arginine, a NOS substrate. We conclude that PTX exerts beneficial, gastroprotective effect against WRS-induced gastric lesions due to enhancement in gastric microcirculation, possibly mediated by the enhanced NOS activity as well as local action of NO and by the attenuation of oxidative metabolism and generation proinflammatory cytokines.

Molecular resistance testing of Helicobacter pylori in gastric biopsies.

OBJECTIVE: To evaluate simultaneous diagnosis of infection and molecular resistance testing of Helicobacter pylori. METHODS: Gastric biopsies were obtained from 26 rapid urease-positive and 51 rapid urease-negative test kits used to diagnose H pylori infection. Following glass bead-assisted DNA isolation, amplification of H pylori 16S ribosomal DNA (rDNA), glmM, and 23S rDNA target genes was performed. RESULTS: Helicobacter pylori DNA was successfully amplified from 100% (26/26) of urease-positive and 3.9% (2/51) of urease-negative gastric biopsies. Subsequent restriction enzyme-mediated digestion of 23S rDNA amplification products revealed that 17% (4/24) of urease-positive and H pylori DNA-positive biopsy specimens contained point mutations (A2142G or A2143G) associated with clarithromycin resistance. Helicobacter pylori DNA from gastric biopsies was successfully amplified 8 weeks following rapid urease testing. CONCLUSION: Helicobacter pylori genotyping may be used to detect macrolide-resistant H pylori in individuals prior to initiation of therapy or in patients refractory to anti-H pylori therapy. Two urease-negative specimens yielded Helicobacter DNA distinct from that of H pylori and indicated the need for further investigations of Helicobacter species present in the human stomach.

Metabolism of ethanol and some associated adverse effects on the liver and the stomach.

Current knowledge of alcohol oxidation and its effects on hepatic metabolism and its toxicity are summarized. This includes an evaluation of the relationship of the level of consumption to its interaction with nutrients (especially retinoids, carotenoids, and folate) and the development of various stages of liver disease. Ethanol metabolism in the stomach and its link to pathology and Helicobacter pylori is reviewed. Promising therapeutic approaches evolving from newly gained insight in the pathogenesis of medical complications of alcoholism are outlined. At present, the established approach for the prevention and treatment of alcoholism are outlined. At present, the established approach for the prevention and treatment of alcoholic liver injury is to control alcohol abuse, with the judicial application of selective antioxidant therapy, instituted at early stages, prior to the social or medical disintegration of the patient, and associated with antiinflammatory agents at the acute phase of alcoholic hepatitis. In addition, effective antifibrotic therapy may soon become available.

Prevalence and clinical characterization of gastric Helicobacter species infection of dogs and cats in Korea.

This study was carried out to evaluate the prevalence and clinical characterizations of gastric Helicobacter spp. infection of dogs and cats in Korea. The prevalence of Helicobacter spp. infection of dogs and cats determined by urease test was 78.4% and 64%, respectively, although Helicobacter genus-specific PCR assay showed that it was 82.3% and 84%. Urease mapping results based on urease test showed that total positive rate of tested tissues from clinically abnormal dogs was significantly higher than that from clinically normal dogs (p=0.0018; Odds ratio = 6.118; 95% Confidence Interval = 1.96-19.103). These findings were consistent with the results of Helicobacter genus-specific PCR assay which showed that positive rate of the fundus (100%) and the antrum (100%) of clinically abnormal dogs was significantly higher than that of same gastric regions of clinically normal dogs (77.5 and 67.5% respectively). In comparison of gastric regions between clinically normal dogs and abnormal dogs, positive rate of urease test for the fundus (100%) and body (90.9%) in clinically abnormal dogs was significantly higher than that of abnormal dogs (72.5% and 57.5% respectively; p<0.05). The results of urease mapping in dogs and cats also indicated that Helicobacter colonization in the fundus was more dense compared with the density in the body and antrum. In Helicobacter species-specific PCR assay for dogs, 32 of 42 fundic tissues (76.2%) were positive for H. heilmannii and two (4.8%) were positive for H. felis. In cats, 18 of 21 fundic tissues (85.7%) were positive for H. heilmannii and 2 (9.5%) were positive for H. felis. Gastritis scores of fundic tissues from clinically abnormal infected dogs were similar to that from noninfected dogs and evidence of upregulation of IL-1beta, IL-8, and TNF-alpha mRNA was not detected in gastric fundic tissues from clinically abnormal infected dogs. This study suggested that Helicobacter spp. infection in domestic dogs including private owned pet dogs and cats is highly prevalent usually with no clinical sign but high density of colonization can be related to gastrointestinal signs

Clinical implications of serum pepsinogen and progastricsin in man.

The serum pepsinogens in man have been reviewed with respect to clinical and physiological significance. The many places of synthesis of pepsinogen (PG A) and progastricsin (PG C) are described. The major part of serum pepsinogen and progastricsin is synthezized in the stomach, and the findings after antrectomy indicate that the majority of the pepsinogens in serum originates from the corpus of the stomach. The concentrations of pepsinogen and progastricsin in serum in relation to stomach diseases, e.g. ulcer disease, gastritis, and cancer of the stomach, are described. Despite typical findings, i.e. hyperpepsinogenemia in duodenal ulcer disease, or hypopepsinogenemia in atrophic gastritis or stomach cancer, there is a big overlap in serum concentrations between the groups reducing the clinical value of routine measurements of pepsinogens. Most promising are the findings in stomach cancer disease, where the combined measurement of pepsinogen levels and the isozymogen Pg5 is found to be highly indicative for the presence of a gastric carcinoma. Reports state that pepsinogens are excellent markers of recurrence of gastric cancer somewhere in the body after total gastrectomy. Genetical studies have--concerning pepsinogen--proved the multiple gene/multiple loci model. There is only a single progastricsin gene in humans and no genetic heterogenity has been found. Finally, the relationship between gastric infection with the bacterium Helicobacter pylori, and elevated pepsinogen and progastricsin levels in the blood, and the search for serologic markers of gastric diseases is discussed.

[Antioxidant enzyme activity in the gastric mucosa in precancerous conditions]. / Aktivita antioxidacných enzýmov v sliznici zalúdka u prekanceróznych stavov.

BACKGROUND: The primary defense against oxidation damage of tissues are anti-oxidant enzymes, e.g. superoxide dismutase, catalase and glutathione peroxidase. Some non-enzymatic substances have a significant anti-oxidant action (e.g. vitamin C, E, beta-carotene and others). The objective of the present work was to follow up the Cu/Zn superoxide dismutase activity, catalase and glutathione peroxidase (anti-oxidant enzymes of the gastric mucosa) in subjects with the risk of developing gastric cancer, e.g. those suffering from atrophic gastritis, hyperplastic polyps and gastric adenoma. METHODS AND RESULTS: The authors examined 80 subjects (50 men and 30 women) aged 25 - 71 years. In all during endoscopic examination bioptic specimens of the mucosa were taken at standard sites of the gastric corpus and antrum for histological and enzymological examination. Enzymological examination: activity of Cu/Zn-superoxide dismutase (Randox Lab. Ltd. GB kit), catalase activity (modified method of Cavarocchia et al.) and glutathione peroxidase activity (method according to Paglia and Valentine). The Cu/Zn-superoxide dismutase activity was elevated in the group of patients with gastritis after gastrectomy (67%) and with gastric adenoma (35%), the catalase activity in patients with gastritis after gastrectomy (40%) and the glutathione peroxidase activity in patients with the diagnosis of gastritis after gastrectomy (185%), atrophic gastritis (46%) hyperplastic polyp (50%) and gastric adenoma (50%). CONCLUSIONS: The increased activity of anti-oxidant enzymes was due to a higher concentration of the superoxide anion radical, hydrogen peroxide and organic peroxides (lipoperoxides); the source of active types of oxygen are phagocytic leucocytes in the chronically inflamed gastric mucosa.

[Lactate dehydrogenase isozyme profile in gastric mucosa as an early marker of possible neoplastic pathology in children with chronic gastroduodenal diseases]. / Izofermentnyi spektr laktatdegidrogenazy slizistoi obolochki zheludka kak rannii marker vozmozhnoi onkopatologii u detei s khronicheskimi gastroduodenal'nymi zabolevaniiami.

The lactate dehydrogenase (LDH) isoenzyme profile was studied in bioptic samples of gastric mucosa taken from 57 infantile patients suffering from chronic gastroduodenal pathology and 7 children with gastric functional disorders. The investigation showed LDH1 level to decrease and that of LDH5 to increase, the LDH5/LDH1 ratio increasing accordingly, in cases of erosive gastro-like gastroduodenitis and duodenal ulcers. The degree of said changes was found to correlate with the extent of morphological lesions of gastric mucosa and the most pronounced changes were recorded in cases of gastric mucosa gland atrophy. Similar changes in LDH isoenzyme profile had been identified in patients with gastric tumors. Said findings may be used in identification of groups at high risk for gastric carcinoma.