Superoxide dismutases in chronic gastritis.

Human gastric diseases have shown significant changes in the activity and expression of superoxide dismutase (SOD) isoforms. The aim of this study was to detect Mn-SOD activity and expression in the tissue of gastric mucosa, primarily in chronic gastritis (immunohistochemical Helicobacter pylori-negative gastritis, without other pathohistological changes) and to evaluate their possible connection with pathohistological diagnosis. We examined 51 consecutive outpatients undergoing endoscopy for upper gastrointestinal symptoms. Patients were classified based on their histopathological examinations and divided into three groups: 51 patients (archive samples between 2004-2009) with chronic immunohistochemical Helicobacter pylori-negative gastritis (mononuclear cells infiltration were graded as absent, moderate, severe) divided into three groups. Severity of gastritis was graded according to the updated Sydney system. Gastric tissue samples were used to determine the expression of Mn-SOD with anti-Mn-SOD Ab immunohistochemically. The Mn-SOD expression was more frequently present in specimens with severe and moderate inflammation of gastric mucosa than in those with normal mucosa. In patients with normal histological finding, positive immunoreactivity of Mn-SOD was not found. Our results determine the changes in Mn-SOD expression occurring in the normal gastric mucosa that had undergone changes in the intensity of chronic inflammatory infiltrates in the lamina propria.

Role of zinc in chronic gastritis.

Oxidative stress occurs in inflammation of gastric mucosa. The role of zinc in modulating oxidative stress has recently been recognized. Zn deficiency results in an increased sensitivity to oxidative stress and have a higher risk of musoca damage in inflammation. The aim of this study was to determine wheather chronic inflammation affects on the concentration of Zn2+ ions in gastric mucosa of patients with chronic gastritis. Forthy-three patients with chronic gastitis were enrolled. Patients were endoscoped. Histology and scoring of gastritis was performed following the guidelines of the updated Sydney system. Endoscopic finding of mucosa were scored according to a Lanza scoring system. The diagnosis of Helicobacter pylori (H. pylori) infection, histopathologic changes, intensity of inflammation and zinc concentration were determined from biopsies of gastric mucosa. The atomic absorption spectrophotometer was used to determine tissue concentrations of zinc. Twenty of 43 patients with chronic gastritis were uninfected by H. pylori. There was no statistically significant difference in tissue concentrations of zinc between H. pylori-positive and H. pylori-negative patients. From those infected patients 53.3% had chronic active gastritis. There was no statistically significant difference in tissue concentrations of zinc between patients with chronic active gastritis and patients with chronic inactive gastritis (p = 0.966). Zn in antrum showed positive correlation with density of H. pylori in antrum (Spearman' rho = 0.481, p = 0.020), negative correlation with density of H. pylori in corpus (Spearman' rho = -0.492, p = 0.017) and with zinc in corpus (Spearman' rho = 0.631, p =0.001). Tissue concentration of zinc was not affected by chronic inflammation of gastric mucosa in patients with chronic gastritis.

Helicobacter pylori and trace elements.

The metabolism of the trace elements is altered in infection or inflammation. Helicobacter pylori infection is a causative in chronic gastritis, duodenal ulcer disease and gastric cancer. It is not known whether H. pylori infection is associated with the changes in the serum levels of trace elements. The aim of this study was to determine serum concentrations of zinc and copper, using atomic absorption spectrophotometer, in patients with H. pylori positive chronic gastritis, patients with H. pylori negative chronic gastritis and healthy individuals. Serum Zn was significantly higher in patients with H. pylori positive chronic gastritis compared to both patients with H. pylori negative chronic gastritis and to healthy individuals, while serum Cu and Cu/Zn ratio was not significantly different in any study group. The serum zinc and copper concentrations were not altered in patients with chronic gastritis.

[The role of zinc in the treatment of hyperactivity disorder in children]. / Uloga cinka u lijecenju hiperaktivnog poremecaja u djece.

Zinc is an essential cofactor of more than 100 enzymes, including metalloenzymes and metalloenzyme complexes, which are necessary in the metabolism of carbohydrates, fatty acids, proteins and nucleic acids. It is an important factor in the metabolism of neurotransmitters, prostaglandins, and for maintaining brain structure and function. Dopamine is one of the most important factors in the pathophysiology of hyperactivity disorder, and the hormone melatonin has an important role in the regulation of dopamine. Because zinc is necessary in the metabolism of melatonin, it can be assumed that zinc is a very important factor in the treatment of attention deficit and hyperactivity disorder (ADHD). It is known that deficit of some minerals and vitamins is connected with hyperkinetic disorder. Preliminary investigations in humans show that many children with ADHD have lower zinc concentration in relation to healthy children. Zinc sulfate as an adjunct to methylphenidate has favorable effects in the treatment of ADHD children, pointing to the possible association of zinc deficit and ADHD pathophysiology. Zinc concentration can only point to some other factors (malnutrition) that can lead to ADHD, but is not a factor that has a causative role in ADHD. Therefore, zinc supplementation to nutrition or to ADHD therapy may be of great benefit in ADHD children with zinc deficit or low plasma zinc concentration. ADHD occurs in different cultures, mostly before seven years of age. In children younger than five years it is difficult to make an accurate diagnosis because their behavior is more variable than in older children. Hyperactive disorder is mostly observed in younger age, i.e. in childhood and adolescence. The majority of the main characteristics are less pronounced or completely lost in adult age. In the 1960s, the disorder was named "minimal cerebral dysfunction" and was most often the consequence of head trauma or low birth weight. Later, the term was changed as hyperactive reaction in childhood. Recent studies estimate its prevalence to three of ten hyperactive children, and there are data that about 4% of children have the complete frame of the disorder. The condition is more common in boys than in girls. The reason probably lies in the fact that girls primarily develop attention disorder and cognitive problems (concentration, memory, thinking), and less often have symptoms of aggressive and impulsive behavior, thus boys being earlier referred for examination. There are many theories about the possible origin of hyperactive disorder, and one of the most widely studied is the theory of the role of dopamine, which is supported by the results of treatment in these children with dopamine agonists like methylphenidate and amphetamines. Recent studies do not neglect the influence of maternal intake of food and drink additives, alcohol consumption and smoking during pregnancy, soil contamination, and low birth weight. Zinc is a coenzyme of the enzyme delta-6 desaturase, which is important in the anabolism of polyunsaturated long chain fatty acids, linolic and linolenic acids that constitute neuronal membrane. Studies point to the possible association of zinc deficiency and ADHD pathophysiology. In ADHD children with zinc deficiency or low plasma zinc concentration, zinc dietary supplementation or during therapy for ADHD may be of great benefit. A study of ADHD treatment with zinc sulfate as a supplement to methylphenidate showed beneficial effects of zinc supplementation in the treatment of children with ADHD. The dose of zinc sulfate used was 55 mg/day, which is equivalent to 15 mg zinc. The improvement achieved in ADHD children with the use of zinc sulfate appears to confirm the role of zinc deficiency in the etiopathogenesis of ADHD. Additional studies are needed to identify the real and efficient dose of zinc.