Expression of melatonin synthesizing enzymes in Helicobacter pylori infected gastric mucosa.

Cezary Chojnacki,Russel J Reiter,Grazyna Klupinska,Jan Chojnacki,Janusz Blasiak,Tomasz Popławski

doi:10.1155/2013/845032

Abstract

Helicobacter pylori colonization of gastric mucosa causes pain of unknown etiology in about 15–20% of infected subjects. The aim of the present work was to determine the level of expression of enzymes involved in the synthesis of melatonin in gastric mucosa of asymptomatic and symptomatic H. pylori infected patients. To diagnose H. pylori infection, histological analysis and the urea breath test (UBT C13) were performed. The levels of mRNA expression of arylalkylamine-N-acetyltransferase (AA-NAT) and acetylserotonin methyltransferase (ASMT) were estimated in gastric mucosa with RT-PCR. The level of AA-NAT expression and AMST was decreased in H. pylori infected patients and was increased after H. pylori eradication. We conclude that decreased expression of melatonin synthesizing enzymes, AA-NAT and ASMT, in patients with symptomatic H. pylori infection returns to normal level after H. pylori eradication.

Highlights

Melatonin is a molecule with numerous beneficial properties which is produced both in the pineal gland and in the gastrointestinal tract [1, 2]
The concentration of melatonin may depend on the number of enterochromaffin cells (EC), which are the main source of melatonin in the gastrointestinal tract [2]
We have found no report on the expression of arylalkylamine N-acetyltransferase (AA-NAT) and acetylserotonin methyltransferase (ASMT) in gastric mucosa

Summary

Introduction

Melatonin is a molecule with numerous beneficial properties which is produced both in the pineal gland and in the gastrointestinal tract [1, 2]. Melatonin synthesizing enzymes are found in other organs of mammals [3,4,5,6]. This indoleamine is produced from L-tryptophan in a metabolic pathway shared with serotonin. Reductions in AA-NAT and ASMT expression were observed under similar experimental conditions [15]. This apparent discrepancy may be due to nature and severity of inflammatory changes [8, 16]

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