Abstract
Hydrogen sulphide (H2S) is produced endogenously via two enzymes dependent on pyridoxal phosphate (PLP): cystathionine beta-synthase (CBS, EC 4.2.1.22), cystathionase γ-liase (CTH, EC 4.4.1.1), and a third, 3-mercaptopyruvate sulfurtransferase (MPST, EC 2.8.1.2). H2S strengthens the defence mechanisms of the gastric mucosal barrier, and plays an important role in gastroprotection, including the increased resistance to damage caused by various irritants and non-steroidal anti-inflammatory drugs. The study was conducted to determine the role of H2S in ulcerated gastric mucosa of rats caused by immobilization in cold water (WRS). The activity and expression of γ-cystathionase, cystathionine β-synthase, 3-mercaptopyruvate sulfurtransferase, and rhodanese was compared with healthy mucosa, together with H2S generation, and cysteine, glutathione, and cystathionine levels. The results showed that the defence mechanism against stress is associated with stimulation of the production of H2S in the tissue and confirmed the observed advantageous effect of H2S on healing of gastric ulcers. In case of animals pretreated with exogenous sources of H2S and NaHS, and some changes observed in the ulcerated gastric mucosa tend to return to values found in the healthy tissue, a finding that is in accordance with the previously determined gastroprotective properties of H2S. The results presented in this paper point to the possible role of rhodanese in H2S production in the gastric mucosa of rats, together with the earlier mentioned three enzymes, which are all active in this tissue.
Highlights
The gastrointestinal tract is exposed to various substances and factors which often cause gastric mucosal damage
The results showed an increased production of H2S, administered to animals before Water immersion restraint stress (WRS), resulted in the reversion of some investigated of hydrogen sulphide (H2 S) as a defence against damage of the gastric mucosa caused by WRS
The results presented in this paper show that the defence against WRS-induced gastric mucosal lesions includes the acceleration of endogenous H2 S formation
Summary
The gastrointestinal tract is exposed to various substances and factors which often cause gastric mucosal damage. Long-term exposure to these factors, or to stress, can result in pathological inflammation, such as erosions, haemorrhages, or ulcers. An important role in maintaining the integrity of the gastric mucosa is played by hydrogen sulphide (H2 S). H2 S is produced from L-cysteine enzymatically in pathways involving three enzymes: cystathionine β-synthase (CBS, EC 4.2.1.22), cystathionine γ-lyase (CTH, EC 4.4.1.1), and 3-mercaptopyruvate sulfurtransferase (MPST EC 2.8.1.2). CBS and CTH are enzymes dependent on pyridoxal phosphate (PLP). The MPST reaction converts 3-mercaptopyruvate produced from cysteine in a PLP-dependent transamination reaction (Scheme 1). CBS produces cystathionine and H2 S from L-cysteine or homocysteine
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