Hydrogen sulfide formation in experimental model of acute pancreatitis

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Abstract

Acute pancreatitis (AP) is a disease defined as acute or chronic inflammatory process of the pancreas characterized by premature activation of digestive enzymes within the pancreatic acinar cells and causing pancreatic auto-digestion. In mammalian tissues, H2S is synthesized endogenously from L-cysteine in regulated enzymatic pathways catalyzed by pyridoxal phosphate-dependent enzymes: cystathionine beta-synthase (CBS), gammacystathionase (CTH) and cysteine aminotransferase (CAT) coupled with 3-mercaptopyruvate sulfurtransferase (MPST). In the mitochondria, hydrogen sulfide is oxidized to sulfite, which is then converted to thiosulfate (a sulfane sulfur-containing compound) by thiosulfate sulfurtransferase (rhodanese; TST). Activity and expression of CBS, CTH, MPST, and TST have been determined in vivo in pancreas of the control rats, rats with acute pancreatitis and a sham group. Levels of low-molecular sulfur compounds, such as the reduced and oxidized glutathione, cysteine, cystine and cystathionine, were also determined. This study revealed a significant role of MPST in H2S metabolism in the pancreas. Stress caused by the surgery (sham group) and AP cause a decrease in H2S production associated with a decrease in MPST activity and expression. Markedly higher level of cysteine in the AP pancreas may be caused by a reduced rate of cysteine consumption in a reaction catalyzed by MPST, but it can also be a sign of proteolytic processes occurring in the changed tissue.

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Bronowicka-Adamska, P., Hutsch, T., Gawrys-Kopczynska, M., Maksymiuk, K., & Wróbel, M. (2019). Hydrogen sulfide formation in experimental model of acute pancreatitis. Acta Biochimica Polonica, 66(4). https://doi.org/10.18388/ABP.2019_2900

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