Oral Phosphatidylcholine Pretreatment Decreases Ischemia-Reperfusion-Induced Methane Generation and the Inflammatory Response in the Small Intestine

Abstract

We have shown that phosphatidylcholine (PC) metabolites may have a function in counteracting the production of reactive oxygen species (ROS), and that this mechanism can lead to the generation of methane from choline. The aims were to establish whether the dietary administration of PC can protect the reperfused small bowel mucosa by its acting as an anti-inflammatory agent and to investigate this possibility in association with in vivo methane generation. Group 1 (n = 5) of anesthetized dogs served as sham-operated controls, whereas in groups 2 (n = 6) and 3 (n = 6), complete small intestinal ischemia was induced by occluding the superior mesenteric artery for 60 min. Groups 1 and 2 were fed with normal laboratory chow for 1 week before the experiments, whereas the animals in group 3 received a special diet containing 1% soybean PC. The intramucosal pH and the difference of the arterial and local PCO2 (PCO2 gap) were detected by indirect tonometry. Intestinal superoxide production and myeloperoxidase (MPO) activity (a marker of tissue leukocyte infiltration) were ascertained on ileal biopsy samples 180 min after reperfusion. The content of methane in the exhaled air was determined by gas chromatography. I/R was characterized by significant tissue acidosis with ROS generation and elevated MPO activity. These changes were accompanied by increased methane production in the exhaled air during reoxygenation. The PC-enriched diet prevented the decrease in intramucosal pH, diminished the intestinal superoxide generation and the MPO activity, and significantly decreased the exhaled methane concentration. The increased dietary uptake of PC exerts an anti-inflammatory influence in the gastrointestinal tract. Exhaled methane is linked to abnormal ROS generation; a decreased methane production is associated with significantly reduced inflammatory activation during I/R.

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

“…Several techniques are available to study the microcirculation of the intestine. Deteriorations of the intestinal microcirculation can be assessed indirectly by analyzing tissue oxygenation with Clark electrodes or by monitoring intramucosal pH (pHi) and pCO 2 (PiCO 2 ) using tonometry [17][18][19][20]. In addition, tissue reflectance spectrophotometry may give information on microvascular hemoglobin oxygen saturation (HbO 2 ) and Laser Doppler velocimetry can assess relative changes of microvascular blood perfusion [21,22].…”

A novel pathway of direct methane production and emission by eukaryotes including plants, animals and fungi: An overview

“…Then, the methyl group splits off with the generation of CH 4 , and NADH is oxidised to NAD þ (Table 1). It is also important to note that the dietary administration of phosphatidylcholine can have a protective function during intestinal ischaemiaereperfusion injury by acting as an anti-inflammatory agent with a significantly decreased concentration of exhaled CH 4 (Ghyczy et al, 2008b). Acting as the most bioavailable choline source in various tissues (Bauernschmitt and Kinne, 1993), L-aglycerylphosphorylcholine treatment lowered the CH 4 production level during hypoxia-induced injuries in rat cells (Tuboly et al, 2013b).…”

l-Alpha Glycerylphosphorylcholine as a Potential Radioprotective Agent in Zebrafish Embryo Model

“…12,18 GPC has exhibited protective activity in different experimental models against damage occurring due to inflammatory reaction. 19 Experiments of T} okés et al 20 and Ghyczy et al 21 have shown PC to be effective in stopping the production of reactive oxygen species both in vitro and in vivo and may exhibit anti-inflammatory properties.…”