The kinetics of glutathione in the gastrointestinal tract of weaned piglets supplemented with different doses of dietary reduced glutathione

Abstract

This study aimed to investigate the kinetics of dietary GSH in the gastrointestinal tract and the effect of GSH on the intestinal redox status of weaned piglets. Forty-eight piglets with an average age of 26 days and an average body weight of 7.7 kg were used in this study. The piglets were divided into three treatment groups including the control group with a basal diet (CON) and two GSH groups with a basal diet supplemented with 0.1% GSH (LGSH) and 1.0% GSH (HGSH), respectively. The basal diet did not contain any GSH. The experiment lasted for 14 days, with eight animals sampled from each group on d5 and 14. The parts of 0–5%, 5–75%, and 75–100% of the length of the small intestine were assigned to SI1, SI2, and SI3. The results showed that GSH almost completely disappeared from the digesta at SI2. However, no difference in the GSH level in mucosa, liver, and blood erythrocytes was found. The level of cysteine (CYS) in SI1 digesta was significantly higher in HGSH than CON and LGSH on d14, and similar findings were observed for cystine (CYSS) in SI3 digesta on d5. The CYSS level in HGSH was also significantly higher than LGSH in the stomach on d14, while no CYS or CYSS was detected in the stomach for control animals, indicating the breakdown of GSH to CYS already occurred in the stomach. Irrespective of the dietary treatment, the CYS level on d14 and the CYSS level on d5 and 14 were increased when moving more distally into the gastrointestinal tract. Furthermore, the mucosal CYS level was significantly increased at SI1 in the LGSH and HGSH group compared with CON on d5. Glutathione disulfide (GSSG) was recovered in the diets and digesta from the LGSH and HGSH group, which could demonstrate the auto-oxidation of GSH. It is, therefore, concluded that GSH supplementation could not increase the small intestinal mucosal GSH level of weaned piglets, and this could potentially relate to the kinetics of GSH in the digestive tract, where GSH seemed to be prone to the breakdown to CYS and CYSS and the auto-oxidation to GSSG.