Effects of N-Acetyl-Cysteine Supplementation through Drinking Water on the Glutathione Redox Status during the Weaning Transition of Piglets.

Jeroen Degroote,Wei Wang,Joris Michiels,Noémie Van Noten,Stefaan De Smet

doi:10.3390/antiox8010024

Abstract

This study investigated the effect of N-acetyl-cysteine (NAC) supplementation through drinking water on animal performance and the glutathione (GSH) redox system in weaned piglets, particularly in relation to the immediate post-weaning feed intake. To this end, 168 piglets were weaned and either fed ad libitum or fasted the first two days, and either or not administered 200 mg/L NAC via the drinking water until d14 post-weaning. Next to animal performance until day 42 (d42), the GSH redox system was measured in erythrocytes, small intestinal mucosa, liver, lung, and kidney tissue at d0, d2, and d14 post-weaning. Animal performance and GSH levels were not affected by NAC, nor by fasting. Irrespective of treatment, a significant drop in GSH at d2 post-weaning was found as compared to d0, in particular in liver (−69%), distal jejunal mucosa (−72%), and lung tissue (−80%). Post-weaning changes of the GSH redox status were strongly tissue-dependent. To conclude, this research indicates that GSH redox homeostasis was largely affected in multiple organs during the weaning transition. NAC supplementation did not increase GSH levels in any tissue, not even in fasted animals, questioning the fact if cysteine is the first or only limiting factor determining the rate of GSH synthesis in the early post-weaning phase.

Highlights

Increasing evidence implicates that weaning triggers the occurrence of oxidative stress and redox imbalance in piglets [1,2]
No animals had to be removed from the study, antibiotic treatments were limited to a few individual intramuscular injections, and no mortality occurred during the experiment
The average fecal consistency score tended to be higher in NAC-supplemented piglets (p = 0.098), where an increase from 1.19 (NAC−) to 1.33 (NAC+) was observed on a scale from 1 to 3

Summary

Introduction

Increasing evidence implicates that weaning triggers the occurrence of oxidative stress and redox imbalance in piglets [1,2]. Cells tightly regulate the synthesis of GSH, which involves two ATP-requiring enzymatic steps. The first and most important step is the γ-linkage of glutamate with cysteine, catalyzed by glutamate cysteine ligase (GCL) This step is considered rate limiting, since cysteine is generally the limiting precursor [8], and since GCL activity is controlled at multiple levels [9]. GSH serves as an electron donor, resulting in the generation of its oxidized counterpart glutathione disulphide (GSSG). An increased GSH/GSSG Eh can be interpreted as a more oxidized cell environment [3]. While almost all mammalian cells can synthesize GSH, its Antioxidants 2019, 8, 24; doi:10.3390/antiox8010024 www.mdpi.com/journal/antioxidants

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