The Effect of Antioxidant Supplementation in Intravenous Nutrition on Gastrointestinal Health in a Neonatal Piglet Model

Lay Summary 
Intravenous (IV) nutrition is a lifesaving tool used by clinicians to treat premature infants. However, the use of IV nutrition presents with adverse consequences including changes to the structure and function of the intestinal tract. This subsequently reduces the infant's ability to absorb nutrients from the diet once normal feeding into the gastrointestinal (GI) tract is resumed. The loss of GI function is due in part to a decrease in blood flow to the intestinal tract during IV nutrition. Blood flow is regulated by a compound called nitric oxide (NO), so greater availability of NO may help sustain blood flow during IV feeding. However, IV feeding introduces pro-oxidant compounds that contribute to tissue damage and cell death. NO is known to react with pro-oxidant compounds and the resultant compound, peroxynitrite, can also cause tissue damage. These negative effects must be mitigated by the infant's own antioxidant system. Glutathione is the compound within the antioxidant system that reacts with the pro-oxidant compounds. In premature infants, this glutathione system is under-developed and unable to overcome the production and presence of these pro-oxidant compounds. In this study, we will be using newborn piglets that are supported with IV nutrition supplemented with glutathione (versus un-supplemented). We predict that the addition of glutathione will enhance antioxidant capabilities which in turn, will protect NO so it can function as a blood flow regulator rather than contributing to oxidative tissue damage. Glutathione supplementation is potentially an innovative method of reducing intestinal injury caused by oxidative damage and poor intestinal blood flow, and could be applied clinically to aid in the survival and growth of premature infants. 


Canadian Institute For Health Research
Newfoundland and Labrador
Industry Sectors 
Health Care and Social Assistance
Start date 
1 Sep 2019
End date 
31 Dec 2020