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Published on: June 27, 2018
Peroxynitrite decomposition catalyst FeTMPyP provides partial protection against intestinal ischemia and reperfusion
Giorgio Stefanutti1, Agostino Pierro, Virpi V Smith
1Units of Paediatric Surgery, Institute of Child Health, London, WC1N 1EH, United Kingdom.
Insights
Peroxynitrite decomposition catalyst FeTMPyP offers limited protection against infant intestinal ischemia-reperfusion (I/R) injury. It reduced inflammation and oxidative stress in the ileum and lungs, preserving antioxidant capacity in neonatal rats.
Area of Science:
- Biomedical Science
- Gastroenterology
- Pediatric Research
Background:
- Free radicals contribute significantly to intestinal ischemia-reperfusion (I/R) injury, causing damage to both the intestines and lungs.
- Understanding the role of reactive oxygen species in I/R injury is crucial for developing therapeutic strategies, especially in vulnerable infant populations.
Purpose of the Study:
- To evaluate the protective effects of the peroxynitrite decomposition catalyst, FeTMPyP, against intestinal I/R injury in a neonatal rat model.
- To investigate the impact of FeTMPyP on key markers of inflammation, oxidative stress, and antioxidant capacity following I/R.
Main Methods:
- Suckling rats were subjected to 40 minutes of intestinal ischemia followed by 90 minutes of reperfusion.
- Animals received either saline or FeTMPyP at the onset of reperfusion.
- Histological injury, ICAM-1, P-selectin, myeloperoxidase, malondialdehyde, and glutathione levels were assessed in the ileum and lungs.
Main Results:
- FeTMPyP administration reduced P-selectin expression, neutrophil infiltration (myeloperoxidase), and lipid peroxidation (malondialdehyde) in the ileum.
- While glutathione levels were decreased in all I/R groups, FeTMPyP treatment led to higher oxidized and total glutathione compared to saline.
- Systemic nitric oxide production (nitrate+nitrite) was elevated in the saline group but not in the FeTMPyP group.
Conclusions:
- FeTMPyP demonstrates limited protective efficacy in neonatal rat intestinal I/R injury.
- The compound mitigates I/R-induced damage by decreasing P-selectin expression, systemic nitric oxide, neutrophil infiltration, and lipid peroxidation.
- FeTMPyP helps preserve intestinal antioxidant capacity, suggesting a potential role in managing I/R-related complications in infants.
Abstract:
Free radicals are important in development of intestinal ischemia-reperfusion (I/R) injury, leading to intestinal and pulmonary damage. We evaluated the effects of peroxynitrite decomposition catalyst FeTMPyP in infant intestinal I/R. Suckling rats underwent 40 min intestinal ischemia + 90 min reperfusion. At reperfusion, animals received saline or FeTMPyP. Groups were (n = 11 per group): 1) control+saline; 2) I/R+saline; 3) I/R+FeTMPyP. Increased histologic injury and ICAM-1 expression were observed in ileum of both I/R+saline and I/R+FeTMPyP rats, but P-selectin expression was increased in I/R+saline animals only versus controls. Myeloperoxidase (neutrophil infiltration marker) was increased in ileum and lungs of I/R+saline rats, but FeTMPyP prevented this in the ileum. I/R+saline animals showed higher malondialdehyde (lipid peroxidation marker) in ileum and lungs versus both control+saline and I/R+FeTMPyP rats. Glutathione was decreased in all I/R animals, but oxidized and total glutathione were higher in I/R+FeTMPyP than the I/R+saline group. Nitrate+nitrite concentration (systemic nitric oxide production) was elevated in I/R+saline but not in I/R+FeTMPyP animals. FeTMPyP provides limited protection against intestinal I/R in neonatal rats by reducing ileal P-selectin expression, systemic nitric oxide production, neutrophil infiltration in ileum and lipid peroxidation in both lungs and ileum; and preserving intestinal antioxidant capacity.
