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Total glutathione is not decreased in infants with necrotizing enterocolitis
Nigel J Hall1, Jamal Ali, Agostino Pierro
1Department of Paediatric Surgery, Institute of Child Health and Great Ormond Street Hospital for Children NHS Trust, WC1N 1EH London, UK.
Insights
Infants with necrotizing enterocolitis (NEC) do not have lower erythrocyte glutathione (GSH) levels than controls. A relative deficiency in antioxidant compounds, not an absolute one, may contribute to NEC development in infants.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Pediatric Surgery
Background:
- Glutathione (GSH) is a primary intracellular antioxidant crucial for combating free radical damage.
- Oxidative stress is a key factor in necrotizing enterocolitis (NEC) pathogenesis.
- A potential GSH deficiency could exacerbate NEC-related damage.
Purpose of the Study:
- To investigate erythrocyte glutathione (GSH) levels in infants diagnosed with necrotizing enterocolitis (NEC).
- To compare GSH levels in NEC infants with those of a control group.
Main Methods:
- Erythrocyte GSH concentration was measured per gram of hemoglobin (g Hb) in blood samples.
- Samples were obtained from 16 infants with NEC requiring surgery and 10 nonseptic control infants.
Main Results:
- No significant difference in mean erythrocyte GSH levels was observed between infants with NEC (0.076 ± 0.004 μmol/g Hb) and controls (0.078 ± 0.005 μmol/g Hb).
- GSH levels did not correlate with weight, gestational age, or C-reactive protein.
- No differences in GSH levels were found based on NEC disease stage or patient survival, though a trend toward lower levels in more extensive disease was noted.
Conclusions:
- Total erythrocyte glutathione (GSH) levels are comparable between infants with NEC and control infants.
- The findings suggest that a relative, rather than absolute, deficiency in antioxidant compounds may play a role in NEC development.
Background:
Glutathione (GSH) is the major intracellular antioxidant protecting against free radical-mediated damage. Oxidative stress is implicated in the pathogenesis of necrotizing enterocolitis (NEC), and damage could be enhanced by a relative deficiency of GSH. We hypothesized that infants with NEC would have lower levels of erythrocyte GSH when compared with controls.
Methods:
Total erythrocyte GSH concentration (per gram of hemoglobin [g Hb]) was determined in blood samples from infants with NEC (n = 16) referred for surgical intervention. Nonseptic infants referred for other conditions (eg, patent ductus arteriosus ligation) served as controls (n = 10).
Results:
Controls and infants with NEC were demographically similar. Mean erythrocyte GSH concentration in infants with NEC was 0.076 +/- 0.004 micromol/g Hb and in controls it was 0.078 +/- 0.005 micromol/g Hb (P = .73). There was no significant correlation between GSH concentration and weight, gestational age, or C-reactive protein levels. In infants with NEC, there was no difference in GSH levels between infants with stage 2 and stage 3 diseases nor between those who died and survived, but a trend toward lower GSH levels in infants with more extensive diseases exists.
Conclusions:
Total GSH levels are similar in infants with NEC and controls. It is possible that a relative rather than absolute deficiency of antioxidant compounds exists and may contribute to the development of NEC.
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