Dipanwita Saha1, Mohit Mehndiratta2, Dheeraj Shah1, Piyush Gupta3. 1. Department of Pediatrics, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi, 110095, India. 2. Department of Biochemistry, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi, India. 3. Department of Pediatrics, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi, 110095, India. prof.piyush.gupta@gmail.com.
Abstract
OBJECTIVES: To assess oxidative stress, mitochondrial dysfunction, and premature ageing in children with severe acute malnutrition (SAM). METHODS: This cross-sectional study was conducted in children (1 mo-5 y) with SAM (defined as per WHO criteria) presenting to Pediatrics inpatient department. Oxidative stress, mitochondrial dysfunction, and premature ageing were assessed by measuring and comparing total antioxidant status (TAOS), mitochondrial DNA (mtDNA) content, and telomere length (TL), respectively in 40 under-five children with SAM and 40 age- and sex-matched non-malnourished controls. RESULTS: Oxidative stress was significantly increased in children with SAM, reflected by lower median (IQR) TAOS in cases as compared to controls [10.78 (9.08, 12.3) vs. 16.63 (15.20, 18.03) mM Trolox, p < 0.001]. Median (IQR) mtDNA content was significantly increased in children with SAM [188.7 (105.2, 398.9) vs. 116.2 (67.2, 154.6), p < 0.001]. There was no significant difference in telomere length between cases and controls [1184.5 (894, 1408) vs.1082.6 (823.3, 1479), p = 0.747]. CONCLUSION: Children with SAM had significantly increased oxidative stress that possibly caused mitochondrial dysfunction but no premature ageing.
OBJECTIVES: To assess oxidative stress, mitochondrial dysfunction, and premature ageing in children with severe acute malnutrition (SAM). METHODS: This cross-sectional study was conducted in children (1 mo-5 y) with SAM (defined as per WHO criteria) presenting to Pediatrics inpatient department. Oxidative stress, mitochondrial dysfunction, and premature ageing were assessed by measuring and comparing total antioxidant status (TAOS), mitochondrial DNA (mtDNA) content, and telomere length (TL), respectively in 40 under-five children with SAM and 40 age- and sex-matched non-malnourished controls. RESULTS: Oxidative stress was significantly increased in children with SAM, reflected by lower median (IQR) TAOS in cases as compared to controls [10.78 (9.08, 12.3) vs. 16.63 (15.20, 18.03) mM Trolox, p < 0.001]. Median (IQR) mtDNA content was significantly increased in children with SAM [188.7 (105.2, 398.9) vs. 116.2 (67.2, 154.6), p < 0.001]. There was no significant difference in telomere length between cases and controls [1184.5 (894, 1408) vs.1082.6 (823.3, 1479), p = 0.747]. CONCLUSION: Children with SAM had significantly increased oxidative stress that possibly caused mitochondrial dysfunction but no premature ageing.