ArticleIndian journal of pediatrics2022
Oxidative Stress, Mitochondrial Dysfunction, and Premature Ageing in Severe Acute Malnutrition in Under-Five Children.
Article in Indian journal of pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Association between preoperative prognostic nutritional index and postoperative delirium in older adults with hip fractures: a real-world study.Annals of medicine · 2026Article
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidative Stress and Endothelial Dysfunction: The Pathogenesis of Pediatric Hypertension.International journal of molecular sciences · 2025Review
- Relationship between composite dietary antioxidants index and growth indicators in children aged 3-12 years: results from two observational studies.Frontiers in nutrition · 2025Article
- Oxidative Stress in Children and Adolescents: Insights Into Human Biology.American journal of human biology : the official journal of the Human Biology Council · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo assess oxidative stress, mitochondrial dysfunction, and premature ageing in children with severe acute malnutrition (SAM).
methodsThis 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.
resultsOxidative 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].
conclusionChildren with SAM had significantly increased oxidative stress that possibly caused mitochondrial dysfunction but no premature ageing.
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