Mitochondrial Dysfunction, Oxidative Stress and Premature Aging in Children With Nutritional Rickets
Raaj Lakshmi1, - Aaradhana1, Mohit Mehndiratta2
1Department of Pediatrics, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi, India.
Indian Pediatrics
|June 11, 2024
Summary
Children with nutritional rickets exhibit mitochondrial dysfunction and high oxidative stress. However, they do not show signs of premature aging, as indicated by telomere length.
Area of Science:
- Biochemistry
- Pediatrics
- Cell Biology
Background:
- Nutritional rickets is a significant pediatric condition.
- Mitochondrial dysfunction and oxidative stress are implicated in various diseases.
- The relationship between rickets, oxidative stress, and aging is not fully understood.
Purpose of the Study:
- To investigate mitochondrial dysfunction, oxidative stress, and premature aging in children with nutritional rickets.
- To compare markers of these conditions between children with rickets and healthy controls.
Main Methods:
- A cross-sectional study involving 40 children with nutritional rickets and 40 healthy controls (aged 6 months - 5 years).
- Assessment of mitochondrial DNA (mtDNA) content, total antioxidant status (TAOS), and telomere length (TL).
Main Results:
- Children with rickets showed significantly higher mtDNA content, indicating mitochondrial dysfunction.
- Significantly lower TAOS levels in children with rickets suggest increased oxidative stress.
- Telomere length was significantly longer in children with rickets, refuting premature aging.
Conclusions:
- Children with nutritional rickets experience significant mitochondrial dysfunction and oxidative stress.
- Despite these cellular changes, premature aging is not evident in these children.
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