Mitochondrial Dysfunction, Oxidative Stress and Premature Aging in Children With Nutritional Rickets.

OBJECTIVES

To assess the mitochondrial dysfunction, oxidative stress and premature aging in children with nutritional rickets.

METHODS

This cross-sectional study enrolled children aged 6 months - 5 years with nutritional rickets attending a tertiary care hospital between January 2021 and August 2022. Mitochondrial dysfunction, oxidative stress and premature aging were assessed by measuring the mitochondrial DNA (mtDNA) content, total antioxidant status (TAOS) and telomere length (TL) in 40 children with nutritional rickets and 40 age- and sex- matched healthy children without rickets (controls).

RESULTS

The median (IQR) mtDNA content was significantly higher in children with rickets as compared to controls [152.27 (111.83, 218.66) vs 93.7 (72.5, 134.14); P < 0.001], implying mitochondrial dysfunction attributed to increased mitochondrial biogenesis in children with rickets. The median (IQR) TAOS ( mM Trolox equiv.) was significantly lower in children with rickets than controls [4.54 (3.93, 5.73) vs 7.86 (5.09, 9.58); P < 0.001)]. The median (IQR) TL in cases was significantly longer in children with rickets compared to controls [417.31 (111.83,218.66) vs 93.7 (72.5,134.14); P < 0.001] implying that children with rickets do not have premature aging.

CONCLUSIONS

Children with rickets have high oxidative stress and mitochondrial dysfunction but no evidence of premature aging.