RESUMO
OBJECTIVE: To assess the mitochondrial dysfunction, oxidative stress and premature aging in children with nutritional rickets. METHODS: This cross-sectional study enrolled children between 6 months - 5 years of age with nutritional rickets attending a tertiary care hospital between 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 was significantly lesser 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. CONCLUSION: Children with rickets have high oxidative stress and mitochondrial dysfunction but no evidence of premature aging.
