{"title":"营养性佝偻病儿童的线粒体功能障碍、氧化应激和早衰。","authors":"Raaj Lakshmi, - Aaradhana, Mohit Mehndiratta, Dheeraj Shah, Piyush Gupta","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>To assess the mitochondrial dysfunction, oxidative stress and premature aging in children with nutritional rickets.</p><p><strong>Methods: </strong>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).</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>Children with rickets have high oxidative stress and mitochondrial dysfunction but no evidence of premature aging.</p>","PeriodicalId":13291,"journal":{"name":"Indian pediatrics","volume":" ","pages":"750-755"},"PeriodicalIF":1.7000,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Mitochondrial Dysfunction, Oxidative Stress and Premature Aging in Children With Nutritional Rickets.\",\"authors\":\"Raaj Lakshmi, - Aaradhana, Mohit Mehndiratta, Dheeraj Shah, Piyush Gupta\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>To assess the mitochondrial dysfunction, oxidative stress and premature aging in children with nutritional rickets.</p><p><strong>Methods: </strong>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).</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>Children with rickets have high oxidative stress and mitochondrial dysfunction but no evidence of premature aging.</p>\",\"PeriodicalId\":13291,\"journal\":{\"name\":\"Indian pediatrics\",\"volume\":\" \",\"pages\":\"750-755\"},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-08-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Indian pediatrics\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/6/7 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"PEDIATRICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Indian pediatrics","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/7 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PEDIATRICS","Score":null,"Total":0}
引用次数: 0
摘要
目的:评估营养性佝偻病患儿的线粒体功能障碍、氧化应激和早衰:评估营养性佝偻病患儿的线粒体功能障碍、氧化应激和早衰:这项横断面研究招募了 2021 年 1 月至 2022 年 8 月期间在一家三级医院就诊的 6 个月至 5 岁营养性佝偻病患儿。通过测量40名营养性佝偻病患儿和40名年龄和性别匹配的非佝偻病健康儿童(对照组)的线粒体DNA(mtDNA)含量、总抗氧化状态(TAOS)和端粒长度(TL),对线粒体功能障碍、氧化应激和早衰进行评估:与对照组相比,佝偻病患儿mtDNA含量的中位数(IQR)明显升高[152.27(111.83,218.66) vs 93.7(72.5,134.14);P <0.001],这意味着佝偻病患儿线粒体生物生成增加导致线粒体功能障碍。佝偻病患儿的 TAOS 中位数(IQR)明显低于对照组 [4.54 (3.93, 5.73) vs 7.86 (5.09, 9.58); P < 0.001]。与对照组相比,佝偻病患儿的病例TL中位数(IQR)明显更长[417.31 (111.83,218.66) vs 93.7 (72.5,134.14); P < 0.001],这意味着佝偻病患儿不会过早衰老:结论:佝偻病儿童的氧化应激和线粒体功能障碍较高,但没有早衰的迹象。
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.
期刊介绍:
The general objective of Indian Pediatrics is "To promote the science and practice of Pediatrics." An important guiding principle has been the simultaneous need to inform, educate and entertain the target audience. The specific key objectives are:
-To publish original, relevant, well researched peer reviewed articles on issues related to child health.
-To provide continuing education to support informed clinical decisions and research.
-To foster responsible and balanced debate on controversial issues that affect child health, including non-clinical areas such as medical education, ethics, law, environment and economics.
-To achieve the highest level of ethical medical journalism and to produce a publication that is timely, credible and enjoyable to read.