Related Experiment Video
Updated: May 28, 2026

An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model
Published on: March 9, 2022
Novel large-range mitochondrial DNA deletions and fatal multisystemic disorder with prominent hepatopathy
Marzia Bianchi1, Teresa Rizza, Daniela Verrigni
1Unit of Molecular Medicine for Neuromuscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, Rome, Italy.
Insights
Mitochondrial DNA deletions can cause multisystem disorders with liver failure in infants. Diagnosis is possible using blood or skin cells, expanding knowledge of mitochondrial genome deletions.
Area of Science:
- Genetics
- Biochemistry
- Pediatrics
Background:
- Mitochondrial cytopathies rarely cause liver issues in adults but are common in children.
- Multiple OXPHOS enzyme defects and reduced mtDNA are often seen in children with liver involvement.
Observation:
- Two infants with multisystem disorders and hepatopathy were studied.
- Novel large-scale mitochondrial DNA (mtDNA) deletions were identified in these infants.
- Highest levels of deleted mtDNA were found in liver, kidney, and pancreas tissues.
Findings:
- mtDNA deletions were detected in cultured skin fibroblasts and blood samples.
- Biochemical analysis revealed impaired complex I enzyme activity.
- The study identified novel mtDNA deletions associated with childhood-onset liver failure.
Implications:
- Less invasive samples like blood or fibroblasts can aid molecular diagnosis in children.
- This research expands the known spectrum of mtDNA deletions linked to liver failure.
- mtDNA analysis should be considered for diagnosing childhood-onset hepatopathies.
Abstract:
Hepatic involvement in mitochondrial cytopathies rarely manifests in adulthood, but is a common feature in children. Multiple OXPHOS enzyme defects in children with liver involvement are often associated with dramatically reduced amounts of mtDNA. We investigated two novel large scale deletions in two infants with a multisystem disorder and prominent hepatopathy. Amount of mtDNA deletions and protein content were measured in different post-mortem tissues. The highest levels of deleted mtDNA were in liver, kidney, pancreas of both patients. Moreover, mtDNA deletions were detected in cultured skin fibroblasts in both patients and in blood of one during life. Biochemical analysis showed impairment of mainly complex I enzyme activity. Patients manifesting multisystem disorders in childhood may harbour rare mtDNA deletions in multiple tissues. For these patients, less invasive blood specimens or cultured fibroblasts can be used for molecular diagnosis. Our data further expand the array of deletions in the mitochondrial genomes in association with liver failure. Thus analysis of mtDNA should be considered in the diagnosis of childhood-onset hepatopathies.
More Related Videos
07:24Genotyping Single Nucleotide Polymorphisms in the Mitochondrial Genome by Pyrosequencing
Published on: February 10, 2023
06:53Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry
Published on: November 23, 2011
Related Concept Videos
Animal Mitochondrial Genetics
Inborn Errors of Metabolism
Lysosomal Hydrolases
Hepatic Encephalopathy
Huntington Disease l: Introduction
Lethal Alleles
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...