Search PubMed⌕ Search

PubMed · 12821823

Tests for mitochondrial function and DNA: potentials and pitfalls.

Abstract

PURPOSE OF REVIEW: In the past few years, mitochondria have been carefully studied to ascertain whether and how in patients affected by HIV antiretroviral therapy is able to alter their functionality and exert a toxic effect on immune cells, as well as on cells present in other districts. RECENT FINDINGS: A variety of in-vivo and ex-vivo models have been developed to investigate the functionality of mitochondria and DNA during a variety of physiopathological situations, including HIV infection and its treatment. Numerous technologies are available to study at the single-cell or at the single-organelle level a variety of parameters, such as membrane potential, the activity of respiratory chain enzymes, and DNA content or its sequence. As far as in-vitro studies are concerned, a substantial homogeneity of data exists, and several changes in different mitochondrial parameters have been described that depend upon the drug used, the cell model and the parameter investigated. On the other hand, different results have been reported on biological material collected from HIV-positive patients and immediately analysed. Ex-vivo studies showed that changes in mitochondrial DNA content or in the functionality of the organelle exist in some tissues or cells, but not in others. SUMMARY: One of the possible causes of the discrepancies is the technologies used to investigate mitochondria, and this paper summarizes some of the pros and cons of the main methods used to study mitochondrial function or DNA.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Andrea Cossarizza. 2003. Tests for mitochondrial function and DNA: potentials and pitfalls.. https://doi.org/10.1097/00001432-200302000-00002

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

A previously undescribed leukodystrophy in Leigh syndrome associated with T9176C mutation of the mitochondrial ATPase 6 gene.

We report two male Taiwanese siblings in whom the T-->C point mutation at nucleotide 9176 of the mitochondrial ATPase 6 gene (m.9176T>C mutation) was associated with early onset hypotonia, lactic acidosis, and death due to respiratory arrest at 7 and 10 months old. Brain MRI showed lesions over diffuse white matter and the bilateral posterior limbs of the internal capsule. The m.9176T>C mutation is suggested as the cause of the bilateral striatal necrosis and Leigh syndrome. However, leukodystrophy in Leigh syndrome associated with m.9176T>C mutation has never been reported before. We suggest that m.9176T>C mutation could be a new aetiology for leukodystrophy in children with Leigh syndrome.

Acidosis, Lactic↗

Lactic acidosis in children with acute exacerbation of severe asthma.

This is a retrospective case series reporting lactic acidosis in four pediatric patients with acute severe asthma treated with nebulized beta2-agonists in a pediatric intensive care unit of a tertiary care teaching facility. During treatment with beta2-agonists, these patients developed lactic acidosis with a peak concentration of 5.2 to 13 mmol/l. Lactic acidosis improved within 24 h after discontinuation or decrease in the dosage of beta2-agonists. We conclude that the intensive use of beta2-agonists for acute severe asthma in children may be the primary and significant cause of lactic acidosis.

Acidosis, Lactic↗