Daily Oral Supplementation with 60 mg of Elemental Iron for 12 Weeks Alters Blood Mitochondrial DNA Content, but Not Leukocyte Telomere Length in Cambodian Women.

There is limited evidence regarding the potential risk of untargeted iron supplementation, especially among individuals who are iron-replete or have genetic hemoglobinopathies. Excess iron exposure can increase the production of reactive oxygen species, which can lead to cellular damage. We evaluated the effect of daily oral supplementation on relative leukocyte telomere length (rLTL) and blood mitochondrial DNA (mtDNA) content in non-pregnant Cambodian women (18-45 years) who received 60 mg of elemental iron as ferrous sulfate ( = 190) or a placebo ( = 186) for 12 weeks.

Optimization of a Relative Telomere Length Assay by Monochromatic Multiplex Real-Time Quantitative PCR on the LightCycler 480: Sources of Variability and Quality Control Considerations.

Telomere length (TL) measurement is central to many biomedical research, population, and epidemiology studies, with promising potential as a clinical tool. Various assays are used to determine TL, depending on the type and size of the sample. We describe the detailed optimization of a monochromatic multiplex real-time quantitative PCR (MMqPCR) assay for relative TL using the LightCycler 480.

Blood and dried blood spot telomere length measurement by qPCR: assay considerations.

Measurement of telomere length is crucial for the study of telomere maintenance and its role in molecular pathophysiology of diseases and in aging. Several methods are used to measure telomere length, the choice of which usually depends on the type and size of sample to be assayed, as well as cost and throughput considerations. The goal of this study was to investigate the factors that may influence the reliability of qPCR-based relative telomere length measurements in whole blood.

Longitudinal effects of thymidine analogues on mtDNA, mtRNA and multidrug resistance (MDR-1) induction in cultured cells.

Objectives: HIV nucleoside reverse transcriptase inhibitors (NRTIs) can cause mitochondrial toxicity. In spite of several studies performed on cells, little is known about their long-term effects on mitochondrial DNA (mtDNA), mitochondrial gene expression (mtRNA) and cellular protective mechanisms that such exposure may trigger. Our aim was to investigate the longitudinal effects of two thymidine analogue NRTIs, zidovudine and stavudine, on human cells, measuring their effects on the levels of mtDNA, mtRNA and on induction of the multidrug resistance (MDR) gene MDR-1.