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Donato Lacedonia1, Giovanna E Carpagnano2, Elisabetta Crisetti3

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Obstructive Sleep Apnea (OSAS) patients show increased mitochondrial DNA (MtDNA) damage due to heightened oxidative stress. Intermittent hypoxia appears to be the primary driver of this mitochondrial alteration in OSAS.

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Area of Science:

  • Cellular Biology
  • Sleep Medicine
  • Cardiovascular Research

Background:

  • Obstructive Sleep Apnea (OSAS) is linked to increased cardiovascular risk.
  • OSAS is characterized by intermittent hypoxia (IH), leading to oxidative stress and inflammation.
  • Mitochondria, crucial for cellular respiration, contain their own DNA (MtDNA).

Purpose of the Study:

  • To investigate if oxidative stress in OSAS patients causes mitochondrial DNA (MtDNA) alterations.
  • To assess the relationship between oxidative stress markers and MtDNA levels in OSAS.

Main Methods:

  • Compared 46 OSAS patients with 36 controls, measuring blood cell mitochondrial DNA (MtDNA) and nuclear DNA (nDNA) content via Real Time PCR.
  • Calculated the MtDNA/nDNA ratio.
  • Assessed oxidative stress by measuring Reactive Oxygen Metabolites (ROMs) using the d-ROM test.

Main Results:

  • OSAS patients exhibited a higher MtDNA/nDNA ratio (150.94 ± 49.14) compared to controls (128.96 ± 45.8; p=0.04).
  • Levels of ROMs, indicating oxidative stress, were significantly higher in OSAS subjects (329.71 ± 70.17) than in controls (226 ± 36.76; p=0.04).
  • A positive correlation was found between MtDNA/nDNA ratio and ROMs (R=0.5, p<0.01).

Conclusions:

  • OSAS patients experience mitochondrial DNA damage.
  • Increased oxidative stress in OSAS is a key factor in inducing this MtDNA damage.
  • Intermittent hypoxia is suggested as the primary mechanism driving mitochondrial DNA alterations in OSAS.