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Abstract Details

Development of a minimally invasive muscle O2 nanosensor for Mitochondrial Myopathy
General Neurology
S32 - General Neurology: Advances in Neurology: From the Clinic to the Bench (4:58 PM-5:09 PM)
009
An opportunity for in vivo intramuscular measurements of oxygen (O2) levels in Mitochondrial Myopathy (MM) patients has not previously been possible.  In MM, compromised mitochondrial oxidative phosphorylation (OXPHOS) function results in elevation of whole body and tissue O2 levels.

We report results of a pre-clinical study to test the safety and efficacy of a prototype O2 sensor to quantify muscle O2 levels at rest and after exercise in an MM mouse model.

We have fabricated and characterized a prototype Clark-type O2 nanosensor that was manually inserted in gluteus muscle of MM mice under isoflurane (1.5%) anesthesia within 90 seconds from completion of 20 minutes of treadmill-exercise.  Specific mice studied included control C57BL/6J mice and MM mice homoplasmic for an MT-ND6 complex I subunit mutation.

The partial pressure of muscle O2 in control (C57BL/6J) mice measured by other techniques was reported to be 50 Torr (Reinke, 1985).  Prior to and after in vivo measurement in gluteal muscle, nanosensor measurement in room air (21% O2) was obtained and confirmed to be ~160 Torr.  In control (C57BL/6J) mice, sedentary and exercised muscle O2 levels, respectively, were 33.97 ± 3.3 Torr and 39.1 ± 4.05 Torr (n=8 each).  In MT-ND6 mutant mice, muscle O2 levels were 37.5 ± 2.8 Torr when sedentary (n=5) and 73.5 ± 0.7 Torr following treadmill-exercise (n=3).

MT-ND6 mutant mice have a significant increase in muscle O2 levels following moderate exercise, but not at sedentary baseline. This is the first study to directly confirm elevated muscle O2 levels in MM mice, modeling similar observations in human MM subjects previously made by other techniques (Bank, 1994).  These preliminary results demonstrate the feasibility and efficacy of our prototype O2 nanosensor to accurately measure muscle O2 levels and distinguish MM from healthy controls in exercised mice.

 

Authors/Disclosures
Zarazuela Zolkipli-Cunningham, MBChB (The Children's Hospital of Philadelphia, Human Genetics)
PRESENTER
Dr. Zolkipli-Cunningham has nothing to disclose.
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
Marni Falk No disclosure on file