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High-resolution Respirometry to Assess Mitochondrial Function in Permeabilized and Intact Cells
Published on: February 8, 2017
Oxygen sensitivity of mitochondrial function in rat arterial chemoreceptor cells
Keith J Buckler1, Philip J Turner
1Department of Physiology, Anatomy & Genetics, Parks Road, Oxford, UK. keith.buckler@dpag.ox.ac.uk
The Journal of Physiology
|May 15, 2013
Summary
Mitochondria in arterial chemosensory cells show high oxygen sensitivity, challenging previous assumptions. This study reveals their crucial role in sensing oxygen levels, particularly under hypoxic conditions.
Area of Science:
- Cellular Biology
- Physiology
- Neuroscience
Background:
- The mechanism of oxygen sensing in arterial chemoreceptors remains largely unknown.
- Mitochondrial function is often implicated, but its sensitivity to physiological hypoxia is debated.
Purpose of the Study:
- To investigate the oxygen sensitivity of mitochondrial function in neonatal rat type-1 cells.
- To determine if mitochondria in these cells can sense physiological levels of hypoxia.
Main Methods:
- Autofluorescence was used to monitor mitochondrial NADH levels.
- Rhodamine 123 was used to measure mitochondrial membrane potential (Δψm).
- Specific inhibitors and electron donors were employed to assess cytochrome oxidase activity.
Main Results:
- Mitochondrial NADH increased in hypoxia with a P50 of 15 mm Hg.
- Hypoxia depolarized Δψm with P50 values between 2.8 and 3.3 mm Hg.
- Cytochrome oxidase activity was inhibited by hypoxia (P50 = 2.6 mm Hg), while NADH, electron transport, and cytochrome oxidase in sympathetic neurons were largely unaffected.
Conclusions:
- Type-1 cell mitochondria exhibit remarkable oxygen sensitivity, supporting their role in oxygen sensing.
- This sensitivity is significantly higher than previously thought and contrasts with sympathetic neurons.
- The precise mechanisms underlying this extraordinary mitochondrial oxygen sensitivity require further investigation.
