Bundgaard 2016 Abstract IOC115

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Does nitrite protect the turtle heart from oxidative damage in the spring?

Link: Mitochondr Physiol Network 21.10

Bundgaard AG, James AM, Murphy MP, Fago A (2016)

Event: IOC115

Nitrite protects the heart from toxic oxygen radicals when oxygen returns after a period of oxygen deprivation, such as after heart attack or infarct. During anoxia, nitrite can inhibit inactive proteins, such as complex I in the electron transport chain, by a post-translational modification termed S-nitrosation, where an NO-moiety binds protein cysteines. Inhibition of complex I have been shown to limit the production of oxygen radicals, thereby protecting the heart from oxidative damage [1].

Some extreme animals, such as the red-eared slider turtle, survive the winter at the bottom of frozen ponds, and remain completely deprived of oxygen for several months. Unlike mammals, these turtles are not maimed by reoxygenation, but wake up in the spring with healthy hearts. Nitrite is naturally accumulated in the hearts of these animals during anoxia, which might protect them from reperfusion damage [2].

In this study, we investigate the protective effects of nitrite on the turtle heart. In vitro studies on isolated mitochondria have shown that the artificial S-nitrosating agent MitoSNO S-nitrosates turtle complex I which decreases activity of the enzyme and reduces ROS production upon reoxygenation, but does not affect respiration rate. Further, we have shown that succinate is accumulated in the anoxic turtle heart, which has been shown in mice to fuel the ROS production that occurs upon reoxygenation. This would corroborate the need for inhibition of complex I in the turtle.

We further wish to investigate whether the accumulated nitrite in the anoxic turtle mimics the protective effect of S-nitrosation in vitro and whether this is involved in keeping the turtle heart healthy upon awakening in the spring after a long, oxygen-deprived winter. Using extreme animals such as the turtle as models for coping with extreme situations like oxygen deprivation might teach us how to protect the more sensitive human heart.


Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Reptiles  Tissue;cell: Heart  Preparation: Isolated mitochondria  Enzyme: Complex I 


1-Dept Bioscience, Aarhus Univ, Denmark; 2-Medical Research Council Mitochondrial Biol Unit, Cambridge, UK. - [email protected]


IOC115 2016 Bundgaarrd Figure.png

Figure 1: During anoxia, nitrite is accumulated in the turtle heart. We hypothesise that nitrite S-nitrosates complex I, which inhibits the main ROS production site, the FMN site, upon reoxygenation by electron transfer from NADH or by reverse electron transfer from succinate via the ubiquinone pool (Q).


  1. Chouchani ET, Methner C, Nadtochiy SM, Logan A, Pell VR, Ding S, James AM, Cochemé HM, Reinhold J, Lilley KS, Partridge L, Fearnley IM, Robinson AJ, Hartley RC, Smith RA, Krieg T, Brookes PS, Murphy MP (2013) Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I. Nat Med 19:753-9.
  2. Jensen FB, Hansen MN, Montesanti G, Wang T (2016) Nitric oxide metabolites during anoxia and reoxygenation in the anoxia-tolerant vertebrate Trachemys scripta. J Experim Biol 217:423-31.