Key result
Gadolinium ions reduce frog myocardial contractility and preserve mitochondrial membrane potential under calcium stress.
Why the study?
The effects of gadolinium ions on heart muscle contractility and mitochondrial functions related to calcium-dependent processes in vertebrate myocardium were not fully understood.
Animal data link gadolinium to cardiac and mitochondrial effects; leaves open human relevance and safety.
We studied the inotropic and chronotropic effects of gadolinium ions (Gd3+) on contractility of frog Rana ridibunda heart muscle preparations. In addition, the influence of Gd3+ on oxygen uptake rates, swelling and the mitochondrial inner membrane potential (ΔΨmito) were studied in glutamate- and malate-energized rat heart mitochondria (RHM). It was found that Gd3+ decreases the amplitude and frequency of spontaneous heart contractions. At the same time, Gd3+ prevents Ca2+-induced swelling of these organelles in saline media and falling of ΔΨmito. In this case, regardless of the presence of Ca2+ in the medium, Gd3+ has a weak effect on mitochondrial state 3 or 3UDNP respiration (in the presence of 2,4-dinitrophenol). In calcium free experiments, Gd3+ stimulates passive swelling of RHM. These effects of Gd3+ may indicate that Gd3+ has no toxic effect on RHM but, on the other hand, inhibits opening of the mitochondrial permeability transition pore (MPTP) in the inner membrane. Our data provide better insight into the mechanisms of action of rare earth elements on Ca2+-dependent processes in the myocardium of vertebrates.
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Korotkov et al. (2020) studied this question. Gadolinium ions (Gd3+) was evaluated on Contractility, oxygen uptake rates, swelling, and mitochondrial inner membrane potential. Gadolinium ions decreased the amplitude and frequency of spontaneous frog heart contractions and prevented Ca2+-induced swelling and falling of inner membrane potential in rat heart mitochondria.
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