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The Intracellular Signaling System Controlling Cell Hydration as a Biomarker for EMF Dosimetry
Published in Marko Markov, Dosimetry in Bioelectromagnetics, 2017
Since Na+/Ca2+ exchange functions in stoichiometry of 3Na:1Ca, the activation of R Na+/Ca2+ exchange could cause cell dehydration. However, our previous study has shown that IP injection of 10−9 M ouabain-induced activation of R Na+/Ca2+ exchange is accompanied by hydration in brain cortex and heart muscle tissues. Furthermore, it has been shown that 10−9 M ouabain-induced tissue hydration is more pronounced than 10−4 M ouabain-induced cell hydration (Narinyan et al., 2014; Ayrapetyan et al., 2015; Nikoghosyan et al., 2015). It is known that 10−4 M ouabain increases cell hydration, which is due to inhibition of Na+/K+ pump, having electrogenic character (Ayrapetyan and Sulejmanian, 1979; Carpenter et al., 1992). But the fact that 10−9 M ouabain has a more pronounced effect on cell hydration than 10−4 M ouabain serves as additional evidence that nM ouabain-induced cell hydration cannot be considered as the result of Na+/K+ pump inactivation. We came to the same conclusion by studying the activation of R Na+/Ca2+ exchange as a result of decrease of Na+ concentration in cell aqua medium ([Na+]0) (Nikoghosyan et al., 2015). It has been shown that the decrease of [Na+]o has a double effect on cell hydration: from one side, through activation of R Na+/Ca2+ exchange it brings dehydration, from the other side through activation of oxidative processes in the cell it causes hydration because of H2O release in cytoplasm. It is worth noting that as a consequence of these two effects water efflux from the cell takes place, which in its turn inhibits inward going INa and ICa (Ayrapetyan et al., 1988). The activation of R Na+/Ca2+ exchange leading to membrane hyperpolarization (Baker et al., 1969; Saghian et al., 1996) and resulting in cell shrinkage (Iwasa et al., 1980) is the next mechanism through which the decrease of membrane permeability takes place. Thus, it can be assumed that nM ouabain-induced activation of cAMP-dependent R Na+/Ca2+ exchange has a multisided protective function for cells. However, this protective reaction has a transient character as its continuous activation brings an increase of [Ca2+]i which poisons intracellular metabolism and leads to the impairment of endogenous H2O release.
Effects of exposure to sediment-associated fipronil on cardiac function of Neotropical armored catfish Hypostomus regani
Published in Journal of Environmental Science and Health, Part A, 2023
Lucas Abreu Ferro, Suzana Luisa Alves Fernandes, Ana Lúcia Kalinin, Diana Amaral Monteiro
The amplified role of NCX in cardiomyocytes of Fp-exposed fish was confirmed after the addition of 0.01 and 0.1 µM of ouabain, which significantly increased force development (49% and 37%, respectively) (Fig. 5A). This ouabain-induced inotropic stimulation was not detected in the ventricular strips from the Ct group, which maintained a similar force development at low doses of ouabain. In both experimental groups, a subsequent development of toxicity with decrease in contractile force were observed at concentrations of 1.0 µM and higher. Previous studies have demonstrated that high concentrations of ouabain induced toxicity in heart muscle.[77,78] The inhibition of the NCX activity with ouabain increases the thermodynamic drive for Ca2+ influx by exchanger NCX (in reverse-mode) due to the intracellular Na+ rise and shifts the burden of Ca2+ removal to sarco/endoplasmic reticulum Ca2+-ATPase (SERCA).[79–81] Consequently, a higher SR Ca2+ loads induce increases in Ca2+ transient and contractile force.[81,82] The effects of glycosides depend on the degree of NCX activity and expression since ouabain changes Ca2+ cycling via this exchanger protein,[83] which may explain the positive inotropic effects of ouabain only in Fp-exposed fish. Moreover, in isolated ventricular myocytes, the reversal of the Na+/Ca2+-exchanger causes transient increase in cellular energy expenditure, oxygen consumption, and [Ca2+]i.[84] In cardiomyocytes, cytoplasmic [Ca2+], thermodynamically controlled by the NCX, is a major regulator of the respiratory rate.[85] These fipronil-induced changes can greatly affect fish energy budget, which may cause negative impacts at population and community levels.