RESUMO
Snails are effective bioindicators due to their prolific distribution, high level of endemism, and capacity to accumulate contaminants. Freshwater snails have unique ecological niches which are imperiled by land-use change and the introduction of hazardous chemicals. To assess how environmental alterations affect gastropods, lab-based studies are needed to characterize the toxicity of specific stressors. This can help guide policy decisions and remediation efforts. The aim of this research was to characterize acute toxicity of nickel (Ni) on endemic snails (Somatogyrus georgianus [Walker, 1904], Elimia cahawbensis [Lea, 1861], and Elimia spp.) and measure the accumulation of Ni and mineral elements including calcium (Ca), magnesium, potassium, and sodium (Na). Snails were exposed to six concentrations (25-800 µg/L) of Ni for 96 h. Among the studied snail species, E. cahawbensis was the most sensitive to Ni, with the lowest lethal concentration where 50% of the organisms died (LC50) at 88.88 µg/L Ni after 96 h. The LC50 at 96 h for S. georgianus was 167.78 µg/L Ni, and 393.13 µg/L Ni for Elimia spp. Except for Elimia spp., mortality of the other two snail species corresponded to the whole-body uptake of Ni. Nickel exposure also influenced Ca and Na uptake for Elimia spp. All three endemic species are potential candidate species for evaluating localized effects of human activities, and the present study provides a first step in characterizing how snails would be affected by environmental alterations. More research could further characterize potential effects of other human stressors on these endemic snail species. Future research into subindividual responses and routes of exposure can further elucidate variations in species sensitivity. Environ Toxicol Chem 2024;00:1-11. © 2024 SETAC. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.
RESUMO
Cardiac glycosides (CG) are traditionally known as positive cardiac inotropes that inhibit Na+/K+-ATPase-dependent ion transport. CG also trigger-specific signaling pathways through the cardiac Na+/K+-ATPase, with beneficial effects in ischemia/reperfusion (I/R) injury (e.g., ouabain preconditioning, known as OPC) and hypertrophy. Our current understanding of hypersensitivity to CG and subsequent toxicity in the ischemic heart is mostly based on specific I/R-induced alterations of the Na+/K+-ATPase enzymatic function and has remained incomplete. The primary goal of this study was to investigate and compare the impact of I/R on Na+/K+-ATPase enzymatic and signaling functions. Second, we assessed the impact of OPC on both functions. Langendorff-perfused rat hearts were exposed to 30 min of ischemia and 30 min of reperfusion. At the inotropic concentration of 50 µmol/L, ouabain increased ERK and Akt phosphorylation in control hearts. In I/R hearts, this concentration did not induced positive inotropy and failed to induce Akt or ERK phosphorylation. The inotropic response to dobutamine as well as insulin signaling persisted, suggesting specific alterations of Na+/K+-ATPase. Indeed, Na+/K+-ATPase protein expression was intact, but the enzyme activity was decreased by 60% and the enzymatic function of the isoform with high affinity for ouabain was abolished following I/R. Strikingly, OPC prevented all I/R-induced alterations of the receptor. Further studies are needed to reveal the respective roles of I/R-induced modulations of Na+/K+-ATPase enzymatic and signaling functions in cardiomyocyte death.