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Environmental hazard profile of Gadolinium: Mechanistic insights into its ecotoxicity towards Euglena gracilis from a multi-level investigation

ABSTRACT:

As emerging environmental contaminants, rare earth elements (REEs) pose a growing ecotoxicological threat, making a mechanistic understanding of their toxicity in aquatic primary producers like microalgae crucial for accurate ecological risk assessment. This study investigated the multi-level adverse effects of gadolinium (Gd³⁺), a representative REE contaminant, on Euglena gracilis by integrating physiological, ultrastructural, and non-targeted metabolomic approaches. While background environmental concentrations of Gd are low, levels in anthropogenically impacted systems can exceed ~60 mmol/L, providing the context for this toxicological investigation. Gd³⁺ exhibited potent, dose-dependent toxicity, causing a 35.77% inhibition of growth at 80 µmol/L, with a calculated EC₅₀ for growth inhibition of 110.5 µmol/L (95% CI: 95.8 to 127.5 µmol/L), alongside detrimental morphological shifts and severe chloroplast damage. While total photosynthetic pigments and paramylon decreased in the culture, their per-cell levels paradoxically increased, signifying a severe cellular stress response. Non-targeted metabolomics revealed extensive metabolic reprogramming, with lipid metabolism identified as the primary target of Gd³⁺-induced cellular damage, accounting for 65.8% of the differential metabolites. This disruption included the significant upregulation of lysophospholipids, a nearly 400-fold increase in the signaling molecule 12-HETE, and the perturbation of key bioenergetic pathways like oxidative phosphorylation. In conclusion, Gd³⁺ exerts multi-target toxicity in E. gracilis through direct chloroplast damage, drastic reprogramming of lipid metabolism leading to membrane disruption and altered signaling, and consequent disorders in energy metabolism. These findings advance REE ecotoxicology and highlight that the disruption of lipid metabolism is a key toxic mechanism and a potential sensitive biomarker for REE-induced hazardous effects, providing crucial evidence to inform environmental risk assessments and establish water quality benchmarks for these materials.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS12918 | MetaboLights | 2025-09-03

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS12918_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS12918_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS12918_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS12918_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:Background: Genetic elimination of c-Met signaling in the liver has been shown to impact many cellular pathways involved in repair, regeneration, lipid homeostasis and redox balance. In this study, we analyzed a nutritional model of hepatic steatosis in Met fl/fl ; Alb-Cre +/- (MetKO) mice in a 129SV/C57BL/6 background fed a high cholesterol diet for 30 days. Methods: Liver injury was determined by histopathology and plasma enzymes, transcriptomic changes were examined using gene expression microarrays, and evaluation of key molecules involved in liver damage and lipid homestasis were evaluated by Western blot analysis. Results: We observed that in comparison with wild type mice subjected to the same diet, MetKO mice developed a strong liver lipid deposition, inflammatory infiltration and increment in total bile acids synthesis and liver damage markers. Global transcriptomic changes analysis confirmed the steatosis and cholestasis induced by the high cholesterol diet. In addition, we found affected pathways related to amino acids, glutathione and lipid metabolism, oxidative stress and mitochondria dysfunction. Oxidative stress exacerbation was corroborated by lipid and protein oxidation in liver tissue. To address further, Western blot studies revealed downregulation on Erk, NF-kB and Nrf2 survival pathways and target genes (cyclin D1, SOD1, gamma-GCS), an increment in proapoptotic proteins (p53, caspase 3) and changes in nuclear receptors such as RAR and RXR, which were increased, and CAR, FXR and PPAR alfa, which were decreased, in the MetKO diet. These results are in agreement with the steatosis and cholestasis phenotype. Conclusion: Our data provide evidence of c-Met signaling involvement in lipid metabolism, and bile acids synthesis and excretion. Disruption of these pathways leads to liver dysfunction, improper metabolism and hepatocellular damage. Global transcriptome changes between WT mice vs. c-Met KO mice fed a 2% cholesterol and 0.5% sodium cholate diet (high cholesterol) or a Chow regular diet (Chow) as control. Mice were fed a high cholesterol or chow regular diet for 30 days. Liver tissue was obtained, and RNA was extracted and subjected to Illumina microarray analysis.

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Environmental hazard profile of Gadolinium: Mechanistic insights into its ecotoxicity towards Euglena gracilis from a multi-level investigation

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