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Ionic liquids (ILs) are thought to have negative effects on human health. Researchers have explored the effects of ILs on zebrafish development during the early stages, but the intergenerational toxicity of ILs on zebrafish development has rarely been reported. Herein, parental zebrafish were exposed to different concentrations (0, 12.5, 25, and 50 mg/L) of [Cnmim]NO3 (n = 2, 4, 6) for 1 week. Subsequently, the F1 offspring were cultured in clean water for 96 h. [Cnmim]NO3 (n = 2, 4, 6) exposure inhibited spermatogenesis and oogenesis in F0 adults, even causing obvious lacunae in the testis and atretic follicle oocytes in ovary. After parental exposure to [Cnmim]NO3 (n = 2, 4, 6), the body length and locomotor behavior were measured in F1 larvae at 96 hours post‐fertilization (hpf). The results showed that the higher the concentration of [Cnmim]NO3 (n = 2, 4, 6), the shorter the body length and swimming distance, and the longer the immobility time. Besides, a longer alkyl chain length of [Cnmim]NO3 had a more negative effect on body length and locomotor behavior. RNA‐seq analysis revealed several downregulated differentially expressed genes (DEGs)—grin1b, prss1, gria3a, and gria4a—enriched in neurodevelopment‐related pathways, particularly the pathway for neuroactive ligand–receptor interaction. Moreover, several upregulated DEGs, namely col1a1a, col1a1b, and acta2, were mainly associated with skeletal development. Expression of DEGs was tested by RT‐qPCR, and the outcomes were consistent with those obtained from RNA‐Seq. We provide evidence showing the effects of parental exposure to ILs on the regulation of nervous and skeletal development in F1 offspring, demonstrating intergenerational effects. [ABSTRACT FROM AUTHOR]

Ionic liquids (ILs) are thought to have negative effects on human health. Researchers have explored the effects of ILs on zebrafish development during the early stages, but the intergenerational toxicity of ILs on zebrafish development has rarely been reported. Herein, parental zebrafish were exposed to different concentrations (0, 12.5, 25, and 50 mg/L) of [C n mim]NO 3 (n = 2, 4, 6) for 1 week. Subsequently, the F1 offspring were cultured in clean water for 96 h. [C n mim]NO 3 (n = 2, 4, 6) exposure inhibited spermatogenesis and oogenesis in F0 adults, even causing obvious lacunae in the testis and atretic follicle oocytes in ovary. After parental exposure to [C n mim]NO 3 (n = 2, 4, 6), the body length and locomotor behavior were measured in F1 larvae at 96 hours post-fertilization (hpf). The results showed that the higher the concentration of [C n mim]NO 3 (n = 2, 4, 6), the shorter the body length and swimming distance, and the longer the immobility time. Besides, a longer alkyl chain length of [C n mim]NO 3 had a more negative effect on body length and locomotor behavior. RNA-seq analysis revealed several downregulated differentially expressed genes (DEGs)-grin1b, prss1, gria3a, and gria4a-enriched in neurodevelopment-related pathways, particularly the pathway for neuroactive ligand-receptor interaction. Moreover, several upregulated DEGs, namely col1a1a, col1a1b, and acta2, were mainly associated with skeletal development. Expression of DEGs was tested by RT-qPCR, and the outcomes were consistent with those obtained from RNA-Seq. We provide evidence showing the effects of parental exposure to ILs on the regulation of nervous and skeletal development in F1 offspring, demonstrating intergenerational effects., (© 2023 Wiley Periodicals LLC.)

Objectives: This study intended to investigate the effects of Ginsenoside-Rbl (Gs-Rbl) on fatty acid β-oxidation (FAO) in rat failing heart and to identify potential mechanisms of Gs-Rbl improving heart failure (HF) by FAO pathway dependent on AMP-activated protein kinase (AMPK)., Materials and Methods: Rats with chronic HF, induced by adriamycin ( Adr ), were randomly grouped into 7 groups. Gs-Rb1, adenine 9-β-D-arabinofuranoside ( Ara A , specific AMPK inhibitor), and 5'-aminoimidazole-4-carboxamide riboside ( Aicar , specific AMPK activator) were administered to rats with HF, singly and/or combinedly. Myocardial high-energy phosphate (such as phosphocreatine, ADP, and ATP), free L-Carnitine, malonyl-CoA, and the activity of FAO-related enzymes in left ventricle from different groups were measured by using the corresponding molecular biological techniques., Results: Gs-Rb1 improved HF significantly, accompanied by a significant increase in phosphocreatine (PCr), ADP, ATP, PCr/ATP ratio, free carnitine, malonyl-CoA, mRNA, activity of carnitine palmitoyltransferase (Cpt), medium-chain Acyl-CoA Dehydrogenase (MCAD) and long-chain acyl-CoA Synthetase (ACSL) and a significant decrease of the ADP/ATP ratio in the left ventricular myocardium. However, all those effects were almost abolished by Ara A and were not further improved by Aicar ., Conclusion: Taken together, it suggests that Gs-Rb1 may modulate cardiac metabolic remodeling by improving myocardial fatty acid β-oxidation in failing heart. In addition, the effects of Gs-Rb1 may be mediated via activating AMPK.

To investigate the effects of hypoxia on the apoptosis and glucose intake of mesenchymal stem cells (MSCs), MSCs derived from bone marrow of rats were incubated in the atmosphere of 1% O(2) for a series of time points and their glucose-intaking capacity, ultrastructural changes and apoptotic proportions were analyzed by (3)H-labeling assay, electron microscopy and flow cytometry, respectively. The results showed that the cultured cells took the fibroblast-like morphology and could be induced into osteoblasts and adipocytes under appropriate conditions. The proportions of apoptotic cells after hypoxia treatment for 1, 4 and 8 hours were 13.7 +/- 2.26%, 14.1 +/- 2.78% and 14.7 +/- 4.01%, respectively, all of which were significantly higher than that observed in normoxic counterparts (0.09 +/- 2.03%, p < 0.05). Also, cell death occurred after hypoxia treatment and the death rates were 3.11 +/- 2.14%, 4.72 +/- 2.05% and 4.91 +/- 3.72% for 1, 4 and 8 hours incubation respectively. Under hypoxia culture in vitro, cell membrane microvillus began to fall off and the mitochondrias became swelling at 1 hour, and the above changes increasingly aggravated along with hypoxia time prolongation. The (3)H-glucose intaking ratios of MSCs at different hypoxia time points significantly decreased than those in normoxic cells (p < 0.01). It is concluded that the acute hypoxia can induce down-regulation of glucose-intaking capacity, ultrastructural changes and apoptosis of MSCs.