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Polystyrene nanospheres-induced hepatotoxicity in swamp eel (Monopterus albus): From biochemical, pathological and transcriptomic perspectives
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Researchers exposed swamp eels to polystyrene nanoplastics for 28 days and found significant liver damage including oxidative stress, tissue abnormalities, and disrupted gene expression related to immune response and metabolism. Higher concentrations caused more severe liver injury, with changes detectable at both the biochemical and genetic levels. This study adds evidence that nanoplastic exposure can harm liver function in freshwater species important to aquaculture and local food supplies.
As ubiquitous emerging pollutants, microplastics (MPs) in aquatic environments have aroused critical global concerns. Despite the occurrence and characteristics of MPs in freshwater agroecosystems well-described by our previous study, their ecotoxicological implications in Monopterus albus remains unfathomed. Herein, we dissected toxic effects and mechanisms of PS-NPs exposure against M. albus hepatic tissues at concentrations of 0.5 (L), 5 (M), 10 (H) mg/L for 28 days using physiochemical measurements, histopathological analysis and transcriptomic sequencing. Results showed that upon PS-NPs treatments, levels of ROS, MDA, 8-OHdG and MFO activity were significantly enhanced relative to the control (C) group, while SP content and T-AOC activity were dramatically suppressed, suggesting ROS burst, lipid peroxidation and DNA damage may occur in liver tissues. This oxidative damage further triggered impaired hepatic function and histopathology, disordered lipid metabolism and hepatocyte apoptosis, as reflected by significantly diminished activities of GPT, GOT, ACP, AKP and LDH, paralleled with augmented levels of TG, TC and HSI as well as Cytc and Caspase-3,8,9 activities. Noticeably, concentration-dependent rises of apoptotic rate, vacuolar degeneration and lipid deposition were manifest in TUNEL, H&E and ORO staining. In addition, a total of 375/475/981 up-regulated as well as 260/611/1422 down-regulated DEGs in C vs L, C vs M and C vs H categories were identified based on RNA-seq, respectively. These DEGs were significantly annotated and enriched into GO terms (membrane, cytoplasm, response to stimuli, oxidation-reduction process) as well as KEGG pathways (ether lipid metabolism, apoptosis, chemical carcinogenesis-reactive oxygen species, non-alcoholic fatty liver disease). Moreover, signaling cascades Keap1-Nrf2, p53 and PPAR were either substantially initiated or dysregulated to orchestrate PS-NPs hepatotoxicity featuring oxidative damage, hepatocyte apoptosis and lipid steatosis. Collectively, this study not only expounded on toxicological mechanisms whereby PS-MPs exerted deleterious effects on M. albus, but also pointed to ecological risks of PS-MPs-induced hepatoxicity and lipid steatosis in this commercially-important species.
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