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Microplastics as vectors for microcystin-LR: Enhanced bioavailability, oxidative damage, and immune dysregulation in zebrafish spleen
Summary
Researchers studied the combined effects of the algal toxin microcystin-LR and polystyrene microplastics on zebrafish spleen over 60 days. They found that microplastics enhanced the bioavailability of the toxin, worsening oxidative damage and suppressing immune function beyond what either pollutant caused alone. The study suggests that microplastics can act as vectors for harmful algal toxins, amplifying their biological impact in aquatic organisms.
The co-occurrence of eutrophication and plastic pollution has emerged as a critical global water quality challenge. In the present study, we systematically investigated the joint effects of microcystin-LR (MC-LR) and polystyrene microplastics (PSMPs) on antioxidant defense mechanisms and innate immunity function through an orthogonal experimental design (MC-LR: 0, 0.8, 4, 20 μg/L; PSMPs: 0, 100 μg/L). After 60 d exposure, our results found that the presence of PSMPs enhanced the MC-LR bioavailability in the spleen of zebrafish. Besides, the severity of splenic injuries exhibited a concentration-dependent response to MC-LR exposure and was further exacerbated in co-exposure groups, primarily manifested with increased melano-macrophage centers and mitochondrial edema. Compared to the MC-LR-only group, the MC-LR-co-PSMPs exposure groups showed remarkably increased malondialdehyde (MDA) content, indicating enhanced oxidative damage. These results were further supported by significantly reduced glutathione (GSH) levels and downregulated gpx1a mRNA expression. Simultaneously, co-exposure to MC-LR and PSMPs significantly decreased complement C3 content and downregulated the transcriptional level of c3b, il1β and ifn in relative to the single MC-LR exposure groups, which indicated that they could jointly result in immune inhibition. Our results revealed that PSMPs significantly enhanced MC-LR bioavailability in the spleen, functioning as vectors that exacerbated splenic histopathological damage, oxidative stress as well as immune dysfunction. These findings highlight the non-negligible combined toxicity of these pollutants in eutrophic aquatic systems.