Polystyrene nanoplastics decrease molting and induce oxidative stress in adult Macrobrachium nipponense.

The widespread occurrence and accumulation of plastic waste have been globally recognized as a critical issue. However, few researches have evaluated the adverse effects of nanoplastics to freshwater organisms. Thus, here, the effects of polystyrene nanoplastics (PS-NP) on the physiological changes (i.e., molting) and enzyme activity of oxidative stress were investigated in the adult freshwater prawn Macrobrachium nipponense. Based on a previous study and environmental microplastic concentrations, the prawn was exposed to 0, 0.04, 0.4, 4, and 40 mg/L waterborne PS-NP for 21 days. The results showed that growth and survival-related parameters were not affected by all PS-NP groups, while the molting rate were significantly decreased in the 4 and 40 mg/L PS-NP group. Meanwhile, the expression of molting-related gene (calcium-calmodulin-dependent protein kinase I, ecdysteroid receptor, and leucine-rich repeat-containing G-protein-coupled receptor 2) were significantly decreased. H2O2 content was significantly increased in all PS-NP groups relative to the control. Lower concentrations of PS-NP increased the activity of superoxide dismutase (SOD), glutathione S-transferase (GST), and glutathione peroxidase (GSH-Px), whereas increased concentrations, decreased SOD, GST, and GSH-Px activity. These results suggest that chronic exposure to PS-NP at an environmental concentration impaired molting and induced oxidative stress in the adult river prawn Macrobrachium nipponense. The findings provided basic information for assessing the risk assessment of nanoplastics and revealing the molecular mechanisms of nanoplastics toxicity.

Microcystin-LR and polystyrene microplastics jointly lead to hepatic histopathological damage and antioxidant dysfunction in male zebrafish.

The co-occurrence of cyanobacterial blooms and nano-microplastic pollution in the water is becoming an emerging risk. To assess the combined hepatotoxicity of microcystin-LR (MC-LR) and polystyrene microplastics (PSMPs) on zebrafish (Danio rerio), male adult zebrafish were exposed to single MC-LR (0, 1, 5, 25 µg/L) and a mixture of MC-LR and PSMPs (100 µg/L). After 60 d exposure, the results indicated that PSMPs significantly increased the MC-LR bioaccumulation in the livers in contrast to the single 25 µg/L MC-LR treatment group. Moreover, the severity of hepatic pathological lesions was aggravated in the MC-LR + PSMPs treatment groups, which were mainly characterized by cellular vacuolar degeneration, swollen hepatocytes, and pyknotic nucleus. The ultrastructural changes also proved that PSMPs combined with MC-LR could enhance the swollen mitochondria and dilated endoplasmic reticulum. The biochemical results, including increased malondialdehyde (MDA) and decreased glutathione (GSH), indicated that PSMPs intensified the MC-LR-induced oxidative damage in the combined treatment groups. Concurrently, alterations of sod1 and keap1a mRNA levels also confirmed that PSMPs together with MC-LR jointly lead to enhanced oxidative injury. Our findings demonstrated that PSMPs enhanced the MC-LR bioavailability by acting as a vector and exacerbating the hepatic injuries and antioxidant dysfunction in zebrafish.

Polystyrene microplastics enhance the microcystin-LR-induced gonadal damage and reproductive endocrine disruption in zebrafish.

The coexistence of eutrophication and plastic pollution in the aquatic environment is becoming a realistic water pollution problem worldwide. To investigate the microcystin-LR (MC-LR) bioavailability and the underlying reproductive interferences in the presence of polystyrene microplastic (PSMPs), zebrafish (Danio rerio) were exposed to individual MC-LR (0, 1, 5, and 25 µg/L) and combined MC-LR + PSMPs (100 µg/L) for 60 d. Our results showed that the existence of PSMPs increased the accumulation of MC-LR in zebrafish gonads compared to the MC-LR-only group. In the MC-LR-only exposure group, seminiferous epithelium deterioration and widened intercellular spaces were observed in the testis, and basal membrane disintegration and zona pellucida invagination were noticed in the ovary. Moreover, the existence of PSMPs exacerbated these injuries. The results of sex hormone levels showed that PSMPs enhanced MC-LR-induced reproductive toxicity, which is tightly related to the abnormal increase of 17ß-estradiol (E2) and testosterone (T) levels. The changes of gnrh2, gnrh3, cyp19a1b, cyp11a, and lhr mRNA levels in the HPG axis further proved that MC-LR combined with PSMPs aggravated reproductive dysfunction. Our results revealed that PSMPs could increase the MC-LR bioaccumulation by serving as a carrier and exaggerate the MC-LR-induced gonadal damage and reproductive endocrine disruption in zebrafish.