Effects of polystyrene nanoplastics and PCB-44 exposure on growth and physiological biochemistry of Chlorella vulgaris.

Both NPs and PCBs are emerging contaminants widely distributed in the environment, and it is worth exploring whether the combination of the two contaminants causes serious pollution and harm. Therefore, we studied the effects of PS-NPs and PCB-44 alone and together after 96 h and 21 d of exposure to C. pyrenoidosa. The results showed that PS-NPs and PCB-44 affected the cell cycle of C. pyrenoidosa and inhibited its normal growth. Under PS-NPs and PCB-44 stress, the relative conductivity of the algal solution increased, the hydrophobicity of the algal cell surface decreased, and the synthesis of chlorophyll a and chlorophyll b was reduced. In addition to physiological, there are biochemical effects on C. pyrenoidosa. PS-NPs and PCB-44 exposure induced oxidative stress with significant changes in the enzymatic activities of SOD and CAT together with MDA content. Moreover, the relative expression of photosynthesis-related genes (psbA, rbcL, rbcS) all responded, negatively affecting photosynthesis. In particular, significant toxic effects were observed with single exposure to PCB-44 and co-exposure to PS-NPs and PCB-44, with similar trends of effects in acute and chronic experiments. Taken together, exposure to PS-NPs and PCB-44 caused negative effects on the growth and physiological biochemistry of C. pyrenoidosa. These results provide scientific information to further explore the effects of NPs and PCBs on aquatic organisms and ecosystems.

Trophic transfer of nanoplastics and di(2-ethylhexyl) phthalate in a freshwater food chain (Chlorella Pyrenoidosa-Daphnia magna-Micropterus salmoides) induced disturbance of lipid metabolism in fish.

Nanoplastics and di(2-ethylhexyl) phthalate (DEHP) are ubiquitous emerging contaminants that are transferred among organisms through food chain in the ecosystem. This study evaluated the trophic transfer of polystyrene nanoplastics (PSNPs) and DEHP in a food chain including Chlorella pyrenoidosa, Daphnia magna and Micropterus salmoides (algae-crustacean-fish) and lipid metabolism at a higher trophic level in fish. Our results showed that the PSNPs and DEHP accumulated in C. pyrenoidosa or D. magna were transferred to the M. salmoides, of which the DEHP were not biomagnified, while the PSNPs were trophically amplified by the food chain. It is suggested that more PSNPs might be accumulated by higher level consumers in a longer food chain. Additionally, the trophic transfer of PSNPs and DEHP resulted in antioxidant response and histopathological damage in M. salmoides. Moreover, the lipid biochemical parameters and lipid metabolism related genes (fasn, hsl, cpt1a, atgl, apob, fabp1, lpl, cetp) of M. salmoides were significantly affected, which indicated disturbance of lipid metabolism. This study offers great insight into the transfer of contaminants by trophic transfer and their negative effects on organisms at higher trophic levels, which cause human exposure to MNPs and organic contaminants in the ecosystem.

Combined exposure to polystyrene nanoplastics and bisphenol A induces hepato- and intestinal-toxicity and disturbs gut microbiota in channel catfish (Ictalurus punctatus).

The widespread consumption of nanoplastics (NPs) and bisphenol A (BPA) affected the aquatic ecosystem and imposed risks to the safety of aquatic organisms. This study was aimed at assessing the ecotoxicological effects of single and combined exposure to BPA and polystyrene nanoplastics (PSNPs) on the channel catfish (Ictalurus punctatus). A total of 120 channel catfish were separated into four groups with triplicate (each contains 10 fish) and exposed to chlorinated tap water (control group), PSNP single exposure (0.3 mg/L), BPA single exposure (500 µg/L) and PSNPs (0.3 mg/L) + BPA (500 µg/L) co-exposure for 7 days. Our results showed a relatively higher intestinal accumulation of PSNPs in co-exposure group, compared to PSNP single exposure group. Histopathological analysis showed that single exposure to PSNPs and BPA caused breakage of intestinal villi and swelling of hepatocytes in channel catfish, while the co-exposure exacerbated the histopathological damage. In addition, co-exposure significantly increased SOD, CAT activities and MDA contents in the intestine and liver, inducing oxidative stress. In terms of immune function, the activities of ACP and AKP were significantly decreased. The expressions of immune-related genes such as IL-1ß, TLR3, TLR5, hepcidin and ß-defensin were significantly up-regulated, and the expression of IL-10 was down-regulated. Additionally, the co-exposure significantly altered the composition of the intestinal microbiota, leading to an increase in the Shannon index and a decrease in the Simpson index. In summary, this study revealed that mixture exposure to PSNPs and BPA exacerbated toxic effects on histopathology, oxidative stress, immune function and intestinal microbiota in channel catfish. It emphasized the threat of NPs and BPA to the health of aquatic organisms and human food safety, with a call for effective ways to regulate the consumption of these anthropogenic chemicals.

Parental exposure to polystyrene nanoplastics and di(2-ethylhexyl) phthalate induces transgenerational growth and reproductive impairments through bioaccumulation in Daphnia magna.

The ubiquitous presence of polystyrene nanoplastics (PSNPs) and di(2-ethylhexyl) phthalate (DEHP) in the aquatic environment may cause unpredictable negative effects on aquatic organisms and even continue to the offspring. This study assessed the transgenerational impacts of parental exposure to PSNPs and DEHP over four generations (F0-F3) of Daphnia magna. A total of 480 D. magna larvae (F0, 24 h old) were divided into four groups with six replicates (each of them contains 20 D. magna) and exposed with dechlorinated tap water (control), 1 mg/L PSNPs, 1 µg/L DEHP, and 1 mg/L PSNPs + 1 µg/L DEHP (PSNPs-DEHP) until spawning begins. Subsequent to exposure, all the surviving F1 offspring were transferred to new water and continued to be cultured until the end of F3 generation births in all groups. The results showed that the PSNPs accumulated in F0 generation and were inherited into F1 and F2 generations, and disappeared in F3 generation in PSNPs and PSNPs-DEHP groups. However, the accumulation of DEHP lasted from F0 generation to F3 generation, despite a significant decline in F2 and F3 generations in DEHP and PSNPs-DEHP groups. The accumulation of PSNPs and DEHP caused overproduction of reactive oxygen species in F0-F2 generations and fat deposition in F0-F3 generations. Additionally, single and in combination parental exposure to PSNPs and DEHP induced regulation of growth-related genes (cyp18a1, cut, sod and cht3) and reproduction-related genes (hr3, ftz-f1, vtg and ecr) in F0-F3 generations. Survival rates were decreased in F0-F1 generations and recovered in F2 generation in all treatment groups. Furthermore, the spawning time was prolonged and the average number of offspring was increased in F1-F2 generaions as a defense mechanism against population mortality. This study fosters a greater comprehension of the transgenerational and reproductive effects and associated molecular mechanisms in D. magna.

Physiological Measurements and Transcriptome Survey Reveal How Semi-mangrove Clerodendrum inerme Tolerates Saline Adversity.

Salinity adversity has been a major environmental stressor for plant growth and reproduction worldwide. Semi-mangrove Clerodendrum inerme, a naturally salt-tolerant plant, can be studied as a successful example to understand the biological mechanism of saline resistance. Since it is a sophisticated and all-round scale process for plants to react to stress, our greenhouse study interpreted the response of C. inerme to salt challenge in the following aspects: morphology, osmotic protectants, ROS production and scavenging, ion homeostasis, photosynthetic efficiency, and transcriptome reprogramming. The results drew an overview picture to illustrate the tolerant performance of C. inerme from salt acclimatization (till medium NaCl level, 0.3 mol/L) to salinity stress (high NaCl level, 0.5 mol/L). The overall evaluation leads to a conclusion that the main survival strategy of C. inerme is globally reshaping metabolic and ion profiles to adapt to saline adversity. These findings uncover the defense mechanism by which C. inerme moderates its development rate to resist the short- and long-term salt adversity, along with rebalancing the energy allocation between growth and stress tolerance.