Bisphenol A induces hepatic triglyceride level in adult male rare minnow Gobiocypris rarus.

Bisphenol A (BPA), an endocrine disruptor, exist in almost all waters. In the present study, we expose adult male Gobiocypris rarus rare minnow to 15 µg/L BPA to study the effect BPA on fish hepatic lipid metabolism. Following 1, 3 and 5 weeks exposure, the liver tissue of rare minnow was separated. The change of the hepatic morphology, hepatosomatic index, lipid composition and expression of lipid metabolism related genes were analyzed through paraffin section, oil red O staining, lipidomic analysis, and quantitative real-time PCR. BPA can cause significant hepatic lipid deposition in male rare minnow, leading to an increase in triglyceride (TG) level (1.84-22.87-fold), but it is also accompanied by a decrease in diglyceride level (1.67-4.78-fold). The expression of lipid metabolism related genes showed that BPA exposure can up-regulate TG synthesis related genes expression, and down-regulate TG degradation genes expression. Expression of TG transport related genes were also disrupted by BPA. It suggests that BPA can up-regulate rare minnow hepatic TG level through multi-path, and ultimately lead to lipid accumulation in the liver. The results of the present study enrich the mechanisms of environmental endocrine disruptors affecting lipid accumulation in fish.

Acute BPA exposure-induced oxidative stress, depressed immune genes expression and damage of hepatopancreas in red swamp crayfish Procambarus clarkii.

Bisphenol A is a typical endocrine disrupting chemicals (EDCs) and produce various toxic effects on animals due to its potential endocrine disruption, oxidative damage effect, mutagenic effect and hypomethylation. To study its effect on the immune system of crustaceans, the Procambarus clarkii were utilized to detect the immune related indicators after 225 µg/L BPA exposure for 1 week. Hepatopancreatic histology and ultrastructure analysis showed that the brush border disappeared, the lumen increased, and the connection between the hepatic tubules fade away in BPA treated group. BPA could significantly increase the level of ROS, inhibit the activities of antioxidant-related enzymes (SOD, POD, and CAT), and thereby cause the oxidative stress. The enzyme activities of AKP, ACP and lysozyme in hepatopancreas after BPA exposure were also depressed even after Aeromonas hydrophila infections. The relative expression profiles of immune-related genes after BPA exposure and bacterial infection showed suppressed trends of most selected genes. Under A. hydrophila infections, the cumulative mortality of 225 µg/L BPA-treated crayfish was significantly higher than other groups. All these results indicated that BPA exposure had adverse effects on the immune ability of P. clarkii. The present study will provide an important foundation for further understanding the effects of EDCs on crustacean immune functions.

Toxicity comparison of nano-sized and micron-sized microplastics to Goldfish Carassius auratus Larvae.

Plastic pollution is one of the most serious environmental issues worldwide. The negative influence of plastics on aquatic organisms has increasingly concerned, especially the influence of microplastic (MPs). In the present study, the toxicology of nano-sized MPs (nMPs) and micron-sized MPs (mMPs) were comparatively studied. Goldfish larvae were exposed to 10, 100 and 1000 µg/L nMPs and mMPs for 1, 3 and 7 days. The enrichment of MPs, body length, heart rate, motor ability, microscopic and ultrastructure of intestine, liver, gill and muscle tissue, as well as the oxidative stress were analyzed. Results showed that both 70 nm and 50 µm MPs were accumulated in the digestive tract of larvae. MPs at high concentrations could induce oxidative stress, destroy intestine, liver and gill tissues, increase heart rate, and inhibit growth and swimming speed of the larvae. The most important finding was that nMPs could enter into the muscle tissue through the epidermis of the larvae. It could cause damage to muscle tissue, destroy nerve fibers, inhibit acetylcholinase (AchE) activity, and show great adverse effects on larval movement than mMPs. In conclusion, both nMPs and mMPs at higher concentrations can cause damage to fish larvae and nMPs are potentially more hazardous.

The surface syndecan protein from Macrobrachium rosenbergii could function as mediator in bacterial infections.

Due to the aquatic animal pathogens are numerous and specific, the pathogen invasion mechanisms are more complicated. The cell surface receptors play vital roles to understand these mechanisms. Syndecan is a cell surface protein and could function as a receptor involved bacteria and virus infections. But there are few studies on the function of syndecan in shrimp and their interaction with aquatic bacterial pathogens. In the present study, we identified a syndecan receptor gene from Macrobrachium rosenbergii and analyzed its functions during the bacterial infections. The MrSDC was expressed in various tissues and presented a constitutive expression distribution except in eyestalk. Recombinant MrSDC-his tag protein was expressed in the E. coli BL21 with pET30a/MrSDC plasmid and exhibited a broad bacterial binding activities. The inhibition of MrSDC expression by dsRNA interference and antibody blocked could significantly reduce the number of Aeromonas hydrophila in hepatopancreas compared with the control. The overexpression of MrSDC by mRNA injection could significantly increase the number of A. hydrophila. In addition, the functional role of syndecan heparan sulfate chains in bacterial recognition was also studied. After extra injection of heparan sulfate in vivo, the bacterial numbers and accumulative mortality of M. rosenbergii were significantly higher than control groups and exhibit a dose effect. All these data could indicate that the cell surface syndecan protein could function as mediator in bacterial infections by the heparan sulfate chains. Our present study will provide new insights into the functions of shrimp syndecan.

Characterization of a classical 2-cysteine peroxiredoxin1 gene from Chinese soft-shelled turtle Pelodiscus sinensis with its potent antioxidant properties and putative immune response.

Peroxiredoxin family members could function in host defense against oxidative stress, and modulate immune response. In the present study, a 2-cysteine peroxiredoxin gene named PsPrx1 was isolated from Chinese soft-shelled turtle Pelodiscus sinensis. The PsPrx1 cDNA was composed of 1130 bp, consisted of 199 amino acid residues and included a Redoxin and AphC-TSA domain. As detected by qPCR, PsPrx1 was ubiquitously expressed in the examined tissues with the higher levels in liver and spleen. Upon the immune challenge with A. jandaei bacteria and oxidative stress with ammonia pressure, both mRNA and protein expression level in liver could be significantly enhanced. The results of immunohistochemical examinations showed PsPrx1 was mainly distributed at the junction between the hepatic cells. The general functional properties of PsPrx1 were confirmed using purified rPsPrx1 protein. From the results, rPsPrx1 protein was confirmed to exhibit antioxidant activity and antibacterial properties. The potential for scavenging extracellular H2O2 was evidenced by the purified rPsPrx1 protein in vitro system. In the mixed-function oxidase assay, rPsPrx1 also exhibited a dose-dependent inhibition of DNA damage. These results suggest that rPsPrx1 was implicated defense against microbial pathogens and oxidants, and would provide important information to further understand the functional mechanism of Prx1 in P. sinensis immunity.