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The bioaccumulation of erythromycin (ETM) and cadmium (Cd) in Chinese mitten crab (Eriocheir sinensis) and subsequent toxicity on pathological changes and enzymatic activities were investigated during 21-day exposure to ETM, Cd, and Cd + ETM mixture. The bioaccumulation of Cd and ETM residues in crab tissues decreased as gill > hepatopancreas > muscle > ovary, with higher Cd bioaccumulation than ETM. The highest Cd bioaccumulation in crab reached 1.15 mg/g dry weight in gill and 461.29 μg/g in hepatopancreas, on the 14th day of Cd treatment. Cd exposure promoted the bioaccumulation of ETM in four tissues. ETM exposure caused tubular vacuolization in epithelial and edema and degeneration of hepatic ducts in hepatopancreas, and disconnected gill epithelial layer and indistinctly cellular structure in gill. During Cd exposure, mitochondria acted as a main biomarker to identify the damage, including reduced and swollen mitochondria, and broken mitochondrial structure. Moreover, Chinese mitten crab showed defence capability against ETM and Cd exposure by physiological adjustment of metabolic enzymes glutathione S-transferase activity.

Microplastic contamination poses a great threat to the health of aquatic species, which may affect their reproduction and result in ecological consequences. There is a need to further elucidate the potential impact microplastics can impose on aquatic species. In this study, the effects of exposure to polystyrene microplastics on reproductive organs, and the underlying response mechanisms, were investigated using zebrafish Danio rerio. After 21 days of continuous waterborne exposure, no significant difference was observed at the lower concentration of 10 μg/L. At concentrations above 100 μg/L, significantly enhanced reactive oxygen species (ROS) level was found in both male and female liver and gonads. At the concentration of 1000 μg/L, significantly increased apoptosis levels were observed in male testes, triggering increased expression of p53-mediated apoptotic pathways; histological alteration in the form of a significant decrease in testis basement membrane thickness was also observed. This study demonstrated that exposure to microplastics can induce molecular responses and histological alterations in fish gonads, implying potential adverse impact on fish reproductive organs. This work provided new insights on the reproductive damage microplastics can cause in fish and have implications in fields of freshwater ecology and environmental toxicology.

Exposure to polybrominated diphenyl ether (PDBE) and methylmercury (MeHg) can occur simultaneously as both contaminants are found in the same food sources, especially fish, seafood, marine mammals and milk. The aim of this study was to assess the effects of exposure to low levels of MeHg (2.0 μg mL(-1) in drinking water) and BDE-99 (0.2 mg kg(-1) d(-1)) from gestational day 6 to postnatal day (PND) 21, alone and in combination, on neurobehavioral development and redox responses in offspring. The present study demonstrated an interaction due to co-exposure with low doses of MeHg and BDE-99 enhanced developmental neurotoxic effects. These effects were manifested as the delayed appearance of negative geotaxis reflexes, impaired motor coordination, and induction of oxidative stress in the cerebellum. In particular, the cerebellum may be a sensitive target for combined MeHg and BDE-99 toxicity. The neurotoxicity of low dose MeHg was exacerbated by the presence of low dose of BDE-99. It is concluded that prenatal co-exposure to MeHg and BDE-99 causes oxidative stress in the cerebellum of offspring by altering the activity of different antioxidant enzymes and producing free radicals. Hg retention was not affected by co-exposure to BDE-99. However, MeHg co-exposure seemed to increase BDE-99 concentrations in selected brain regions in pups compared to pups exposed to BDE-99 only. These results showed that the adverse effects following prenatal co-exposure to MeHg and BDE-99 were associated with tissue concentrations very close to the current human body burden of this persistent bioaccumulative compound.

Exposure to methylmercury (MeHg) and perfluorooctanoic acid (PFOA) can occur simultaneously as both contaminants are found in the same food sources, especially fish, seafood, marine mammals and milk. The aim of this study was to assess the effects of exposure to MeHg (10 μg mL(-1) in drinking water) and PFOA (10 μg mL(-1) in drinking water) from gestational day 1 to postnatal day (PND) 21, alone and in combination, on neurobehavioral development and the expression of c-Fos/Jun in different brain regions in the offspring. Our findings showed that exposure to MeHg alone, and exposure to MeHg combined with PFOA significantly induced cliff avoidance reflexes and negative geotaxis reflexes. And these effects appeared to be greater following exposure to MeHg alone. MeHg and/or PFOA exposure did not significantly impair motor coordination functions, or cause significant changes in c-Fos expression in the hippocampus and cerebellum, and spatial learning tests were similar to those in the controls, thus it was impossible to determine whether combined exposure to MeHg and PFOA had any additional effects on both hippocampus and cerebellum regions. However, a significant increase in the frequency of line crossing was observed in rats treated with MeHg or PFOA alone, and there were no significant differences between the MeHg+PFOA-treated group and the controls, suggesting that PFOA was antagonistic to MeHg toxicity in the locomotor activity test. Co-exposure to MeHg and PFOA decreased all tissue Hg concentrations in pups compared to the group exposed to MeHg only, suggesting that PFOA impaired Hg retention in different tissues.

Polybrominated diphenyl ethers (PBDEs) have recently been shown to be on the increase in the environment and in human milk. The most commonly found PBDE congener in human milk is 2,2',4,4',5-penta BDE (BDE-99). The aim of the present study was to investigate the neurotoxic effects of BDE-99 (2 mg kg(-1)d(-1)) administration, from gestational day 6 to postnatal day (PND) 21, on neurobehavioural development and redox responses in offspring. Neurobehavioural development analysis revealed a delayed appearance of cliff drop and negative geotaxis reflexes in the exposed group. Furthermore, developmental exposure to BDE-99 also affected learning and memory functions during adolescence. On PND 37, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) was reduced, while increases in hydrogen peroxide, lipid peroxidation, nitric oxide and electron spin resonance signal intensities were observed in the hippocampus of BDE-99-treated animals. However, the activity of SOD and GSH-Px in the cerebellum and cerebral cortex was not significantly different between treated and control animals. The present study demonstrated that developmental BDE-99 exposure causes oxidative stress in the hippocampus of offspring by altering the activity of different antioxidant enzymes and producing free radicals. We demonstrated adverse effects of developmental exposure to BDE-99 associated with tissue concentrations very close to the current human body burden of this persistent and bioaccumulative compound.