Exposure to aluminium causes behavioural alterations and oxidative stress in the brain of adult zebrafish.

Aluminium (Al) water pollution is an increasing environmental problem. Accordingly, this study aimed to find out more about its toxic effects on aquatic organisms. Adult zebrafish were exposed to 11 mg/L of Al and the behavioural responses and its correlation with brain oxidative stress, antioxidant-defences, changes in metabolism and neurotransmission were assessed at 10, 15 and 20 days of exposure. The behavioural and locomotory responses, suggest an increase in the anxiety state, especially observed in animals exposed to Al for 15 days. The reactive oxygen species increased in a time-dependent trend, while the oxidative damage varied over exposure time. The activity of antioxidant enzymes, as superoxide dismutase, glutathione peroxidase and glutathione S-transferases, and the metallothioneins levels increased after short-term exposures and tended to decrease or stabilize at longer times. The results contribute to understand the toxic mechanisms activated by Al highlighting correlations like behavioural disorders and oxidative state.

Eobania vermiculata as a potential indicator of nitrate contamination in soil.

The effects of nitrates were analysed on the land snail Eobania vermiculata, a good bioindicator to assess the effects of certain pollutants in soil. It is known that the molluscs are very sensitive to contamination substances and can be used as sentinel organism for environmental pollution assessment. The nitrates are present in fertilizers and in food additives and their excess can not only be harmful to the environment but also dangerous for the humans. Indeed, in the mammals the nitrates are converted into nitrites and can cause a series of complications as the formation of methaemoglobin and cancers. In this study, adult organisms of E. vermiculata were exposed to soil containing 2000 mg/L of nitrates for 30 days to evaluate the stool microbiome and the histological changes at the level of the foot. Eggs of these snails were similarly treated to observe their hatching, survival and development. Histological changes were observed at level of the foot of adult snails exposed to nitrate and in their stools was evident an increase of bacteria, especially those that have a high ability to exploit nitrates and nitrogen as nutrients. Instead, the treated eggs showed changes in hatching, hypopigmentation of newborn snails and a decrease of their survival in time. The overall information obtained from these endpoints can provide important information regarding the quality of the environment. In addition, they also showed that the invertebrate organism E. vermiculata despite being a simple organism is very useful and efficient for ecotoxicological studies.

Impact of copper in Xenopus laevis liver: Histological damages and atp7b downregulation.

Copper is an essential micronutrient but its excess in the dietary can be toxic. Both copper deficiency and abundance can occur in natural conditions and can lead to pathological dysfunctions. Many of the toxic effects of copper, such as increased lipid peroxidation in cell membranes and DNA damage, are due to its role in the generation of oxygen free radicals. Copper is released into the environment by both natural sources and human activities and it can damage organisms and ecosystems. In the present work the effects of copper has been studied on Xenopus laevis, an interesting model organism, after three weeks of exposure at 1 mg/L of CuCl, concentration allowed in the water for human use. The effects of this metal were analysed on the liver at light microscope by Hematoxylin-Eosin, Mallory, Pas and Perls stainings to evaluate the general histology, the glycogen metabolism and presence of hemosiderin. Moreover the number and area of melanomoacrophages, known as inflammation parameters, were assessment. Finally, we investigated the expression of atp7b gene and localization of respective ATP7B protein, the membrane protein involved in Cu detoxication. The achieved results showed that copper, even at a low concentration, causes serious histological alterations of liver. It induces an increase in the size and number of melanomacrophages and higher amount of hemosiderin in the treated than controls. Moreover, it alters the gene expression and localization of ATP7B protein. The data are indicative that an exposition at low and chronic concentration of copper in Xenopus laevis damages seriously the liver. For this reason it's important to consider this metal one of the pollutants involved in the decline of the amphibians and for its possible effects in other vertebrates including humans.

Effects of aluminium and cadmium on hatching and swimming ability in developing zebrafish.

Aluminium and cadmium are biologically non-essential metals with a role in neurodegenerative and neuromuscular diseases. As an attractive model for neurobehavioural studies, zebrafish at 6 h post fertilization were exposed to 9, 18, 36 and 72 µM CdCl2 and 50, 100 and 200 µM AlCl3, respectively, for 72 h, and motility such as distance moved, mean velocity, cumulative movement, meander and heading were measured by DanioVision equipment. The hatching time was also analysed. A delay in the exit from the chorion was observed in all treated larvae with respect to the controls. CdCl2 acted on the exit from the chorion of larvae with a dose-dependent delay. By contrast, the delay caused by AlCl3 was greater at low concentrations. A dose-dependent reduction in swimming performance was observed in the larvae exposed to CdCl2. Instead, for those exposed to AlCl3, swimming performance improved at higher concentrations although values were in general lower than those of control. All the parameters had a similar trend except the meander parameter which showed a dose-dependent reduction. These data show that cadmium and aluminium can delay hatching and alter swimming ability in the early developmental stages of zebrafish, albeit with different effects, suggesting that exposure to sublethal concentrations of both metals can change behavioural parameters.