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The structure of the zebrafish retina appears to be very similar to that of mammals, that is why it is used as a model for studying the eye. Indeed, the zebrafish retina can regenerate itself through mechanisms of Müller cell reprogramming. In this research, adult zebrafish were exposed to aluminum to cause damage in the retina and thus evaluate the regenerative capacity of the damaged tissue. Histological and histochemical analyses assessed the retinal structure and the neurodegenerative process, respectively. An expression analysis of PARPs was carried out to verify whether a potential oxidative DNA damage happens. In addition, some genes involved in the regeneration process (pax6a, pax2a, ngn1, and notch1a) were analyzed. The data confirmed the toxicity of aluminum which caused retinal neurodegeneration, but also highlighted the ability of zebrafish to regenerate the retinal structure, repairing the damage and confirming its use as a good model for translational studies., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Danio rerio is a small tropical freshwater fish, also known as Brachydanio rerio and commonly referred to as zebrafish, described for the first time in 1822 by Francis Hamilton in the Ganges River but widespread throughout the entire Great Himalayan region of Southeast Asia [...].

In this study, we present data on the effects of condensed tannins (CTs) and hydrolysable tannins (HTs), polyphenols extracted from plants, at different concentrations on zebrafish development to identify the range of concentrations with toxic effects. Zebrafish embryos were exposed to CTs and HTs at two different concentration ranges (5.0-20.0 μgL -1 and 5.0-20.0 mgL -1 ) for 72 h. The toxicity parameters were observed up to 72 h of treatment. The uptake of CTs and HTs by the zebrafish larvae was assessed via HPLC analysis. A qRT-PCR analysis was performed to evaluate the expressions of genes cd63 , zhe1 , and klf4 , involved in the hatching process of zebrafish. CTs and HTs at 5.0, 10.0, and 20.0 μgL -1 were not toxic. On the contrary, at 5.0, 10.0, and 20.0 mgL -1 , HTs induced a delay in hatching starting from 48 h of treatment, while CTs showed a delay in hatching mainly at 48 h. The analysis of gene expression showed a downregulation in the group exposed to HTs, confirming the hatching data. We believe that this study is important for defining the optimal doses of CTs and HTs to be employed in different application fields such as the chemical industry, the animal feed industry, and medical science.

Insulin-like peptide 3 (INSL3) is a biomarker for Leydig cells in the testes of vertebrates, and it is principally involved in spermatogenesis through specific binding with the RXFP2 receptor. This study reports the insl3 gene transcript and the Insl3 prepropeptide expression in both non-reproductive and reproductive tissues of Danio rerio . An immunohistochemistry analysis shows that the hormone is present at a low level in the Leydig cells and germ cells at all stages of Danio rerio testis differentiation. Considering that the insl3 gene is transcribed in Leydig cells, our results highlight an autocrine and paracrine function of this hormone in the Danio rerio testis, adding new information on the Insl3 mode of action in reproduction. We also show that Insl3 and Rxfp2 belonging to Danio rerio and other vertebrate species share most of the amino acid residues involved in the ligand-receptor interaction and activation, suggesting a conserved mechanism of action during vertebrate evolution.

Environmental air pollution and resulting acid rain have the effect of increasing aluminum levels in water bodies. We studied the effects of aluminum on fish gills, the tissue most exposed to aluminum, using zebrafish as an experimental model. Adult zebrafish were exposed to an aluminum concentration found in polluted environments (11 mg/L) for 10, 15 and 20 days and the effects on gill morphology, redox homeostasis (ROS content, NADPH oxidase, NOX, activity, oxidative damage, antioxidant enzymes, total antioxidant capacity, in vitro susceptibility to oxidants) and on behavioural and metabolic parameters (routine respiratory oxygen consumption rMO 2 , tail-beating frequency, cytochrome oxidase activity and muscle lactate content) were evaluated. Exposure to aluminum affects branchial histology, inducing alterations in primary and secondary lamellae and redox homeostasis, modifying ROS levels, NOX activity, lipid and protein oxidative damage, antioxidant enzymes, and total antioxidant capacities, and increases rMO 2 . The effects exhibited a time-dependent behaviour, suggesting the activation of an adaptive response. These changes are associated with a transition of muscle metabolism from aerobic to anaerobic, as suggested by the increase in muscle lactate content, which is probably functional to preserve locomotor performance. Overall, the results here reported provide new insights into the toxicity mechanisms of Al exposure on gill tissue and the subsequent adaptive response of aquatic species., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

Poly(ADPribosyl)ation is a post-translational protein modification, catalyzed by poly(ADP-ribose) polymerase (PARPs) enzymes, responsible for ADP-ribose polymer synthesis (PAR) from NAD + . PAR turnover is assured by poly(ADPR) glycohydrolase (PARGs) enzymes. In our previous study, the altered histology of zebrafish brain tissue, resulting in demyelination and neurodegeneration also with poly(ADPribosyl)ation hyperactivation, was demonstrated after aluminum (Al) exposure for 10 and 15 days. On the basis of this evidence, the aim of the present research was to study the synthesis and degradation of poly(ADP-ribose) in the brain of adult zebrafish exposed to 11 mg/L of Al for 10, 15, and 20 days. For this reason, PARP and PARG expression analyses were carried out, and ADPR polymers were synthesized and digested. The data showed the presence of different PARP isoforms, among which a human PARP1 counterpart was also expressed. Moreover, the highest PARP and PARG activity levels, responsible for the PAR production and its degradation, respectively, were measured after 10 and 15 days of exposure. We suppose that PARP activation is related to DNA damage induced by Al, while PARG activation is needed to avoid PAR accumulation, which is known to inhibit PARP and promote parthanatos. On the contrary, PARP activity decrease at longer exposure times suggests that neuronal cells could adopt the stratagem of reducing polymer synthesis to avoid energy expenditure and allow cell survival.

Aluminium (Al) is among the most abundant metals in nature, and its presence in the environment is further increasing by anthropogenic activities. In water bodies, the Al concentrations ranged between 0.001 and 50 mg/L, raising concerns about the health of aquatic organisms. For this reason, zebrafish was chosen as the model, since it is well suited for ecotoxicological studies. Adult specimens were exposed to 11 mg/L of Al for 10, 15 and 20 days to assess both the morphology and the oxidative state of muscle tissue. Considering the involvement of ROS, the activity of the main antioxidant enzymes, metallothioneins contents, but also oxidative damage and enzymes involved in energy consumption and neuromuscular transmission were assessed. Collected data showed an increase in the thickness of the endomysium and resorbed myofibrils in the organisms exposed to Al for 10 days, and an increase of myotomes' size in the organisms exposed to Al for 15 days. Moreover, the organisms exposed for less time to Al, it was evident an activation of anaerobic metabolism and the increased activity of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and glutathione S-transferases. However, these effects stabilized with increasing exposure time. In addition, only after 20 days of treatment did the oxidative damage to the proteins and the activity of acetylcholinesterase increase while the levels of metallothioneins and the lipid peroxidation were lower for all treated animals when compared to the control group. Overall, the biochemical and histological changes induced by aluminium exposure in the muscular tissue represent a relevant contribution to understanding the environmental risk due to the diffusion of this metal within the aquatic compartment., (Copyright © 2022 Elsevier B.V. All rights reserved.)

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., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Cadmium is a biologically non-essential metal. It is also toxic to many organs including the brain. The aim of this study was to analyse the neurodegenerative effects of this metal in embryos and adults of zebrafish exposed to sub-lethal concentrations of cadmium. The study was performed by cytochemical stainings. Six hours after fertilisation (hpf) zebrafish embryos were treated for 24 hours with 9 μM of cadmium and subsequently stained with Acridine orange in whole mount to detect apoptosis in the brain. Adult zebrafish were treated for 16 days with the same concentration of cadmium, and cell death in the brain was detected by Fluoro-Jade B staining at 2, 7 and 16 days of treatment. An increase in cell death was observed only at 16 days of treatment in adults, while an increase in apoptotic events was revealed in the brain of embryos after 24 h of treatment. This evidence is indicative that cadmium, even at a sub-lethal concentration, induces cell death in the brain of embryos but also in adults of zebrafish in which the phenomenon appears time-dependent.Â.

Embryos at shield stage and larvae at protruding mouth stage were exposed to different concentrations of aluminium chloride (AlCl 3 ) for 72 h with the purpose to analyse their phenotype and lethality. After 24, 48 and 72 h of treatment, higher toxicity of the metal was observed on larvae with minimal lethal concentration of 0.25, 0.20 and 0.08 mm, respectively, while for embryos the corresponding values were 40, 25 and 16 mm. We observed pericardial oedema and alteration of heart rate in 50% of larvae after 48 h of exposure to 100 μm. In larvae exposed to the same concentration, there was also a neurological injury at the level of glial cells, with the number of glial fibrillary acidic protein-positive cells being significantly reduced. This study confirms the toxic nature of this metal and shows that aluminium could also interestingly represent a cardiotoxin in addition to its neurotoxic ability., (© 2016 John Wiley & Sons Ltd.)

Cadmium is an extremely toxic heavy metal that widely occurs in industrial workplaces with various hazardous effects on brain functions. The cytotoxic effects of cadmium chloride (CdCl 2 ) on the neuroglial components of the zebrafish brain were analysed by detecting the glial fibrillary acidic protein (GFAP) expression and the mRNA levels of myelin genes mbp, mpz and plp1 in adult specimens exposed to cadmium for 2, 7 and 16 days. A significant decrease in the GFAP protein by Western blotting experiments was observed after 2 days of treatment, reaching 55% after 16 days. No change was observed in the mRNA levels. Using immunohistochemistry, a reduction in GFAP-positive structures was revealed with a progressive trend in all the brains at 2, 7 and 16 days of treatment. In particular, a considerable reduction in GFAP-positive fibres, with a different course, was observed in the ventricle areas and at the pial surface and in blood vessels after 16 days. Our experiments also showed a structural and chemical alteration of myelin and upregulation of mpz mRNA levels, the oligodendrocyte gene that is upregulated in experiments of neuronal injury, but not of plp1 and mbp mRNA levels, other myelin structural genes. These data confirm the toxic action of cadmium on the zebrafish brain. This action is time-dependent and involves the glial cells, key components of the protection and function of nerve cells, hence the basis for many neurological diseases. Copyright © 2016 John Wiley & Sons, Ltd., (Copyright © 2016 John Wiley & Sons, Ltd.)