No abstract

The aim of this research was to study the accumulation of heavy metals (cadmium - Cd, lead - Pb, chromium - Cr, nickel - Ni, and copper - Cu) from water and sediments into living tissues of relevant marine species from different trophic levels of a food web, representative for shallow waters of the Romanian Black Sea Coast where the main anthropogenic impacts exist. The heavy metals concentrations were analysed by using an Atomic Absorption Spectrometer with graphite furnace, the results being further used to calculate the bioconcentration factors for a few key taxa like green and red algae, molluscs and fishes. Seven sampling sites influenced by anthropogenic pollution sources (municipal wastewater treatment plants and diffuse sources) were considered and a total of 300 samples were analysed for the period 2011-2012, this being the first unitary study for the Romanian Black Sea marine ecosystem. In 2011 and 2012 there were no significant differences between the sampling areas considering the heavy metals concentrations in water. For the sediments significant differences were observed between sampling sites for some heavy metals, namely Pb in 2011 and Pb, Cu and Cd in 2012, the highest concentrations being registered in the southern sector of the Romanian Black Sea shore, where the anthropogenic pollution sources are represented by the harbour and wastewater treatment plants. The values of the bioaccumulation factors (BCFsed) shows that algae are good accumulators for Cu>Pb>Ni>Cr>Cd, in comparison with BCFwater where the order of heavy metal accumulation was different: Cr>Ni>Pb>Cd>Cu. Molluscs have higher bioconcentration factors for Cu and Cd for sediments and for Cu and Ni for water. Rapana venosa accumulated more Cd and Cu. For fishes, Pb, Cu and Ni had the highest values in the tissues of benthonic species Mullus barbatus. In bivalve molluscs and fishes, in the majority of cases, there were not recorded exceeding mean concentrations as compared to the maximum allowed concentrations for Cd and Pb.

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The complex yet not fully understood pathophysiology of Parkinson’s disease includes an important molecular component consisting of oxidative status changes, thus leading to oxidative stress occurrence. While no particular evidence has been reported that describes the relationship between oxidative stress and the molecular mechanisms behind Parkinson’s disease development, animal model studies has shown that oxidative stress induction could modulate Parkinson’s disease symptomatology. Despite the inability to perfectly replicate human disease in animals and despite that Parkinson’s disease has not been reported in any animal species, animal modeling is one of the most important tools in understanding the complex mechanisms of human disorders. In this way, this study is aimed at detailing this particular relationship and describing the molecular mechanisms underlying Parkinson’s disease in animal models, focusing on the potential advantages and disadvantages of zebrafish in this context. The information relevant to this topic was gathered using major scientific database research (PubMed, Google Scholar, Web of Science, and Scopus) based on related keywords and inclusion criteria. Thus, it was observed that oxidative stress possesses an important role in Parkinson’s disease as shown by numerous animal model studies, many of which are based on rodent experimental models. However, an emerging impact of the zebrafish model was observed in the research of Parkinson’s disease pathological mechanisms with regard to disease development factors and the cause-effect relationship between oxidative stress and comorbidities (such as depression, hyposmia, fatigue, sleep disturbances, and cognitive deficits) and also with regard to the pharmacological potential of antioxidant molecules in Parkinson’s disease treatment.

Increased interest regarding the biometal mechanisms of action and the pathways in which they have regulatory roles was lately observed. Particularly, it was shown that biometal homeostasis dysregulation may lead to neurodegeneration including Alzheimer's disease, Parkinson disease, or prion protein disease, since important molecular signaling mechanisms in brain functions implicate both oxidative stress and redox active biometals. Oxidative stress could be a result of a breakdown in metal-ion homeostasis which leads to abnormal metal protein chelation. In our previous work, we reported a strong correlation between Alzheimer's disease and oxidative stress. Consequently, the aim of the present work was to evaluate some of the biometals' levels (magnesium, manganese, and iron), the specific activity of some antioxidant enzymes (superoxide dismutase and glutathione peroxidase), and a common lipid peroxidation marker (malondialdehyde concentration), in mild cognitive impairment (n = 15) and Alzheimer's disease (n = 15) patients, compared to age-matched healthy subjects (n = 15). We found increased lipid peroxidation effects, low antioxidant defense, low magnesium and iron concentrations, and high manganese levels in mild cognitive impairment and Alzheimer's disease patients, in a gradual manner. These data could be relevant for future association studies regarding the prediction of Alzheimer's disease development risk or circling through stages by analyzing both active redox metals, oxidative stress markers, and the correlations in between.