Lately, the interest in researching microplastics in the Black Sea has increased, highlighting areas of accumulation in which the amounts of microplastics are alarming, such as seafood consumed by the population. The Black Sea has special characteristics in terms of currents and wave dynamics that create opportunities for the accumulation of microplastics in hotspot points, such as in the context of large rivers discharge that contains large amounts of pollutants and new sources of contamination. This article offers a literature-based profile on plastic pollution in the Black Sea—pollution that originates in the discharge of large rivers, transportation, and other economic activities, even the COVID-19 pandemic—in order to highlight “microplastic hotspots” before the current political crisis that directly involves the Black Sea worsens.

Recent reports focusing on the extent of plastic pollution have shown that many types of fibers and polymers can now be found in most marine species. The severe contamination of plastic nano-/microparticles (NPs/MPs) mainly results in immediate negative outcomes, such as organic impairments and tissue damage, as well as long-termed negative effects, such as developmental retardation and defects, chronic inflammation, oxidative stress (OS), metabolic imbalance, mutagenesis, and teratogenesis. Oxidative responses are currently considered the first line molecular signal to potential toxic stimuli exposure, as the oxidative balance in electron exchange and reactive oxygen species signaling provides efficient harmful stimuli processing. Abnormal signaling or dysregulated ROS metabolism—OS—could be an important source of cellular toxicity, the source of a vicious cycle of environmental and oxidative signaling-derived toxicity. As chemical environmental pollutants, plastic NPs/MPs can also be a cause of such toxicity. Thus, we aimed to correlate the possible toxic effects of plastic NPs/MPs in zebrafish models, by focusing on OS and developmental processes. We found that plastic NPs/MPs toxic effects could be observed during the entire developmental span of zebrafish in close correlation with OS-related changes. Excessive ROS production and decreased antioxidant enzymatic defense due to plastic NPs/MPs exposure and accumulation were frequently associated with acetylcholinesterase activity inhibition, suggesting important neurodevelopmental negative outcomes (cognitive abnormalities, neurodevelopmental retardation, behavioral impairments) and extraneuronal effects, such as impaired digestive physiology.

The effects of exposure to environmental pollutants on neurological processes are of increasing concern due to their potential to induce oxidative stress and neurotoxicity. Considering that many industries are currently using different types of plastics as raw materials, packaging, or distribution pipes, microplastics (MPs) have become one of the biggest threats to the environment and human health. These consequences have led to the need to raise the awareness regarding MPs negative neurological effects and implication in neuropsychiatric pathologies, such as schizophrenia. The study aims to use three zebrafish models of schizophrenia obtained by exposure to ketamine (Ket), methionine (Met), and their combination to investigate the effects of MP exposure on various nervous system structures and the possible interactions with oxidative stress. The results showed that MPs can interact with ketamine and methionine, increasing the severity and frequency of optic tectum lesions, while co-exposure (MP+Met+Ket) resulted in attenuated effects. Regarding oxidative status, we found that all exposure formulations led to oxidative stress, changes in antioxidant defense mechanisms, or compensatory responses to oxidative damage. Met exposure induced structural changes such as necrosis and edema, while paradoxically activating periventricular cell proliferation. Taken together, these findings highlight the complex interplay between environmental pollutants and neurotoxicants in modulating neurotoxicity.

Tartrazine (TZ, also known as FD&C Yellow No. 5 or E102) is a synthetic, water-soluble yellow food dye widely used in the food and pharmaceutical industries. Some studies have associated TZ with allergic reactions, especially among people with dye sensitivities or pre-existing allergies. Recent research also suggests a possible link between TZ consumption and the worsening of behavioral disorders, especially in children, including symptoms such as hyperactivity, irritability, restlessness, and sleep disturbances. Experimental studies in laboratory animals have highlighted potential risks associated with prolonged or high-dose exposure, including toxic effects on the nervous system and liver function. In addition, increasing evidence indicates that TZ can induce oxidative stress (OS) by increasing the production of reactive oxygen species (ROS), which can contribute to cellular damage and inflammation. Although the evidence remains inconclusive, there are recommendations to limit the intake of synthetic food dyes, especially in children’s diets. The purpose of this review is to examine the potential toxic effects on health of tartrazine by analyzing findings from experimental studies in cell cultures and laboratory animals, as well as correlations observed in humans. We focus on documented adverse reactions, including possible neurotoxic, hepatotoxic, oxidative, and behavioral effects. Through this, we aim to contribute to a more comprehensive understanding of the risks associated with exposure to this synthetic food dye.

In recent years, infertility has started to represent a major global public health problem. A growing number of evidences regarding the involvement of environmental factors in the decline of reproductive function have already been highlighted by the specialized literature. Microplastics (MPs) and nanoplastics (NPs) are ubiquitous particles present in all types of ecosystems. They have recently been detected in various human biological samples, including blood, placenta and seminal fluid. This suggests a continuous systemic exposure to this type of pollutant, as well as its capacity to penetrate the key barriers of the human body and trans-generational transfer. The purpose of this work was to critically review the current literature regarding the link between exposure to MPs/NPs and the possible interaction with human infertility. Relevant studies on animal models, as well as the molecular implications and the main access routes of MPs/NPs in the human body, were also highlighted. Studies on animal models have highlighted the toxicity of this type of pollutant manifested through different size-polymer dependent mechanisms of action, including gonadal histological alterations, induction of oxidative stress, cellular apoptosis and hormonal dysfunctions. An integrative perspective on the reproductive risks associated with small-sized polymeric materials is provided. Furthermore, the need to develop standardized methods and protocols for MPs detection in human samples is emphasized, to improve our understanding of the toxic effects on human health and to guide potential preventive or therapeutic strategies for this type of toxicity.

Parkinson’s disease (PD) is an enigmatic neurodegenerative disorder that is currently the subject of extensive research approaches aiming at deepening the understanding of its etiopathophysiology. Recent data suggest that distinct compounds used either as anticonvulsants or agents usually used as dopaminergic agonists or supplements consisting of live active lactic acid bacteria strains might alleviate and improve PD-related phenotypes. This is why we aimed to elucidate how the administration of rotenone (ROT) disrupts homeostasis and the possible neuroactive potential of valproic acid (VPA), antiparkinsonian agents (levodopa and carbidopa – LEV+CARB), and a mixture of six Lactobacillus and three Bifidobacterium species (PROBIO) might re-establish the optimal internal parameters. ROT causes significant changes in the central nervous system (CNS), notably reduced neurogenesis and angiogenesis, by triggering apoptosis, reflected by the increased expression of PARKIN and PINK1 gene(s), low brain dopamine (DA) levels, and as opposed to LRRK2 and SNCA compared with healthy zebrafish. VPA, LEV/CARB, and PROBIO sustain neurogenesis and angiogenesis, manifesting a neuroprotective role in diminishing the effect of ROT in zebrafish. Interestingly, none of the tested compounds influenced oxidative stress (OS), as reflected by the level of malondialdehyde (MDA) level and superoxide dismutase (SOD) enzymatic activity revealed in non-ROT-exposed zebrafish. Overall, the selected concentrations were enough to trigger particular behavioral patterns as reflected by our parameters of interest (swimming distance (mm), velocity (mm/s), and freezing episodes (s)), but sequential testing is mandatory to decipher whether they exert an inhibitory role following ROT exposure. In this way, we further offer data into how ROT may trigger a PD-related phenotype and the possible beneficial role of VPA, LEV+CARB, and PROBIO in re-establishing homeostasis in Danio rerio.