Neuronutrition to improve brain resilience to stress and human health has received considerable attention. The use of specific nutrients is effective in preventing and slowing neurodegenerative and neuropsychiatric disorders. Selective neuronutrients, including polyphenols, short-chain fatty acids (SCFAs), tryptophan, tyrosine, and sulfur metabolites, can modulate the dysregulated nuclear factor erythroid 2 (Nrf2) pathway through neuroepigenetic modifications and altered levels of neurotransmitters such as serotonin, melatonin, and dopamine. In particular, abnormal epigenetic alterations in the promoter function of the NFE2L2/Nrf2 gene may contribute to the onset and progression of various diseases by disrupting cellular homeostasis. Recent evidence has documented that polyphenols are capable of modulating Nrf2 signaling; to do this, they must reverse hypermethylation in the CpG islands of the NFE2L2 gene. This process is achieved by modifying the activity of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs). Furthermore, a diverse group of polyphenolic metabolites can be identified and quantified using innovative mass spectrometry platforms in both in vitro models and human urine samples to investigate redox metabolic homeostasis under physiological and pathophysiological conditions. This review aims to deepen the current understanding of the role of nutrient-derived secondary metabolites. It highlights innovative strategies to effectively prevent, slow, or potentially reverse neuroinflammation and oxidative stress, key drivers of neuronal damage. The targeted application of these metabolites can be considered a novel, personalized neuronutritional approach to promote brain health and neuronal adaptation.

Microplastics (MPs), emerging contaminants of significant global concern, have a substantially increased environmental impact due to their biological persistence and accumulation in the body. Exposure to MPs has been associated with oxidative stress, systemic inflammation, and cellular dysfunction, notably affecting critical tissues such as the stomach, colon, and brain. This review explores the correlation between MPs and cancer risk along the gastric–colon–brain axis, identifying the signaling pathways altered by MP exposure. Furthermore, it highlights the role of functional nutrition and bioactive flavonoids—including chlorogenic acid, coumaric acid, and naringin—as well as the use of highly bioavailable combined polyphenol nanoparticles as potential detoxifying agents. Functional nutrients are effective in enhancing cellular resilience against reactive oxygen species (ROS) production and MP-induced toxicity, offering protective effects at the gastric, intestinal, and brain barriers. Activation of the Nrf2 pathway by bioactive compounds promotes the expression of detoxifying enzymes, suggesting a promising nutritional strategy to mitigate MP-related damage. This review underscores how functional nutrition may represent a viable therapeutic approach to reduce the harmful effects of MP exposure. The integration of advanced technologies—such as microfluidic systems, organ-on-a-chip platforms, and machine learning—and the identification of key molecular targets lay the foundation for developing preventive and personalized medicine strategies aimed at lowering the risk of environmentally induced carcinogenesis.

The therapeutic potential of functional nutrients has garnered considerable attention for enhancing resilience signaling and counteracting the damage to human health caused by microplastic pollutants. The intricate interactions between microplastics (MPs) and nanoplastics (NPs) and functional nutrients, including polyphenols, flavonoids, phenylpropanoids, phenolic acids, diterpenoids, and triterpenoids, have been shown to improve blood–brain barrier (BBB) homeostasis and brain function by inhibiting oxidative stress, ferroptosis, and inflammation linked to the pathogenesis of metabolic and brain disorders. Interestingly, nutrients exhibit biphasic dose–response effects by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway and stress-resilience proteins at minimum doses, thereby preventing or blocking MP and NP-induced damage. Notably, chronic exposure to environmental pollutants causes aberrant regulation of NFE2L2 gene and related antioxidant signaling, which can exacerbate selective susceptibility to brain insulin resistance under inflammatory conditions. This, in turn, impairs glucose metabolism and facilitates β-amyloid (Aβ) plaque synthesis leading to the onset and progression of Alzheimer’s disease (AD), also known as “Type 3 diabetes”. This pathological process triggered by oxidative stress, inflammation, and ferroptosis creates a vicious cycle that ultimately contributes to neuronal damage and loss. The review aims to investigate the therapeutic potential of functional nutrients targeting the Nrf2 pathway and stress resilience proteins to regulate epigenetic alterations, and to explore the underlying molecular mechanisms using innovative in vitro platforms for the development of promising preventive strategies and personalized nutritional interventions to attenuate oxidative stress, ferroptosis, and inflammation, with the goal of ultimately improving clinical outcomes.

The growing spread of antibiotic resistance represents a significant challenge in the medical field, making the treatment of bacterial infections increasingly difficult. Therefore, current research is focused on studying new formulations containing natural antibacterial/antibiofilm agents that can act on both planktonic and sessile bacteria. In this study we developed a soluble formulation of the flavonoid baicalin (BA) by complexation with sulfobutylether-β-cyclodextrin (SBE-β-CD), designed for the treatment of ocular infections. The inclusion complex, prepared by lyophilization, showed a significant increase in BA solubility (110-times higher than free BA) and fast dissolution. In solution studies and the deeper physical-chemical characterization performed at solid state evidenced the formation of a 1:1 inclusion complex with high association constant (about 6000 M^-1). Moreover, NMR spectroscopy and molecular docking simulations evidenced the deeper penetration of benzoyl and cinnamoyl moieties of BA within the macrocycle cavity, whilst the glucuronic residue remained out of the cavity but probably interacting with sulfobutyl groups of the CD. Biological in vitro studies were carried out to verify the activity of the free and complexed BA against Staphylococcus aureus, Staphylococcus epidermidis, Klebsiella pneumoniae and Escherichia coli. High improvement of antibacterial and antibiofilm activity was observed for the inclusion complex respect to the free drug against both Gram + and Gram- bacteria strains assayed.

A new category of polyphenolic compounds, like flavonoids, phenolic acids, phenylpropanoids, terpenoids, and others, referred to as food nutrients, may counteract the harmful effects of micro- and nanoplastics (MNPs) by enhancing cellular stress resilience response and overall human health. These compounds found in functional food help mitigate the cellular damage, inflammation, and oxidative stress caused by MNP exposure, which can contribute to pathological conditions, including diabetes. Importantly, specific food nutrients are able to activate, at the minimum dose, the nuclear factor erythroid-derived 2-like 2 (Nrf2) to prevent or block MNP-induced damage. The Nfe2l2 gene encodes the Nrf2 transcription factor, acting as a master regulator of redox homeostasis by inducing antioxidant response element (ARE)-driven resilience genes, which in turn, promote the expression of detoxification enzymes like heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase 1 (NQO1), and glutathione S-transferase (GST) to scavenge reactive oxygen species (ROS) and shield cells from environmental damage and toxicity. Deregulation of the Nfe2l2 gene due to the accumulation of MNP pollutants may exacerbate the inflammatory conditions associated with diabetes and its chronic complications by rendering cells more sensitive to oxidative stress, apoptosis, and pyroptosis. Furthermore, epigenetic modifications influence gene regulation; chromatin remodeling directly impacts DNA accessibility, allowing or limiting transcription factor access to regulate gene expression. This mechanism may also play a pivotal role in the progression of oxidative stress-related diseases, as it modulates the Nrf2 pathway and the expression levels of its target genes. In contrast to the current literature, which has only addressed the pathological mechanisms induced by MNPs, this research explores, for the first time, how food nutrients interacting with the Nfe2l2 gene can combat or reverse the toxic effects of MNPs in cells, tissues, and organs. The goal is to improve health by attenuating MNP toxicity, which is influenced by individual genetic variations and cellular stress resilience.

Water and wastewater workers encounter complex occupational exposures, but evidence on related injuries and adverse health outcomes remains fragmented. We systematically searched PubMed/MEDLINE, Scopus, Web of Science Core Collection, and Embase on 23 April 2026 and synthesized evidence using a Population–Exposure–Outcome framework and PRISMA 2020. Two reviewers independently screened and extracted data. Methodological quality was evaluated with design-specific Joanna Briggs Institute tools, and certainty for prevention measures was assessed using a GRADE-informed narrative approach. Seventy studies published from 1940 to 2025 were included; most were cross-sectional. The most reproducible findings concerned respiratory effects from bioaerosols, endotoxins, and hydrogen sulfide, musculoskeletal morbidity (12-month low-back-pain prevalence up to 72.8%), and severe acute hazards during chemical handling and confined-space entry. Infectious findings, including hepatitis A/E, Helicobacter pylori, and intestinal parasites, were heterogeneous and particularly vulnerable to confounding by community background prevalence. Employment duration, inadequate personal protective equipment, insufficient training, and unsafe facility design amplified risk. Meta-analysis was precluded by heterogeneity, and confidence was limited by cross-sectional designs and inconsistent adjustment. The review was not registered and received no external funding. Engineering controls, confined-space safeguards, and task-specific protective equipment are priority measures, although intervention-effectiveness evidence remains low or very low certainty.