Maize is frequently contaminated with multiple mycotoxins, especially those produced by Aspergillus flavus and Fusarium verticillioides. As mycotoxin contamination is a critical factor that destabilizes global food safety, the current review provides an updated overview of the (co-)occurrence of A. flavus and F. verticillioides and (co-)contamination of aflatoxin B1 (AFB1) and fumonisin B1 (FB1) in maize. Furthermore, it summarizes their interactions in maize. The gathered data predict the (co-)occurrence and virulence of A. flavus and F. verticillioides would increase worldwide, especially in European cold climate countries. Studies on the interaction of both fungi regarding their growth mainly showed antagonistic interactions in vitro or in planta conditions. However, the (co-)contamination of AFB1 and FB1 has risen worldwide in the last decade. Primarily, this co-contamination increased by 32% in Europe (2010–2020 vs. 1992–2009). This implies that fungi and mycotoxins would severely threaten European-grown maize.

Mycotoxins are considered the most threating natural contaminants in food. Among these mycotoxins, aflatoxin B1 (AFB1) and fumonisin B1 (FB1) are the most prominent fungal metabolites that represent high food safety risks, due to their widespread co-occurrence in several food commodities, and their profound toxic effects on humans. Considering the ethical and more humane animal research, the 3Rs (replacement, reduction, and refinement) principle has been promoted in the last few years. Therefore, this review aims to summarize the research studies conducted up to date on the toxicological effects that AFB1 and FB1 can induce on human health, through the examination of a selected number of in vitro studies. Although the impact of both toxins, as well as their combination, were investigated in different cell lines, the majority of the work was carried out in hepatic cell lines, especially HepG2, owing to the contaminants’ liver toxicity. In all the reviewed studies, AFB1 and FB1 could invoke, after short-term exposure, cell apoptosis, by inducing several pathways (oxidative stress, the mitochondrial pathway, ER stress, the Fas/FasL signaling pathway, and the TNF-α signal pathway). Among these pathways, mitochondria are the primary target of both toxins. The interaction of AFB1 and FB1, whether additive, synergistic, or antagonistic, depends to great extent on FB1/AFB1 ratio. However, it is generally manifested synergistically, via the induction of oxidative stress and mitochondria dysfunction, through the expression of the Bcl-2 family and p53 proteins. Therefore, AFB1 and FB1 mixture may enhance more in vitro toxic effects, and carry a higher significant risk factor, than the individual presence of each toxin.

Cyclotriphosphazenes (CTPs), widely used as flame-retardant electrolyte additives in lithium batteries, have raised significant environmental and health concerns due to their potential release and human exposure. However, the toxicological effects of CTPs, particularly on pulmonary health, remain poorly understood. This study investigates the impact of long-term CTPs exposure at environmentally relevant doses on lung cells and animal models. In vitro experiments revealed that CTPs exposure impaired mitochondrial function in BEAS-2B cells in a time-dependent manner. Proteomic analysis demonstrated significant alterations in oxidative phosphorylation-related proteins, disrupting the electron transport chain (ETC). Untargeted metabolomics further revealed disruptions in the tricarboxylic acid (TCA) cycle, glutathione metabolism, and purine metabolism, with notably decreased levels of key metabolites. Multiomics integration suggested potential associations between high-dose CTPs exposure and diseases including lipoyltransferase 1 deficiency, Alzheimer’s disease, and schizophrenia. In vivo studies confirmed pathological lung damage in mice, including alveolar destruction and pulmonary fibrosis. Additionally, downregulation of N-lauroylsphingosine (NLDP) was identified as a potential metabolic biomarker for CTPs-induced lung injury, offering novel insights for mitigating CTPs’ adverse effects. These findings highlight the pulmonary toxicity of CTPs and provide a foundation for future risk assessment and preventive strategies.

Liquid crystal monomers (LCMs), as core components of liquid crystal displays (LCDs), are emerging as environmental materials due to their widespread use and potential for human and ecological exposure. Even as inquiries pertaining to the environmental and health risks of LCMs are progressing, their direct toxic effects on human organs and ecosystems persist in being inadequately comprehended. The present research underscores the hazards entailed by prolonged LCMs exposure, with specific reference to skin cells and animal models, under daily exposure magnitudes. This study reveals that long-term LCMs exposure disrupts mitochondrial function in skin cells, triggers inflammatory pathways (TNF signaling), and downregulates critical proteins (PLOD2, DDIT4) and metabolites (ATP, glutathione), indicating oxidative stress and cellular dysfunction. In vivo experiments further demonstrate histopathological damage in mouse skin, including disordered skin appendages and adipose disorganization, highlighting LCMs' hazardous potential. Multi-omics analysis links LCMs exposure to diseases such as lung cancer and Alzheimer's, while untargeted metabolomics identifies β-alanylleucine downregulation as a promising biomarker for LCM-induced toxicity. Given LCD e-waste growth, improper disposal releases LCMs, risking ecosystem bioaccumulation. These findings underscore the need for stricter regulation of LCMs throughout their lifecycle-from production to waste management-to mitigate ecological and health risks, with β-alanylleucine serving as a potential monitoring tool for environmental contamination.