Food and Chemical Toxicology最新文献

Nanoplastics (NPs) contamination in food has become a critical issue due to the potential impacts on human health. Currently, NPs have the potential to induce cardiovascular damage, but the exact mechanism at the cellular level is unclear. In addition, environmental factors can modify the surface functional groups of NPs, among which amino-modified NPs (NH₂-NPs) significantly affect their toxicity. This study aimed to investigate the effects of NPs with different particle sizes and amino modifications on human umbilical vein endothelial cells (HUVECs). Results demonstrated that 20 nm NH₂-NPs exerted the most significant effect on the expression levels of pyroptosis-related proteins. The pyroptosis inhibitor VX-765 reduced PI-positive cells and the expression of pyroptosis proteins in HUVECs, supporting a critical role of pyroptosis in NH₂-NPs-induced injury. Subsequently, exposure to 20 nm NH₂-NPs resulted in HUVECs injury, which promoted the recruitment of human acute monocytic leukemia (THP-1) cells, with increased adhesion, migration, and lipid accumulation. These findings indicated that PS-NPs induced injury in HUVECs by NF-κB/NLRP3/GSDMD-mediated pyroptosis pathway and influenced THP-1 cells adhesion, migration, and foam cell formation. This study provided insights into the vascular toxicity mechanisms of PS-NPs and highlighted the critical role of surface chemical modifications in modulating their toxicological effects.

This present paper provides the first integrative evaluation of the occurrence of emodin-induced hormetic-biphasic dose responses in the biological and biomedical literature, their study design and dose-response features, underlying adaptive and toxic mechanistic foundations, and generality across biological models, cell types, as well as across different levels of biological organization (i.e., cell, organ, and organism). Emodin-induced hormetic responses have been reported in numerous cellular experimental systems of broad biomedical interest, as well as in in vivo studies with fish and rodent models. Of particular interest was the generality of the in vivo findings across multiple commercial fish models, in which emodin enhanced growth and development and increased resistance to various physical and environmental stressors. While emodin induces hormetic effects via multiple molecular targets and pathways, a general mechanistic adaptive response strategy involves its capacity to activate peroxisome proliferator-activated receptor gamma and the AMPK/Nrf2 pathway.

Despite health benefits, fish consumption poses risks of exposure to toxic substances. Concentrations of toxic metals were determined in 20 fish species available on the Polish market. Cadmium (Cd) concentrations were within the range 0.003-0.005 mg/kg, lead (Pb) 0.011-0.033 mg/kg, total mercury (THg) 0.014-0.133 mg/kg, methylmercury (MeHg) 0.010 mg/kg - 0.108 mg/kg, inorganic arsenic (iAs) below 0.02 mg/kg. Mercury and methylmercury in tuna were at higher levels. The average contents 0.919 mg/kg and 0.684 mg/kg, were close to the limit for THg 1 mg/kg (Commission Regulation (EU) 2023/915). Risks to consumer health were estimated on the base on toxicity markers non-carcinogenic (THQ) for Cd, Pb, MeHg and iAs, and carcinogenic (CR) coefficient for iAs. Values THQ were low for Cd (0.5 x 10^-3 - 2 x 10^-3), Pb (0.7 x 10^-3 - 2.4 x 10^-3), MeHg (2.8 x 10^-2 - 31 x 10^-2) and for iAs (1.9 x 10^-2). The CR marker for iAs was also low at 0.86 x 10^-5. Low values for toxic metals and toxicity markers in fish from the Polish market confirms their safe consumption. Only in tuna the marker THQ for MeHg was twice the recommended safe value. The high methylmercury contents and high THQ in tuna indicates limitations in consumption this fish. Over the past decade, levels of toxic metals in fishes on the Polish market have remained stable. The only significant change was the increased THg and MeHg in tuna.