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Cancer is a crucial global health problem, and prevention is an important strategy to reduce the burden of the disease. Daily diet is the key modifiable risk factor for cancer, and an increasing body of evidence suggests that specific nutrients in foods may have a preventive effect against cancer. This review summarizes the current evidence on the role of nutrients from foods in cancer intervention. It discusses the potential mechanisms of action of various dietary components, including phytochemicals, vitamins, minerals, and fiber. The findings of epidemiological and clinical studies on their association with cancer risk are highlighted. The foods are rich in bioactive compounds such as carotenoids, flavonoids, and ω-3 fatty acids, which have been proven to have anticancer properties. The effects of steady-state delivery and chemical modification of these food's bioactive components on anticancer and intervention are summarized. Future research should focus on identifying the specific bioactive compounds in foods responsible for their intervention effects and exploring the potential synergistic effects of combining different nutrients in foods. Dietary interventions that incorporate multiple nutrients and whole foods may hold promise for reducing the risk of cancer and improving overall health. [ABSTRACT FROM AUTHOR]

Dandelion has received wide attention in food and medicine fields due to its excellent antioxidant properties. Nonetheless, the underlying mechanism of this action has not yet been fully clarified, particularly at the metabolic level. Herein, the effects of dandelion extract (DE) on H2O2-induced oxidative damage was investigated. The results indicate that the DE alleviated H2O2-induced cell damage (increased by 14.5% compared to H2O2 group), reduced the reactive oxygen species (ROS) level (decreased by 80.1% compared to H2O2 group), maintained the mitochondrial membrane potential (MMP) level, and increased antioxidant-related enzyme activities. Importantly, the metabolic response of PC12 cells indicates that H2O2 disturbed phospholipid metabolism and damaged cell membrane integrity. In addition, energy metabolism, the central nervous system, and the antioxidant-related metabolism pathway were perturbed. In contrast, DE rescued the H2O2-induced metabolic disorder and further alleviated oxidative damage. Collectively, these findings provide valuable stepping stones for a discussion of the mechanism and show the promise of DE as a suitable additive for functional food products. [ABSTRACT FROM AUTHOR]

Carbon quantum dots (CQDs) from heat-treated foods show toxicity, but the mechanisms of toxicity and removal of CQDs have not been elucidated. In this study, CQDs were purified from roasted coffee beans through a process of concentration, dialysis and lyophilization. The physical properties of CQDs, the degree and mechanism of toxicity and the removal method were studied. Our results showed that the size of CQDs roasted for 5 min, 10 min and 20 min were about 5.69 ± 1.10 nm, 2.44 ± 1.08 nm and 1.58 ± 0.48 nm, respectively. The rate of apoptosis increased with increasing roasting time and concentration of CQDs. The longer the roasting time of coffee beans, the greater the toxicity of CQDs. However, the caspase inhibitor Z-VAD-FMK was not able to inhibit CQDs-induced apoptosis. Moreover, CQDs affected the pH value of lysosomes, causing the accumulation of RIPK1 and RIPK3 in lysosomes. Treatment of coffee beans with a pulsed electric field (PEF) significantly reduced the yield of CQDs. This indicates that CQDs induced lysosomal-dependent cell death and increased the rate of cell death through necroptosis. PEF is an effective way to remove CQDs from roasted coffee beans. [ABSTRACT FROM AUTHOR]

Although the presence of foodborne nanoparticles was confirmed in grilled fish in a previous study, the evaluation of potential health risks of these NPs was insufficient. In the present study, the potential toxicity of onion-like carbon nanoparticles (OCNPs) separated from grilled turbot Scophthalmus maximus L. was evaluated using mouse osteoblasts cells model and zebrafish (Danio rerio) model. Cytotoxicity evaluation revealed that the OCNPs penetrated into the MC3T3-E1 cells without arousing cell morphology changes. No evident apoptosis or damage of cells was observed with increasing OCNPs' concentration to 20 mg/mL. In the hemolysis test, OCNPs did not show an obvious hemolysis effect on red blood cells. In the acute toxicity test, the LC50 value (212.431 mg/L) of OCNPs to zebrafish showed a weak acute toxicity. In subacute toxicity test, after exposure to OCNPs (30 mg/L, 40 mg/L) for 10 days, a significant increase of reactive oxygen species level of zebrafish was observed. Meanwhile, redundant ROS content caused inhibition to several antioxidant enzymes and induced lipid and protein peroxidation damages according to the upregulation of malondialdehyde and protein carbonyl levels. The chronic toxicity test results indicated that oxidative stress was only observed in the high concentration group of OCNPs-treated zebrafish. [ABSTRACT FROM AUTHOR]