Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 179, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2023.113952
Keywords
Black phosphorus quantum dots; Ferroptosis; Beas-2B; Pulmonary toxicity
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Black Phosphorus Quantum Dots (BP-QDs) have shown potential biomedical applications but may cause respiratory toxicity when entering the body. This study confirmed the respiratory toxicity of BP-QDs in mice and human bronchial epithelial cells by observing lipid peroxidation and iron overload. The findings suggest that BP-QDs induce ferroptosis by increasing lipid peroxidation and iron accumulation in vitro and in vivo.
Black Phosphorus Quantum Dots (BP-QDs) have potential applications in biomedicine. BP-QDs may enter the body through the respiratory tract during grinding and crushing production and processing, causing respiratory toxicity. Ferroptosis is an oxidative, iron-dependent form of cell death. Here, respiratory toxicity of BP-QDs has been validated in mice and human bronchial epithelial cells. After 24 h of exposure to different doses (4-32 & mu;g/ mL) of BP-QDs, intracellular lipid peroxidation and iron overload occurred in Beas-2B cells. After 4 times exposures by noninvasive tracheal instillation at four doses [0, 0.25, 0.5 and 1 (mg/kg/48h)], all animals were sacrificed, organs were removed, processed for pathological examination and molecular analysis. Iron overload, glutathione (GSH) depletion and lipid peroxidation in the lung tissue of mice in the exposure group. Furthermore, based on the ferroptosis-associated protein and mRNA expression, it was hypothesized that BP-QDs induced ferroptosis through increasing intracellular free iron and polyunsaturated fatty acid synthesis. By comparing with previous studies, we speculate that primary cells generally are more sensitive to BP-QDs-induced damage than cancer cells. In summary, findings in the present study confirmed that BP-QDs induce ferroptosis via increasing lipid peroxidation and iron accumulation in vitro and in vivo.
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