Black phosphorus quantum dots induce myocardial inflammatory responses and metabolic disorders in mice

J Environ Sci (China). 2024 Mar:137:53-64. doi: 10.1016/j.jes.2023.01.004. Epub 2023 Jan 10.

Abstract

As an ultrasmall derivative of black phosphorus (BP) sheets, BP quantum dots (BP-QDs) have been effectively used in many fields. Currently, information on the cardiotoxicity induced by BP-QDs remains limited. We aimed to evaluate BP-QD-induced cardiac toxicity in mice. Histopathological examination of heart tissue sections was performed. Transcriptome sequencing, real-time quantitative PCR (RT‒qPCR), western blotting, and enzyme-linked immunosorbent assay (ELISA) assays were used to detect the mRNA and/or protein expression of proinflammatory cytokines, nuclear factor kappa B (NF-κB), phosphatidylinositol 3 kinase-protein kinase B (PI3K-AKT), peroxisome proliferator-activated receptor gamma (PPARγ), and glucose/lipid metabolism pathway-related genes. We found that heart weight and heart/body weight index (HBI) were significantly reduced in mice after intragastric administration of 0.1 or 1 mg/kg BP-QDs for 28 days. In addition, obvious inflammatory cell infiltration and increased cardiomyocyte diameter were observed in the BP-QD-treated groups. Altered expression of proinflammatory cytokines and genes related to the NF-κB signaling pathway further confirmed that BP-QD exposure induced inflammatory responses. In addition, BP-QD treatment also affected the PI3K-AKT, PPARγ, thermogenesis, oxidative phosphorylation, and cardiac muscle contraction signaling pathways. The expression of genes related to glucose/lipid metabolism signaling pathways was dramatically affected by BP-QD exposure, and the effect was primarily mediated by the PPAR signaling pathway. Our study provides new insights into the toxicity of BP-QDs to human health.

Keywords: BP-QDs; Cardiac toxicity; Glucose/lipid metabolism; Inflammatory responses; NF-κB signaling pathway; PPARγ signaling pathway.

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Glucose
  • Humans
  • Metabolic Diseases*
  • Mice
  • NF-kappa B / metabolism
  • PPAR gamma / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Quantum Dots* / toxicity

Substances

  • Proto-Oncogene Proteins c-akt
  • NF-kappa B
  • PPAR gamma
  • Phosphatidylinositol 3-Kinases
  • Cytokines
  • Glucose