Oxidative Stress, Lysosomal Permeability, and Mitochondrial-Derived Vesicles Induced in NL-20 Human Bronchial Cells Exposed to Benzo[ghi]Perylene.

López-Pérez Lizardo, Roldán-Barreto Elisa, Xochiteotzin-Reyes Tania, Torres-Flores Ulises, Licea-Quintero Brandon, Monroy-Quintana Regina, Corona Juan Carlos, Zaragoza-Ojeda Montserrat, Arenas-Huertero Francisco

Journal: Toxicology in vitro : an international journal published in association with BIBRA 2025;104():105999

PMID: 39701484

Full Text on Elsevier Science View on PubMed

Abstract

Benzo[ghi] perylene (b[ghi]p) is classified as non-carcinogenic to humans, and there are currently no occupational exposure models available to identify its effects. The aim of this work was to evaluate the effect of b[ghi]p on the lysosomes of NL-20 cells (a human bronchial cell line) exposed to 4.5 μM for 3 h. The effect was evaluated through an ultrastructural evaluation, morphological changes, and acridine orange staining of lysosomes. Superoxide was quantified; and SOD1, cathepsin B, LAMP1, galectin-3 and LC3α/β, and Rab7 expression was evaluated by immunocytochemistry. The expression of genes related to oxidative stress responses (NRF2, NQO1, HMOX1 and PRDX1) and genes related to autophagy (ULK1, ATG9, BCN1, VMP1, TMEM41B and p62) were quantified by RT-qPCR. The ultrastructural evaluation revealed an increase in autophagic vesicles and phagophores in cells exposed to b[ghi]p, as well as vesicles derived from mitochondria. Based on morphology, there were vesicles in the cytoplasm. B[ghi]p significantly decreased the number of lysosomes (p < 0.05), and NAC reverse this effect (p < 0.05). Superoxide production was observed from 30 min to 3 h (p < 0.05). Immunocytochemistry revealed increased galectin-3 and LC3α/β. All oxidative stress-related genes showed high expression (p < 0.05), and the expression of ATG9 gene was decreased (p < 0.05). These results demonstrate that b[ghi]p induces oxidative stress, responsible for producing the toxic effects in the lysosomes of NL-20 cells.

Address: Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico. Electronic address: [email protected].; Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico; Posgrado en Ciencias Biológicas, Unidad de Posgrado, Edificio D, 1° Piso, Circuito de Posgrados, Ciudad Universitaria, Coyoacán, C.P, 04510 CDMX, Mexico. Electronic address: [email protected].; Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico.; Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico. Electronic address: [email protected].; Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico. Electronic address: [email protected].; Laboratorio de Investigación en Neurociencias, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico.; Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico. Electronic address: [email protected].

DOI: 10.1016/j.tiv.2024.105999

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MeSH Terms: Humans, Oxidative Stress, Lysosomes, Cell Line, Mitochondria, Bronchi, Perylene, Autophagy, Permeability, Superoxides