Sterigmatocystin-induced cytotoxicity via oxidative stress induction in human neuroblastoma cells.

6533b7d3fe1ef96bd126011c

RESEARCH PRODUCT

Sterigmatocystin-induced cytotoxicity via oxidative stress induction in human neuroblastoma cells.

María-josé Ruiz Veronica Zingales Mónica Fernández-franzón

subject

endocrine system Antioxidant Cell Survival medicine.medical_treatment Sterigmatocystin Toxicology medicine.disease_cause Lipid peroxidation 03 medical and health sciences chemistry.chemical_compound 0404 agricultural biotechnology Cell Line Tumor medicine Humans Viability assay 030304 developmental biology Glutathione Transferase chemistry.chemical_classification 0303 health sciences Reactive oxygen species Glutathione Peroxidase Superoxide Dismutase 04 agricultural and veterinary sciences General Medicine Glutathione Mycotoxins Catalase 040401 food science Molecular biology Glutathione Oxidative Stress chemistry Lipid Peroxidation Reactive Oxygen Species Oxidative stress Intracellular Food Science Sterigmatocystin

description

Abstract Sterigmatocystin (STE) is a mycotoxin produced by fungi of the genus Aspergillus. Considering that the effect of STE on neuronal system has not been well studied, the aim of the present study consists to investigate the cytotoxic effects of STE in human neuroblastoma (SH-SY5Y) cells. Moreover, the role of oxidative stress and intracellular defense systems was assessed by evaluating reactive oxygen species (ROS) generation, lipid peroxidation (LPO) and antioxidant no-enzymatic (GSH) levels and enzymatic (GPx, GST, CAT and SOD) activity. Our results revealed that STE decreased cell viability in a dose and time-dependent manner. Furthermore, after 24 h of exposure, STE induced an increase in ROS generation and LPO at all concentrations tested (0.78, 1.56 and 3.12 μM), as well as a depletion of GSH levels, an increase in GSSG content and a decrease in GSH/GSSG ratio at the highest concentrations. The activity of all antioxidant enzymes resulted to be also decreased. Additionally, an enhance of the oxidative damage was caused by BSO, a GSH depletor, while NAC, a GSH precursor, showed a scavenger activity. Our findings suggest that STE could injure SH-SY5Y cells via oxidative stress and highlight the antioxidant role of the glutathione system.

year	journal	country	edition	language
2020-02-01	Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

10.1016/j.fct.2019.110956 https://pubmed.ncbi.nlm.nih.gov/31712107