Dispersion behaviour of molybdenum disulfide (MoS2) nanosheets in different exposure media and determination of its toxicity using in-vitro and in-silico approaches

Abstract

MoS2 nanocomposites have been used in a wide range of environmental, biomedical, and energy-related applications due to their unique physicochemical properties. On the contrary, fewer attempts were made to understand its environmental sustainability, fate, and toxicity. The present study reports the synthesis, characterisation, dispersion behaviour, cellular uptake, toxicity, and in-silico docking of trigonal prismatic (2H) defect-rich MoS2 nanosheets. The applicability of a common European approach to the regulatory testing of nanomaterials (NANoREG) was employed to understand the dispersion stability of MoS2 nanosheets. Particle size analysis was used to understand the interaction between MoS2 nanosheets and biomolecules present in the environmental matrices. Prolonged exposure (48 h) of MoS2 nanosheets to HepG2 cells resulted in a significant increase in cellular uptake of Mo compared to that in cells exposed for 1 h. Significant reduction in the cell viability was noticed in HepG2 cells exposed to 500 mg/L (p ≤ 0.05) and HL-60 cells exposed to 1000 mg/L (p ≤ 0.01) and 500 mg/L (p ≤ 0.05) of MoS2 nanosheets concentrations for 48 h. Forward/side scatter plots in flow cytometric assays (apoptosis and mitochondrial permeability) revealed alterations in cellular morphology of HL-60 cells treated with higher concentrations (≥100 mg/L) of MoS2 nanosheets for 48 h. Loss of mitochondrial membrane potential (ΔΨm) was observed in cells treated with higher concentrations (≥100 mg/L) of MoS2 nanosheets. The results obtained by in vitro analysis suggest that MoS2 nanosheets are toxic at higher doses and not at environmentally relevant concentrations. To the best of our knowledge, this is the first study of its kind that demonstrates the cellular and molecular toxicity of MoS2 nanosheets, along with its in silico interactions with the key sixteen macro-molecules involved in programmed cell death.