Abstract

Overview

Exposure to 2.45 GHz electromagnetic radiation (EMR) is common in everyday devices and is known to induce oxidative stress across various experimental models. This study investigates sulforaphane, a natural compound, for its potential to mitigate the toxic effects of this radiation.

Findings

• Experimental Setup: SH-SY5Y neuronal-like cells and peripheral blood mononuclear cells (PBMCs) were exposed to 2.45 GHz EMR for 24 hours with and without varying concentrations of sulforaphane (5-10-25 μg/mL).
• Cell Health: Measurements included cell viability, mitochondrial activity, levels of redox markers, and apoptosis-related genes.
• Results: Low concentration of sulforaphane (5 μg/mL) provided a protective effect against EMR-induced reductions in cell viability. It decreased ROS production and improved mitochondrial transmembrane potential (Δψm) and NAD+/NADH ratio.
• Adverse Effects: Higher concentrations of sulforaphane showed detrimental effects.
• Hormetic Response: Gene expression analyses of Nrf2, SOD2, and apoptosis markers indicated a hormetic behavior of sulforaphane.

Conclusion

The study highlights the susceptibility of neuronal-like cells and PBMCs to mitochondrial dysfunction and oxidative stress from 2.45 GHz EMR and the potential of sulforaphane supplementation to alleviate these effects. This study provides novel insights into the protective capabilities of sulforaphane against EMR-induced stress in these cells.