The intensity of static electric field (SEF) in the surrounding environment of transmission lines has been greatly increased with the rapid development of ultra-high-voltage direct-current transmission. Therefore, the potential health effects of SEF have stimulated great public attention. It has been proven that SEF exposure can cause reversible damage to the nervous system through oxidative stress; however, the mechanism of its recovery is unclear. This study focused on nuclear factor erythroid 2-related factor 2 (Nrf2), a vital regulator of oxidative stress, and has been identified to notably impact the protection of organisms against many external stimuli. Herein, it was found that 56.3 kV/m SEF exposure for 7 days and 14 days significantly improved the expression levels of Nrf2 protein in the cytoplasm and nucleus of mice' hippocampus, as well as antioxidant genes, superoxide dismutase 2, and glutathione peroxidase 1. No significant difference in the expression level of the Nrf2 gene was found. The results indicated that the body could activate the Nrf2 signalling under SEF exposure by means other than up-regulation of Nrf2 gene expression. Inhibiting Nrf2 signalling by isoniazid could block SEF-induced gene transcription and protein expression, resulting in a decrease in antioxidant capacity, an increase in the level of lipid peroxide product, and irretrievability of learning and memory damage. These results demonstrated that the Nrf2 signalling pathway exhibited a protective role in SEF-induced oxidative damage and decline in learning and memory ability, which provides a potential strategy for preventing and treating SEF-related neurotoxicity.
Keywords: Antioxidation; Cognitive ability; Isoniazid; Nuclear factor erythroid 2-related factor 2 signalling pathway; Self-repair mechanism; Static electric field.
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.