Long-term exposure of 2450 MHz EMR induces stress and anxiety like behavior in rats

zaterdag, 04 mei 2019 - Categorie: Onderzoeken

Bron: www.ncbi.nlm.nih.gov/pubmed/30954502
Neurochem Int. 2019 Apr 4;128:1-13. doi: 10.1016/j.neuint.2019.04.001. (Epub ahead of print)

Gupta SK 1, Patel SK 2, Tomar MS 3, Singh SK 2, Mesharam MK 4, Krishnamurthy S 5.

1. Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, U.P., India.
2. Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, 221005, India.
3. School of Biomedical Engineering, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, U.P., India.
4. Department of Electronics Engineering, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, U.P., India.
5. Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, U.P., India. Electronic address: ksairam.phe@itbhu.ac.in.

Abstract
Long term exposure of electromagnetic radiations (EMR) from cell phones and Wi-Fi hold greater propensity to cause anxiety disorders. However, the studies investigating the effects of repeated exposure of EMR are limited. Therefore, we investigated the effects of repeated exposure of discrete frequencies of EMR in experimental animals. Male rats were exposed to EMR (900, 1800 and 2450 MHz) for 28 (1 h/day) days. Long term exposure of EMR (2450 MHz) induced anxiety like behavior. It deregulated the hypothalamic pituitary adrenal (HPA) axis in rats as observed by increase in plasma corticosterone levels apart from decreased corticotrophin releasing hormone-2 (CRH-2) and Glucocorticoid receptor (GR) expression in amygdala. Further, it impaired mitochondrial function and integrity. The expression of Bcl2 showed significant decrease while Bax and ratio of Bax: Bcl2 were increased in the mitochondria and vice versa in cytoplasm indicating altered regulation of apoptosis. EMR exposure caused release of cytochrome-c and expression of caspase-9 ensuing activation of apoptotic cell death. Additional set of experiments performed to estimate the pattern of cell death showed necrotic and apoptotic amygdalar cell death after EMR exposure. Histopathological studies also revealed a significant decrease in neuronal cells in amygdala. The above findings indicate that long-term exposure of EMR radiation (2450 MHz) acts as a stressor and induces anxiety-like behaviors with concomitant pathophysiological changes in EMR subjected rats.

Copyright © 2019. Published by Elsevier Ltd.
KEYWORDS:
Amygdala; Anxiety; Apoptosis; Electromagnetic radiation; Glucocorticoid receptor; Stress



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