1. Electromagnetic radiation 2450 MHz exposure causes cognition deficit with mitochondrial dysfunction and activation of intrinsic pathway of apoptosis in rats.
- Author
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Gupta SK, Mesharam MK, and Krishnamurthy S
- Subjects
- Acetylcholinesterase genetics, Amyloid beta-Peptides genetics, Animals, Antioxidants metabolism, Caspase 3 genetics, Caspase 9 genetics, Cognitive Dysfunction etiology, Cognitive Dysfunction genetics, Gene Expression Regulation radiation effects, Hippocampus physiopathology, Humans, Mitochondria radiation effects, Oxidative Stress radiation effects, Rats, Reactive Oxygen Species metabolism, Apoptosis radiation effects, Cognitive Dysfunction physiopathology, Electromagnetic Radiation, Hippocampus radiation effects
- Abstract
Electromagnetic radiation (EMR) can induce or modulate several neurobehavioral disorders. Duration and frequency of exposure of EMR is critical to develop cognitive disorders. Even though EMR-2450 is widely used, its effects on cognition in relation to mitochondrial function and apoptosis would provide better understanding of its pathophysiological effects. Therefore, a comparative study of different frequencies of EMR exposure would give valuable information on effects of discrete frequencies of EMR on cognition. Male rats were exposed to EMR (900, 1800 and 2450 MHz) every day for 1 h for 28 consecutive days. The cognitive behavior in terms of novel arm entries in Y-maze paradigm was evaluated every week after 1 h to last EMR exposure. Animals exposed to EMR-2450 MHz exhibited significant cognitive deficits. EMR- 2450 MHz caused loss of mitochondrial function and integrity, an increase in amyloid beta expression. There was release of cytochrome-c and activation of apoptotic factors such as caspase-9 and -3 in the hippocampus. Further, there was decrease in levels of acetylcholine, and increase in activity of acetyl cholinesterase, indicating impairment of cholinergic system. Therefore, exposure of EMR-2450 in rats caused cognitive deficit with related pathophysiological changes in mitochondrial and cholinergic function, and amyloidogenesis.
- Published
- 2018