Abstract
Sleep disturbance is one of the neurobehavioral complications of lead neurotoxicity. The present study evaluated the impacts of chronic lead exposure on alteration of the sleep–wake cycle in association with changes of clock gene expression in the hypothalamus. Sprague–Dawley rats with chronic lead exposure consumed drinking water that contained 250 ppm of lead acetate for five weeks. Electroencephalography and electromyography were recorded for scoring the architecture of the sleep–wake cycle in animals. At six Zeitgeber time (ZT) points (ZT2, ZT6, ZT10, ZT14, ZT18, and ZT22), three clock genes, including rPer1, rPer2, and rBmal1b, were analyzed. The rats with chronic lead exposure showed decreased slow wave sleep and increased wakefulness in the whole light period (ZT1 to ZT12) and the early dark period (ZT13 to ZT15) that was followed with a rebound of rapid-eye-movement sleep at the end of the dark period (ZT22 to ZT24). The disturbance of the sleep–wake cycle was associated with changes in clock gene expression that was characterized by the upregulation of rPer1 and rPer2 and the feedback repression of rBmal1b. We concluded that chronic lead exposure has a negative impact on the sleep–wake cycle in rats that predominantly disrupts sleep homeostasis. The disruption of sleep homeostasis was associated with a toxic effect of lead on the clock gene expression in the hypothalamus.
Highlights
We aim to evaluate the impacts of chronic lead exposure on alteration of the sleep–wake cycle in association with changes of clock gene expression in the hypothalamus in a chronic lead-exposed animal model
Based on a clinically relevant experimental model, the present study demonstrated that rats with lead exposure for five weeks decreased slow wave sleep (SWS) and increased wakefulness in the whole light period (ZT1 to ZT12) and the early dark period (ZT13 to ZT15) that was followed by a rebound of REM sleep at the end of the dark period (ZT22 to ZT24)
The disturbance of sleep–wake cycle was associated with changes in clock gene expression that were characterized by upregulation of rat period 1 gene (rPer1) and rPer2 and feedback repression of rat brain and muscle ARNT-like 1b gene (rBmal1b)
Summary
A toxic metal, is one of the most common cumulative and preventable toxic pollutants of our environment that can induce various adverse clinical consequences in children and adults [1,2,3]. Lead and other heavy metals in bones may serve as a source of exposure during different stages of one’s life and have a potential cumulative effect on adverse clinical outcomes [3,5]. Life exposure to low levels of lead may affect brain development, in impairment of learning and memory function [1]. Chronic lead exposure can manifest with fatigue, headache, irritability, speech problems, cognitive and memory impairment, seizure disorders, and even sleep disturbances [2,20,21,22]
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