Acute enhancement of non‐rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride. Issue 2 (24th January 2013)

• Record Type: Journal Article
• Authors: Unno, Katsuya; Yamoto, Kurumi; Takeuchi, Kouhei; Kataoka, Aya; Ozaki, Tomoya; Mochizuki, Takatoshi; Honda, Kazuki; Miura, Nobuhiko; Ikeda, Masayuki
• Is Part Of: Journal of applied toxicology. Volume 34:Issue 2(2014)
• Page Start: 205
• Page End: 213
• Publication Date: 2013-01-24
• Subjects: Toxicology -- Periodicals; Industrial toxicology -- Periodicals; Environmentally induced diseases -- Periodicals; Toxicology -- Periodicals; 615.9005
• DOI: 10.1002/jat.2853
• Languages: English
• ISSNs: 0260-437X

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <p>Cadmium (Cd) is a heavy metal widely used or effused by industries. Serious environmental Cd pollution has been reported over the past two centuries, whereas the mechanisms underlying Cd‐mediated diseases are not fully understood. Interestingly, an increase in reactive oxygen species (ROS) after Cd exposure has been shown. Our group has demonstrated that sleep is triggered via accumulation of ROS during neuronal activities, and we thus hypothesize the involvement of Cd poisoning in sleep–wake irregularities. In the present study, we analyzed the effects of Cd intake (1–100 ppm CdCl<sub>2</sub> in drinking water) on rats by monitoring sleep encephalograms and locomotor activities. The results demonstrated that 100 ppm CdCl<sub>2</sub> administration for 28 h was sufficient to increase non‐rapid‐eye‐movement (non‐REM) sleep and reduce locomotor activities during the night (the rat active phase). In contrast, free‐running locomotor rhythms under constant dim red light and their re‐entrainment to 12:12‐h light/dark cycles were intact under chronic (1 month) 100 ppm CdCl<sub>2</sub> administrations, suggesting a limited influence on circadian clock movements at this dosage. The relative amount of oxidized glutathione increased in the brain after the 28‐h 100 ppm CdCl<sub>2</sub> administrations similar to the levels in cultured astrocytes receiving H<sub>2</sub>O<sub>2</sub> or CdCl<sub>2</sub> in culture medium. Therefore, we propose Cd‐induced sleep as a consequence of oxidative stress. As oxidized glutathione is an endogenous sleep substance, we suggest that Cd rapidly induces sleepiness and influences activity performance by occupying intrinsic sleep‐inducing mechanisms. In conclusion, we propose increased non‐REM sleep during the active phase as an index of acute Cd exposure. Copyright © 2013 John Wiley & Sons, Ltd.</p> </abstract>