Plasmon-activated water effectively relieves hepatic oxidative damage resulting from chronic sleep deprivation.

Hsiao-Chien Chen,Chih-Ping Yang,Chun-Chao Chang,Wen-Chieh Liao,Fu-Der Mai,Li-You Chen,Yu-Chuan Liu,Hung-Ming Chang,Chung-Yi Cheng

doi:10.1039/c7ra13559a

Abstract

The role of the hepato-protective agent plasmon-activated water (PAW) as an innovative anti-oxidant during chronic sleep deprivation (SD) is realized in this study. PAW possesses reduced hydrogen-bonded structure, higher chemical potential and significant anti-oxidative properties. In vitro tests using rat liver cell line (Clone-9) have demonstrated that PAW is non-cytotoxic and does not change the cellular migration capacity. The in vivo experiment on SD rats suffering from intense oxidative damage to the liver, an extremely common phenomenon in the present-time with deleterious effects on metabolic function, is performed by feeding PAW to replace deionized (DI) water. Experimental results indicate that PAW markedly reduces oxidative stress with enhanced bioenergetics in hepatocytes. PAW also effectively restores hepatocytic trans-membrane ion homeostasis, preserves membranous structures, and successfully improves liver function and metabolic activity. In addition, the hepato-protective effects of PAW are evidently demonstrated by the reduced values of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) and the recovery of total protein and albumin levels. With clear evidences of PAW for protecting liver from SD-induced injury, delivering PAW as a powerful hepato-protective agent should be worthy of trailblazing new clinical trials in a healthier, more natural, and more convenient way.

Highlights

In animals drinking plasmon-activated water (PAW) instead of deionized water (DIW) during the entire chronic SD (CSD) period, both the hepatic H2O2 and malondialdehyde (MDA, a reliable marker of oxidative stress23) levels were drastically reduced to nearly normal untreated values (Fig. 2b and c)
The positive effects of PAW on reducing oxidative stress may arise from the scavenging activity of PAW on H2O2, since the quantity of H2O2
A previous report demonstrates that PAW provides more amount of activity sites for forming hydrogen bonds with other species compared with DIW

Summary

Introduction

Sleep deprivation (SD) has increasingly become a major public health issue, which affects millions of people in many countries worldwide.[1,2] Chronic sleep loss can disturb the cellular function, which unavoidably leads to a variety of neurobiological, cardiovascular, and metabolic diseases.[3,4,5] Previous studies have indicated that SD can signi cantly impair neuroendocrine bioenergetics, hepatic energy metabolism, nicotinamide adenine dinucleotide (NAD) salvage and transmethylation pathways and contributes to the alterations in hepatic lipogenesis and development of metabolic de ciencies.[6,7,8] Clinical reports demonstrate that chronic sleep loss (such as obstructive sleep apnea) is strongly associated with an increased risk of liver cirrhosis through the activation of the hypoxia inducible factor, nuclear factor-kB or unfolded protein response.[9,10,11] By using molecular imaging and spectral analyses, we demonstrate signi cant impairments in ionic homeostasis and phospholipid levels in hepatocytes following SD.[12,13] It is indicated that enhanced cellular stress and intense oxidative damage in the liver may play vital roles in the pathogenesis of SD-related metabolic de ciencies.[12,13,14] Considering the importance of the liver in controlling metabolic homeostasis in mammals, developing natural substances that are highly accessible to the liver and possess effective antioxidative activities may shed important light on advancing therapeutic strategies to prevent or counteract the SD-induced metabolic dysfunction prevailing in our societies nowadays

Results

Discussion

Conclusion