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374 Yeager et al. higher than serum levels, clearly implicating the brain as a primary site of melatonin uptake and action. Rhythmic melatonin production is seen in the chick retina by the end of development; however, the retina is not thought to be a major contributor to the pool of circulating melatonin [25]. Retinal production of melatonin (3 ng or less/eye, embry- onic day 19) may in fact serve as a localized source of antioxidants to combat the continual photo-oxi- dative insult incurred by the retina. Hypothesis: Melatonin as a mediator of red light therapy Considering the presence and regulation of melato- nin during chick development, the responses of glu- tathione, cytochrome c oxidase, and ATP in liver and brain to daily LED treatment after TCDD expo- sure suggest that melatonin, in conjunction with cytochrome c oxidase, is a principle component of the cellular response to LED red light therapy. All indicators noted above are directly affected by red light therapy and may be principle mediating mechanisms involved in red light therapy induced reduction in TCDD toxicity. The effects of TCDD coupled with the ability of LED treatment to re- store both ATP and the glutathione balance could all be linked to melatonin-based mechanisms (Fig. 1). Discussion Melatonin is linked to mitochondrial health via interaction with complexes I and IV [1,26], where- by oxidative phosphorylation and electron trans- port efficiency are enhanced and cytochrome c oxidase activity (complex IV) and ATP production (complex V) are both increased [27]. In addition, melatonin sustains GSH levels in the mitochondria both by scavenging hydroxyl radicals directly [28], thereby sparing GSH, and by inducing the expres- sion of c-glutamylcysteine synthetase, the enzyme responsible for catalyzing the rate-limiting step of GSH synthesis [29]. Melatonin also acts by up-regu- lating superoxide dismutase (SOD) [30] and increas- ing glutathione peroxidase (GPx) and glutathione reductase (GRx) activities [31]. We have observed increased enzyme activities of all three enzymes, SOD, GPx, and GRx, in the developing liver upon daily LED treatment [18]. The coordinated efforts of all three enzymes, in addition to catalase, are responsible for the detoxification of reactive oxy- gen and nitrogen species. TCDD exposure alone has been shown to alter circulating melatonin levels by mechanisms that have yet to be clearly elucidated [32,33]. These re- ports support our own observations of decreased brain ATP and altered glutathione redox balance in TCDD-exposed embryos [12]. If red light treatment stimulates melatonin production, secretion, or uptake by the brain, and/or alters the melatonin Figure 1 Points of proposed interaction of melatonin with cellular metabolism during red light therapy, as elaborated in text.PDF Image | Melatonin as a principal component of red light therapy
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