Laser and life – the effects on telomeres
By Jan Tunér
The knowledge about the complicated cellular events in LPT is increasing. The stimulation of ATP is long established but more recently the regulation of the ATP production by nitric oxide (NO) has been elucidated. The nitric oxide is released when the laser light reaches the mitochondrion, and the increase of ATP starts. But what does the released NO do? Well, a lot of things, such an increasing the lumen of vascular systems. And, probably less known, activate telomerase. And what is telomerase and what does it do? As always, we consult Wikipedia:
Telomerase also called telomere terminal transferase is a ribonucleoprotein that is an enzyme that adds DNA sequence repeats to the 3′ end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes. In linear DNA (circular DNA does not have this problem), when the replication fork reaches the end of the helix, there is no place to produce the RNA primer needed to start the final Okazaki fragment on the lagging strand. Without the presence of telomerase, a section of single-stranded, or “unpaired”, DNA of between 100–200 nucleotides would remain that DNA Polymerase α cannot prime to produce a complementary daughter strand — this would lead to the shortening of the chromosome after each replication cycle.
In short, each time a cell is replicated, the telomere is shortened and when the telomere is gone, the cell can no longer replicate itself and dies. This is no new knowledge, nor is the role of NO in this process. In the year 2000, Vasa et al. reported that NO activates telomerase and delays endothelial senescence [1]. In other words, an endothelial cell aged at a slower rate. And is there any specific studies showing that this is actually happening when LPT is performed? Yes, in 2013 Huang et al. [2] demonstrated this in an in vitro study. And the results in a study by Korraa [3] showed that laser induced telomerase activity in blood mononuclear cells throughout the five consecutive days post laser irradiation, reaching its highest level at 72 hours post laser irradiation and was significantly higher in PHA stimulated cells compared to laser irradiated cells, where 5 J/cm2 displayed the highest activity.
Interested? If so, here is more information about the process, from Axelrad [3]:
Telomeres are repeating DNA sequences at the tip ends of the chromosomes that are diverse in length and in humans can reach a length of 15,000 base pairs. The telomere serves as a bioprotective mechanism of chromosome attrition at each cell division. At a certain length, telomeres become too short to allow replication, a process that may lead to chromosome instability or cell death. Telomere length is regulated by two opposing mechanisms: attrition and elongation. Attrition occurs as each cell divides. In contrast, elongation is partially modulated by the enzyme telomerase, which adds repeating sequences to the ends of the chromosomes. In this way, telomerase could possibly reverse an aging mechanism and rejuvenates cell viability. These are crucial elements in maintaining cell life and are used to assess cellular aging.
The implications of the above is so far vague, but certainly fascinating. Cuddle your telomeres, use LPT!
References
[1] Vasa M, Breitschopf K, Zeiher AM, Dimmeler S. Nitric oxide activates telomerase and delays endothelial cell senescence. Circ Res. 2000 29; 87 (7):540-542.
[2] Huang L, Wu Z, Mo H. [Experimental study of effect of low power laser on telomere length of cells]. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2013; 30 (3): 592-596.
[3] Derasmo Axelrad, Temuri Budagov, Gil Atzmon. Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence. JoVE Biology. 2013. May.
[4] Soheir S Korraa. He:Ne laser irradiation induced survival and cell cycle progression effects on human circulating mononuclear cells in vitro. Arab J. Biotech. 2008; 11 (2): 229-240.