What is deuterium-depleted water and why is it addressed as such?

Before we dig deeper into the main objective of the post, we will like to quickly consider what is meant by DDW. This is for the sake of those not familiar with the term.

In layman terms, deuterium-depleted water (DDW) can be roughly described as water with less than 130 ppm od deuterium content. The name implies it has a lower concentration of naturally occurring deuterium. Deuterium itself is a heavier isotope of hydrogen that has both one proton as well as a neutron that somewhat doubles the mass of the atom of the hydrogen. Now, deuterium-depleted water has been touted for some time to have certain health benefits such as cancer prevention among other things. It is for that reason that we intend under here to look into the neuroprotective effects that it also offers.

A standard concentration of deuterium inside water is 150 parts per million or one atom of deuterium per 6400 atoms of regular hydrogen. To put it better, every single quart of water contains just a little amount with deuterium. On the other hand, deuterium-depleted has 1-120 parts per million of deuterium.

The backdrop of the analysis

As we have stated earlier, we will be considering the neuroprotective effects of deuterium-depleted water. Of course, there has to be what this will be done against and that would be the H203 H2O2-Induced oxidative stress in differentiated PC12 cells via the PI3K/Akt signaling pathway. As we go further, we will further be discussing this topic under two different sections.

First, we will have to consider the role of oxidative stress in the pathogenesis of neurodegenerative disorders and how important the role is (if there is any) to the process. In the concluding part, we will be looking into a lot of assessments that will be used as a background to drive our point under this post and draw out a conclusion.

The role of oxidative stress in the pathogenesis of neurodegenerative diseases

The role that oxidative stress plays when it comes to the pathogenesis of neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease among many others cannot be overemphasized. Inducing endogenous antioxidants to function against oxidative stress-mediated damage of the neuron has been established to be a likely effective strategy when it comes to delaying the progression of such neurodegenerative disorders. As a result of this, we are looking at the neuroprotective abilities of deuterium-depleted water against oxidative stress triggered by H202 in differentiated PC12 cells as well as the pathways that are involved in the whole process.

What happens when you pretreat a differentiated cell line with deuterium-depleted water?

When the differentiated PC12 cell line is pretreated using DDW that contains various concentrations of deuterium and subsequently treated using H202, it induces not only oxidative stress but also neurotoxicity. In the same vein, the post is grounded on the evaluation of things such as survival, TUNEL assay, reactive oxygen species (ROS), copper, and superoxide dismutase that contains zinc among others as well as superoxide dismutase SOD) activity. In addition, it is also based on the performance of western blot analysis. After making all these considerations, the results eventually contributed immensely to the investigation of the neuroprotective effects of deuterium-depleted water.

Results of the various evaluations and analyses

Although we will not describe each process involved in these evaluations made as well as each of the results, we will just quickly draw out how they relate to the subject matter of this post.

The results of all the evaluations and appraisals lend credence to just one thing and that is the fact that deuterium-depleted water has the ability to weaken apoptosis induced by H2O2. Not just this alone, the results also show that that deuterium-depleted water can reduce the formation of ROS and increase CuZn-SOD, CAT as well as CAT activity in PC22 cells treated by H2O2. Furthermore, western blot analysis has likewise shown that deuterium-depleted water treatment significantly increased the expression of Bcl-2, p-Akt, and GSK-3β.

Nevertheless, the ability of deuterium-depleted water to protect the survival of cells as well as the increases in Bcl-2, p-Akt and GSK-3β mediated by deuterium-depleted water can be abolished through pretreatment with the phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002. Without wasting further time and to cut the long story short, the idea that is being established under this post is that deuterium-depleted water has the ability to protect differentiated PC12 cells against oxidative stress induced by H2O2 through the PI3K/Akt signaling pathway.