Hydrogen Sulfide as a Protector of Blood Vessels?

Hydrogen sulfide, H2S, a smelly gas known for example from rotten eggs, appears to be a very important regulatory product in the body. If you read this blog regularly, this will not be any surprise to you. It has been quite a while since, while searching for the mechanism of action of sulfur amino acid restriction, I found studies that surprisingly link the restriction of these amino acids with increased production of H2S as a product of the activity of the enzyme cystathionine-γ-lyase (CSE/CTH).

The main mechanism of hydrogen sulfide is S-sulfhydration of enzymes, that is, a certain change in the “decoration” of these nano-machines, which either further activates or deactivates their function. Today we will look at the effect of hydrogen sulfide on vascular endothelial cells, that is, those that influence cardiovascular diseases generally associated with LDL-C levels, that is, cholesterol. I will not repeat here that cholesterol is a very poor marker of risk for these diseases. Take a look at older posts.

I will start from the end. You can see a diagram of the effects of hydrogen sulfide, which activates the deacetylase SIRT1, apparently precisely through S-sulfhydration, as described by other studies. The authors of this study do not mention this mechanism at all—could it be that they are unaware of it? It is possible; today’s world is strange, some long-known phenomena seem as if they were being concealed in textbooks. Unless one actively searches for them, one does not learn about them.

The deacetylase SIRT1 activates FoxO1 molecules by removing the “decoration” of an acetyl group from them. This triggers its translocation and activates the process of clearing unnecessary material in the cell. It is a kind of major cleanup called autophagy, “self-eating.”

This entire process protects cells from damage and makes them more resilient. This is especially important for cells of the vascular lining. Various substances that damage blood vessels are present in the blood—for example, peroxidized fats, aldehydes, and other toxins. The authors of this study used oxidized LDL particles (Ox-LDL) for in vitro testing, that is, outside a living organism.

We can see that the substance GYY-4137, which releases H2S molecules, protects cells from Ox-LDL, which causes apoptosis, cell death. After adding a blocker of the deacetylase SIRT1, that is, after adding 3-MA molecules, apoptosis increases again, even more than with exposure to Ox-LDL alone. Resveratrol (Res) is a known activator of SIRT1 and also protects cells together with hydrogen sulfide, in contrast to Ex-527, which blocks the deacetylase SIRT1.

If I were to draw some lesson from this research, I would say that the quality and resilience of the vascular wall are influenced by the overall healthy environment in the body. The functionality of all enzymes is key, including the enzymes responsible for hydrogen sulfide production, namely CSE/CTH. We already know that hydrogen sulfide protects against products of omega-6 linoleic acid peroxidation from other studies as well. It protects sites on enzymes where 4-HNE molecules could potentially attach.

For us, this implies that we should avoid an excess of sulfur amino acids, specifically methionine and cysteine. This can also be addressed by supplementation with taurine and glycine. However, this area of metabolic modulation has not yet been thoroughly explored. Another option is the use of vinegar, which can also protect vascular endothelial cells. Acetic acid also works through the deacetylase SIRT1. This is not medical advice. As a layperson, I am interested in the mechanisms of how things work in the body. Therefore, when I find interesting information, I share it with the readers of these pages. Nothing more, nothing less.


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References:

Protective effect of hydrogen sulfide on endothelial cells through Sirt1-FoxO1-mediated autophagy


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