Our cells harbor reserves of pure sulfur, a form of storage that was not even known to exist in mammals.
An international team detected this sulfur in human and mouse cells. It takes the form of small molecules made up of eight atoms arranged in a ring, called Sâ. Until now, the production of elemental sulfur was mainly known in microorganisms, as well as in certain plants and fungi.

Purified sulfur
These rings are not distributed randomly. They accumulate particularly in mitochondria, the structures that supply much of the energy to cells. They are also abundant in lipid droplets, small fat reserves found inside cells. Measured concentrations can reach several millimoles per liter.
To understand their importance, we need to look at what happens to the fats in cell membranes. Some can react with oxygen and break down. This oxidation then produces a chain reaction capable of severely damaging the membrane. If it becomes uncontrollable, it can cause a particular form of cell death linked to iron, called ferroptosis.
Sâ appears to help defend against this process. The cell can draw on this reserve to produce sulfur-containing molecules that act as antioxidants. The researchers found that the accumulation of Sâ in lipid droplets reduced fat oxidation and made cells less sensitive to ferroptosis.

Sâ molecule
Image Wikimedia
Another surprise is that an already well-known enzyme contributes to this production. Called eNOS, it normally produces nitric oxide, a molecule that helps blood vessels relax. The study attributes a second activity to it: it also contributes to the production of sulfur rings in cells.
The researchers also tested this approach in mice with a model of osteoarthritis. Solubilized Sâ injected into the joint reduced fat oxidation in the affected tissues. This result makes it possible to directly study the protective role of this sulfur reserve in a living organism.
Other observations are now opening up new questions. The authors notably measured more Sâ in tissues affected by breast cancer than in noncancerous breast tissue. It remains to be determined why this amount increases and whether it helps some diseased cells resist ferroptosis. This work could thus clarify the role of sulfur in several mechanisms linked to cellular damage.