A new study in mouse models revealed that two newly developed drugs, which selectively target minute quantities of the foul smelling gas hydrogen sulfide inside blood vessel cells, could help prevent heart and blood vessels complications in patients with diabetes.

The study, published in the journal Pharmacological Research, showed that by targeting the minute quantities of hydrogen sulfide, the drugs, AP39 and AP123, could help prevent sugar (glucose) from damaging endothelial cells.

"Some people find it amusing that a substance with such a bad reputation can produce these benefits, but nearly every cell in our body makes and responds to tiny amounts of hydrogen sulfide and we have at least three distinct pathways for making this gas in very small quantities so it is very important," explained Matthew Whiteman, a professor at the University of Exeter Medical School and lead author of the study, in a statement.

For the study, the researchers carefully targeted minute quantities of hydrogen sulfide to the mitochondria inside endothelial cells isolated from the small blood vessels in the brains of mice using AP39 or AP123. The researchers discovered that both drugs were able to restore the efficiency of the mitochondria. Furthermore, both AP39 and AP123 presented long-lasting effects, suggesting that it could be used to treat blood vessel complications in the heart, kidney and eyes of patients with diabetes.

Patients with diabetes have a condition known as hyperglycemia. Due to the excess amount of glucose in their blood, the mitochondria-responsible for energy production and use inside a cell-becomes inefficient and leaky, producing highly toxic metabolites of oxygen known as free radicals. The toxicity produced by the mitochondria in the endothelial cells damages the blood vessels in the circulation and in the heart, depriving some of the organs of blood necessary to function.

The AP39 and AP123 act as a replacement for the loss hydrogen sulfide, re-energizing the mitochondria to keep the metabolism of efficient.