3.2 Metabolism of endogenous hydrogen sulfide
In mammals, hydrogen sulfide is excreted differently in different
systems. In the respiratory tract, hydrogen sulfide is directly excreted
in the form of gaseous molecules; Through the urinary tract,
H2S is mainly excreted in the form of thiosulfate or
free sulfate in the urine. However, in the gastrointestinal tract, most
hydrogen sulfide is still excreted in the form of free sulfide in the
feces[17]. H2S mainly has the
following three metabolic pathways:1). The elimination of hydrogen
sulfide through the mitochondrial sulfide oxidation pathway, with
sulfoquinone oxidoreductase (SQOR) being the key enzyme in this
reaction. Firstly, hydrogen sulfide is oxidized to thiosulfate under the
catalysis of SQOR[35, 36]. In this reaction, the
main sulfur acceptor is glutathione (GSH), and the resulting product is
glutathione disulfide (GSSH)[37, 38]. In the next
step of the reaction, rhodanese (orTST) plays a crucial role as a sulfur
transferase that can further oxidize thiosulfate to sulfite or
sulfate[39, 40]. However, due to the rapid
oxidation of sulfite to sulfate, hydrogen sulfide is ultimately expelled
from the body in the form of thiosulfate or sulfate through this
pathway[17, 40]. 2). Research has found that
methylation occurring in the cytoplasm is another metabolic pathway for
hydrogen sulfide[24]. Thiol-S-methyltransferase
(TSMT) can catalyze the conversion of hydrogen sulfide to methyl
mercaptan and dimethyl sulfide. TSMT is commonly present in cells in the
human body, but has high activity in mucosal cells of the colon and
cecum[41]. Compared to the sulfide oxidation
pathway, the metabolic process of sulfide methylation is slower. In a
study, the rate of sulfide methylation in mammalian colon mucosal cells
was approximately 10000 times slower than the oxidation rate of
H2S[42]. 3). Hydrogen sulfide can
be cleared by methemoglobin, metal containing or sulfur containing
macromolecules. Methemoglobin and myoglobin can promote the binding of
hydrogen sulfide and iron by regulating the reactivity of iron,
accelerating the oxidation rate of hydrogen
sulfide[43].
Figure 2