Accumulating evidence has suggested a dysfunction of synaptic plasticity in the pathophysiology of depression. Hydrogen sulfide (H₂S), an endogenous gasotransmitter that regulates synaptic plasticity, has been demonstrated to contribute to depressive-like behaviors in rodents. The current study investigated the relationship between plasma H₂S levels and the depressive symptoms in patients with depression. Forty-seven depressed patients and 51 healthy individuals were recruited in this study. The 17-item Hamilton Depression Rating Scale (HAMD-17) was used to evaluate depressive symptoms for all subjects and the reversed-phase high-performance liquid chromatography (RP-HPLC) was used to measure plasmaH₂S levels. We found that plasma H₂S levels were significantly lower in patients with depression relative to healthy individuals (P < 0.001). Compared with healthy controls (1.02 ± 0.34 μmol/L), the plasma H₂S level significantly decreased in patients with mild depression (0.84 ± 0.28 μmol/L), with moderate depression (0.62 ± 0.21μmol/L), and with severe depression (0.38 ± 0.18 μmol/L). Correlation analysis revealed that plasma H₂S levels were significantly negatively correlated with the HAMD-17 scores in patients (r = -0.484, P = 0.001). Multivariate linear regression analysis showed that plasma H₂S was an independent contributor to the HAMD-17 score in patients (B = -0.360, t = -2.550, P = 0.015). Collectively, these results suggest that decreased H₂S is involved in the pathophysiology of depression, and plasma H₂S might be a potential indicator for depression severity.

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