There have been studies suggesting the pain attenuating as well as pain inducing actions of hydrogen sulfide (HS). Exogenous administrated HS may be antinociceptive or pronociceptive, while the endogenous HS is pronociceptive. Experimental studies have shown that pharmacological inhibitors of HS biosynthetic enzymes may attenuate nociceptive as well as neuropathic pain. It suggests that nerve injury or inflammatory agents may induce the expression of HS biosynthetic enzymes to increase the endogenous production of HS, which acts as a pain neurotransmitter to produce pain. The endogenous HS may act through different mechanisms including opening of T-type calcium channels, activation of voltage-gated sodium channels, suppression of potassium channels, activation of TRPA1, TRPV1 and TRPC6 channels, upregulation of spinal NMDA receptors and sensitization of purinergic receptors. Exogenous administration of HS/precursors/donors attenuates or facilitates pain. It may be hypothesized that local administration of HS may cause pain; while it's systemic administration may attenuate pain. The doses of HS may also influence the pain response and HS in low doses may contribute in reducing pain, while HS in high doses may contribute in relieving pain. Accordingly, enzymatic inhibitors of HS synthesis or systemic administration of slow HS releasing agents/low dose HS donors may be useful in attenuating nociceptive and neuropathic pain. The present review describes the dual role of HS in pain attenuation and pain induction along with possible mechanisms.