['Hydrogen sulphide (H(2)S), considered as a novel gas transmitter, is produced endogenously in mammalian tissue from L-cysteine by two enzymes, cystathionine β-synthase and cystathionine γ-lyase. Recently, it has been reported that H(2)S contributes to the local and systemic inflammation in several experimental animal models. We conducted this study to investigate on the signalling involved in H(2)S-induced inflammation.', 'L-cysteine or sodium hydrogen sulphide (NaHS) was injected into the mouse hind paw and oedema formation was evaluated for 60\u2003min. In order to investigate H(2)S-induced oedema formation, we used 5-HT and histamine receptor antagonists, and inhibitors of K(ATP) channels or arachidonic acid cascade. Prostaglandin levels were determined in hind paw exudates by radioimmunoassay. Paws injected with L-cysteine or NaHS were examined by histological methods.', 'Both NaHS and L-cysteine caused oedema characterized by a fast onset which peaked at 30\u2003min. This oedematogenic action was not associated with histamine or 5-HT release or K(ATP) channel activation. However, oedema formation was significantly inhibited by the inhibition of cyclooxygenases and selective inhibition of phospholipase A(2). Prostaglandin levels were significantly increased in exudates of hind paw injected with NaHS or L-cysteine. The histological examination clearly showed an inflammatory state with a loss of tissue organization following NaHS or L-cysteine injection.'] Does hydrogen sulphide induce mouse paw oedema through activation of phospholipase A2?