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Recently, cystathionine-γ-lyase (CSE) was found to provide the major physiological pathway for H2S, the third member of the gasotransmitter family. In various pathophysiological conditions, H2S exerted protective effects based on its antioxidant, anti-inflammatory, anti-hypertensive and other regulatory functions. Interestingly, CSE expression had been only poorly studied and only in relation with inflammatory processes. Therefore, the study by Hassan et al. in this issue of the BJP, provides a considerable advance by furnishing direct experimental evidence for the involvement of redox signalling in the regulation of CSE gene expression. They found that PDGF up-regulated CSE expression and activity that was abolished by antioxidants and by deletion of the transcription factor nuclear erythroid-2-related factor-2 (Nrf2). Furthermore, PDGF induced Nrf2 binding to its consensus sequence that was again reversed by antioxidants. As Nrf2 also governs CO biosynthesis, and PDGF inversely affects H2S and NO production, these data could indicate a concerted regulation of the three gasotransmitters by redox signalling. LINKED ARTICLE This article is a commentary on Hassan et al., pp. 2231-2242 of this issue. To view this paper visit [ABSTRACT FROM AUTHOR]

This article summarizes the findings of Kameda et al. (this issue of BJP) that suggest a new avenue for the pharmacological treatment of subarachnoid haemorrhage (SAH) involving the combined use of a proteinase inhibitor (argatroban) that targets thrombin and an antioxidant (vitamin C). The findings are presented in the context of previous modalities of treating SAH that are of modest impact and the possibility that inhibiting proteinase-mediated signalling via proteinase-activated receptors like the thrombin PAR1 receptor combined with blocking oxidative stress may provide a new avenue for the treatment of SAH. LINKED ARTICLE This article is a commentary on Kameda et al., pp. 106-119 of this issue. To view this paper visit [ABSTRACT FROM AUTHOR]

A conference paper about the prevention of H2O2-induced oxidative damage in guinea pig (GP) brain slices by glial antioxidant network is presented. It indicates that GP brain slices are less vulnerable than rat slices to H2O2 toxicity because of glia-mediated antioxidant protection. It also suggests that the loss of glutathione synthesis, glutathione peroxidase and catalase of the antioxidant network can be compensated for by ascorbate.