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|Title:||Synergism between hydrogen sulfide (H2S) and nitric oxide (NO) in vasorelaxation induced by stonustoxin (SNTX), a lethal and hypotensive protein factor isolated from stonefish Synanceja horrida venom|
|Keywords:||Hydrogen sulfide (H2S)|
Nitric oxide (NO)
|Source:||Liew, H.C., Khoo, H.E., Moore, P.K., Bhatia, M., Moochhala, S.M., Lu, J. (2007). Synergism between hydrogen sulfide (H2S) and nitric oxide (NO) in vasorelaxation induced by stonustoxin (SNTX), a lethal and hypotensive protein factor isolated from stonefish Synanceja horrida venom. Life Sciences 80 (18) : 1664-1668. ScholarBank@NUS Repository. https://doi.org/10.1016/j.lfs.2007.01.058|
|Abstract:||Stonustoxin (SNTX) is a 148 kDa, dimeric, hypotensive and lethal protein factor isolated from the venom of the stonefish Synanceja horrida. SNTX (10-320 ng/ml) progressively causes relaxation of endothelium-intact, phenylephrine (PE)-precontracted rat thoracic aortic rings. The SNTX-induced vasorelaxation was inhibited by l-NG-nitro arginine methyl ester (l-NAME), suggesting that nitric oxide (NO) contributes to the SNTX-induced response. Interestingly, d, l-proparglyglycine (PAG) and β-cyano-l-alanine (BCA), irreversible and competitive inhibitors of cystathionine-γ-lyase (CSE) respectively, also inhibited SNTX-induced vasorelaxation, indicating that H2S may also play a part in the effect of SNTX. The combined use of l-NAME with PAG or BCA showed that H2S and NO act synergistically in effecting SNTX-induced vasorelaxation. © 2007 Elsevier Inc. All rights reserved.|
|Source Title:||Life Sciences|
|Appears in Collections:||Staff Publications|
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