Rennenberg H, Filner P
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824.
Plant Physiol. 1982 Apr;69(4):766-70. doi: 10.1104/pp.69.4.766.
The effect of inhibitors of glutathione (GSH) synthesis, namely gamma-methyl glutamic acid, d-glutamic acid, cystamine, methionine-S-sulfoximine (MSX), buthionine-S-sulfoximine, and GSH itself, on the emission of H(2)S was investigated. All these compounds stimulated H(2)S emission from pumpkin (Cucurbita pepo L. cv Small Sugar Pumpkin) leaf discs in response to sulfate. MSX and GSH were the most effective compounds, stimulating H(2)S emission from leaf discs of mature pumpkin leaves by about 80% in response to sulfate. Both inhibitors did not appreciably enhance H(2)S emission in response to l-cysteine and inhibited H(2)S emission in response to sulfite.Treatment with MSX or GSH enhanced the uptake of sulfate by pumpkin leaf discs, but did not affect the incorporation of sulfate into reduced sulfur compounds. Inhibition of GSH synthesis by MSX or GSH caused an increase in the pool size of cysteine, and, simultaneously, reduced the incorporation of labeled sulfate into cysteine. The incorporation of labeled sulfate into the sulfite and sulfide pools of the cells are stimulated under these conditions.These observations are consistent with the idea that inhibition of GSH synthesis leads to an elevated cysteine pool that inhibits further cysteine synthesis. The H(2)S emitted under these conditions appears to arise from diversion of a precursor of the sulfur moiety of l-cysteine. Therefore, stimulation of H(2)S emission in response to sulfate upon inhibition of GSH synthesis may reflect a role of H(2)S emission in keeping the cysteine concentration below a critical level.
研究了谷胱甘肽(GSH)合成抑制剂,即γ-甲基谷氨酸、d-谷氨酸、胱胺、蛋氨酸-S-亚砜亚胺(MSX)、丁硫氨酸-S-亚砜亚胺以及GSH本身对硫化氢(H₂S)释放的影响。所有这些化合物都能刺激南瓜(西葫芦品种小糖南瓜)叶盘因硫酸盐而释放H₂S。MSX和GSH是最有效的化合物,能使成熟南瓜叶盘因硫酸盐而释放的H₂S增加约80%。这两种抑制剂对因l-半胱氨酸而产生的H₂S释放没有明显增强作用,且抑制了因亚硫酸盐而产生的H₂S释放。用MSX或GSH处理可增强南瓜叶盘对硫酸盐的吸收,但不影响硫酸盐掺入还原态硫化合物。MSX或GSH对GSH合成的抑制导致半胱氨酸库大小增加,同时减少了标记硫酸盐掺入半胱氨酸的量。在这些条件下,细胞中亚硫酸盐和硫化物库中标记硫酸盐的掺入受到刺激。这些观察结果与以下观点一致,即GSH合成的抑制导致半胱氨酸库升高,从而抑制进一步的半胱氨酸合成。在这些条件下释放的H₂S似乎源于l-半胱氨酸硫部分前体的转移。因此,GSH合成受抑制时因硫酸盐而刺激的H₂S释放可能反映了H₂S释放在将半胱氨酸浓度维持在临界水平以下的作用。