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Heat Shock Pretreatment Suppresses Cadmium-inducedAmmonium Ion Accumulation and Phenylalanine Ammonia-lyase Activity in Rice Seedling Leaves

水稻幼苗經熱休克前處理可降低鎘所誘導葉片中銨離子之累積與苯丙胺酸氨裂解酶活性之增加

摘要


本研究主要探討水稻幼苗經熱休克處理後,對鎘所誘導葉片中銨離子累積與增加苯丙胺酸氨裂解酶 (PAL) 活性之影響。鎘所誘導葉片中PAL 活性增加之時間早於銨離子累積。鎘所誘導PAL 活性與銨離子含量之增加會因PAL 抑制劑α-aminooxy-β-phenylpropionic acid 處理而降低。另外,水稻幼苗在黑暗中經熱休克前處理3 小時後,可抑制後續鎘所誘導PAL 活性增加與銨離子累積。在不經熱休克前處理情況下,外加過氧化氫,穀胱甘肽(GSH)、抗壞血酸(AsA) 與抗壞血酸之前驅物(L-galactono -1,4-lactone)所顯示之效果與處理熱休克結果相似。我們亦發現水稻幼苗處理imidazole(NADPH oxidase 抑制劑)、buthionine sulfoximine (BSO,穀胱甘肽合成抑制劑)及lycorine (Lyc, 抗壞血酸合成抑制劑)等抑制劑時,可抵銷熱休克處理所減緩鎘誘導之PAL 活性增加與銨離子累積。此外,分別外加GSH 與AsA 亦可恢復被BSO 與Lyc 所抑制的效果。本文亦對水稻經熱休克處理後減緩鎘作用可能的機制加以討論。

並列摘要


We investigated the effects of heat shock (HS) on the subsequent cadmium (Cd)-induced ammonium ion (HN(subscript 4 superscript+)accumulation and the phenylalanine ammonia-lyase (PAL) activity in rice seedling leaves. Increases in PAL activity occurred prior to NH(subscript 4 superscript +) increases in rice leaves. Both of these Cd-induced increases were significantly deterred by the potent PAL inhibitor α-aminooxy-β-phenylpropionic acid. Exposing rice seedlings to 3 h HS in the dark effectively reduced subsequent Cd-induced increases in PAL activity and NH(subscript 4 supercript +) content. The HS effect can be mimicked by pretreating rice seedlings with exogenous H2O2, glutathione (GSH), ascorbic acid (AsA), or L-galactono-1,4-lactone (GalL, a precursor of AsA biosynthesis) under non-HS conditions. The protection that HS provides however, can be counteracted by imidazole, a NADPH oxidase inhibitor, buthionine sulfoximine (BSO, a GSH synthesis inhibitor), or lycorine (Lyc, an AsA synthesis inhibitor). Furthermore, the effects of BSO and Lyc can be reversed by the addition of GSH and AsA, respectively. The mechanisms of the protective effect of HS against subsequent Cd effects are discussed.

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