鐵與水稻幼苗鎘逆境關係之研究

Abstract

中文摘要 本論文係以水稻品種台中在來一號 (Oryza sativa L. cv. Taichung Native 1, TN1) 作為試驗材料，探討 (一) 缺鐵水稻誘導鎘吸收之影響與 (二) 水稻幼苗鎘毒害是否由於鐵含量降低所導致。 缺鐵之水稻幼苗，誘導根形成NO與OsIRT1表現，以及增加根部鎘含量。NO清除劑cPTIO，能降低缺鐵所引起NO之形成、OsIRT1表現與鎘濃度。NOS抑制劑L-NAME有效降低缺鐵水稻幼苗生成NO，以及降低OsIRT1表現與鎘累積，NR抑制劑則無此效應，而外加處理NO提供者SNP，能夠增加缺鐵根部所引起NO形成。這些結果說明，缺鐵水稻幼苗根藉由NOS途徑誘導NO生成，透過OsIRT1基因表現，促進根部鎘累積現象。 水稻幼苗處理5 µM CdCl2能降低地上部與根部鐵含量，同時促進根OsIRT1表現，顯示鎘處理會導致缺鐵狀態。本論文以生物量降低、葉黃化、葉綠素含量降低、氧化逆境之誘導以及銨離子累積作為鎘毒害之指標。根據這些指標，試驗結果顯示外加處理10 µM Fe-citrate有效減緩鎘所引起之毒害。此外，外加處理10 µM Fe-citrate明顯降低水稻幼苗地上部與根部之鎘含量。這些結果證明鎘造成水稻幼苗毒害之原因可能是由於缺鐵所造成。

Abstract In this thesis, rice (Oryza sativa L. cv. Taichung Native 1, TN1) seedlings were used to investigate (a) the effect of iron deficiency on cadmium (Cd) uptake and (b) whether Cd toxicity was resulted from reduction of iron concentration. Iron deficiency resulted in increasing NO production, OsIRT1 expression, and Cd concentration in rice roots. Iron deficiency induced NO production, OsIRT1 expression and Cd accumulation could be blocked by NO scavenger cPTIO, NOS inhibitor L-NAME, but not NR inhibitor Tu. Collective, our results suggested that iron deficiency induced Cd accumulation and OsIRT1 expression are mediated through NOS-catalyzed NO production in rice roots. Application of 5 µM CdCl2 to rice seedlings resulted in decreasing iron concentration in shoots and roots, and induced OsIRT1 expression. These results suggested that Cd-treated rice seedlings were in iron starved status. In this thesis, Cd toxicity was judged by the decrease in biomass production, chlorosis, drcrease in chlorophyll content, induction of oxidative stress, and accumulation of ammonia ion. On the basis of these confidences, we demonstrated that application of 10 µM Fe-citrate reduced toxicity of rice seedlings caused by 5 µM CdCl2. Moreover, we also observed Fe-citrate application decreased Cd concentration in shoots and roots. According to our results, the decrease in iron concentration in rice seedlings may contribute to the toxicity caused by CdCl2.