鉀與水稻鎘逆境關係之研究

Abstract

本論文是以水稻品種台中在來1號（Oryza sativa L. cv. Taichung Native 1, TN1）或台農67號（Oryza sativa L. cv. Tainung 67, TNG67）為材料，探討（一）缺鉀與水稻鎘逆境關係之研究與（二）鎘毒害對水稻幼苗吸收鉀離子之影響。 缺鉀處理之TN1水稻幼苗，其第二片葉片、地上部和地下部之鉀含量均明顯下降，幼苗外觀較對照植物矮小，並且第二片葉片有黃化現象。缺鉀葉片之H2O2含量增加並且抗氧化酵素superoxide dismutase （SOD）、ascorbate peroxidase （APX）、glutathione reductase（GR）、catalase（CAT）之活性提升。若處理NADPH oxidase之抑制劑，imidazole（IMD），能顯著降低缺鉀所誘導之H2O2含量增加和抗氧化酵素SOD、APX、GR、CAT活性之提升，顯示缺鉀所誘導之H2O2含量之增加是藉由NADPH oxidase之活化，並且抗氧化酵素SOD、APX、GR、CAT活性之提升，是經由H2O2所調控。缺鉀導致水稻幼苗葉片脫落酸（ABA）含量上升，並且ABA之合成抑制劑，tungstate能降低缺鉀所誘導ABA和H2O2含量增加，並且降低缺鉀所誘導抗氧化酵素SOD、APX、GR、CAT活性之提升，顯示缺鉀所誘導之H2O2含量增加可能是經由ABA累積所致。缺鉀之水稻幼苗經後續鎘處理，發現鎘毒害減緩，由於缺鉀水稻幼苗之鎘含量並未減少，顯示缺鉀幼苗對於後續鎘逆境之保護作用，不是藉由降低對鎘之吸收，而是經由抗氧化酵素SOD、APX、GR、CAT活性之提升。 TN1和TNG67之水稻幼苗，經後續鎘處理6天，鎘毒害在TN1較TNG67為顯著，顯示TN1為不耐鎘之品種，TNG67為耐鎘之品種。TN1幼苗鎘含量遠高於TNG67，並且TN1之鉀含量在鎘處理下顯著下降，但在TNG67幼苗並沒有顯著影響，說明TN1所受到之鎘毒害，可能是由於鉀含量下降所致。後續以鎘與鉀同時處理TN1水稻幼苗，發現能減緩鎘毒害，進一步證實TN1所受到之鎘毒害，可能是由於鉀含量下降所致。

In this study, rice [ Oryza sativa L. cv. Taichung Native 1（TN1） or cv. Tainung 67（TNG67）] were used as test materials to investigate（a） the interaction between cadmium ( Cd ) and potassium ( K ) deficiency and （b）the effect of Cd on K uptake in rice seedlings. It was found that K deprivation in nutrient solution significantly decreased K concentration in shoots, leaves, and roots of rice seedlings, and K-deficient rice seedlings appeared stunting with chlorosis in the second leaves comparing to control seedlings. H2O2 content in leaves and roots of rice seedlings increased under K deficiency. Similarly, the activities of superoxide dismutase（SOD）, ascorbate peroxidase（APX）, glutathione reductase（GR）, and catalase（CAT）increased under K deficiency, whereas the contents of ascorbate and glutathione were not affected. Imidazole（IMD）, an inhibitor of NADPH oxidase, reduced the increase in H2O2 content and SOD, APX, GR, and CAT activities under K deficiency. IMD is an inhibitor of NADPH oxidase which catalyzes H2O2 generation, suggesting that NADPH oxidase is a H2O2 generating enzyme in K-deficient leaves. Our results also suggest that the increase in SOD, APX, GR and CAT activities under K deficiency is mediated through H2O2. In addition, abscisic acid（ABA）contents increased in leaves of rice seedlings grown under K deficiency. Treatment with tungstate, an inhibitor of ABA biosynthesis, also reduced K deficiency-induced H2O2 accumulation and increase of SOD, APX, GR, CAT activities. These results indicate that H2O2 accumulation in the second leaves is related to ABA under K deficiency. For the subsequent Cd treatment, we found that Cd toxicity in K-deficient leaves was less pronounced than that in K-sufficient leaves, indicating that K deficiency protected from the subsequent Cd toxicity in rice seedlings. However, K-deficient rice seedlings didn’t decrease Cd uptake, indicating that the protection of K deficiency from Cd toxicity in rice seedlings is unlikely due to the reduction of Cd uptake, and is more likely due to the increased activities of antioxidative enzymes. We used two rice cultivars, TN1 and TNG67, cultivars with different sensitivity to Cd stress, to investigate the effect of Cd toxicity on K uptake. TN1 rice cultivar is Cd sensitive, while TNG67 is Cd insensitive. When rice seedlings were treated with CdCl2, it was observed that Cd treatment resulted in a significant decrease in K concentration in TN1, but not in TNG67. In addition, Cd uptake in TN1 was five times higher than that in TNG67. These results suggest that cadmium toxicity of TN1 seedlings might be resulted from the decrease in K uptake. Therefore, we applied additional treatment of K and Cd at the same time to Cd-sensitive cultivar, TN1, and we found that Cd toxicity was decreased by additional K, which further supports the idea that Cd toxicity of TN1 is a result of subsequent reduction in K uptake.