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干旱胁迫下抑制光呼吸对‘赤霞珠’葡萄光抑制的影响 总被引:6,自引:0,他引:6
管雪强;赵世杰;李德全;束怀瑞 《园艺学报》2004,31(4):433-436
选用葡萄(Vitis vinifera L.)品种‘赤霞珠’(Cabernet Sauvignon)的2年生盆栽苗,进行不同程度的干旱处理20d及随后连续3d的光呼吸抑制剂异烟肼(INH)处理后,测定其PSII最大光化学量子产量(Fv/Fm)、实际光化学效率(ФPSII)及净光合速率(Pn),并计算其总光合电子传递(Jr)、羧化电子传递(Jc)、加氧电子传递(Jo)及光呼吸速率(Pr),发现赤霞珠葡萄在干旱胁迫下能够有效调动其光保护机制以避免严重光抑制的发生,而INH抑制光呼吸后,光抑制程度则明显加重,从而证明干旱胁迫下光呼吸对赤霞珠葡萄的光保护机制起重要作用。 相似文献
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AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (105 U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC. 相似文献
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LIU Nian NIU Hui-yan LI Yang ZHANG Cun-tai ZHOU Qiang RUAN Yan-fei PU Jun LU Zai-ying 《园艺学报》2004,20(12):2227-2231
AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, Ito, IK and IK1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of Ito, IK,tail and IK1 were reduced significantly in HMI group (P<0.01), from (6.72±0.42) pA/pF, (1.54±0.13) pA/pF and (25.6±2.6) pA/pF in Sham-operated group to (4.03±0.33) pA/pF, (1.14±0.11) pA/pF and (17.6±2.3) pA/pF, respectively. CONCLUSION: The reduced densities of Ito, IK,tail and IK1 in ventricular myocytes of non-infarcted zone in HMI are responsible for the prolongation of APD and the presentation of EAD, which play important roles in the malignant arrhythmia of HMI. 相似文献