کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4569638 1331348 2007 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Changes in antioxidative system and membrane damage of lettuce in response to salinity and boron toxicity
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک دانش باغداری
پیش نمایش صفحه اول مقاله
Changes in antioxidative system and membrane damage of lettuce in response to salinity and boron toxicity
چکیده انگلیسی

Individual and combined effects of salinity and B toxicity on growth, the major antioxidant enzymes (superoxide dismutase, SOD; catalase, CAT; ascorbate peroxidase, APX) activities, ascorbic acid, proline, and H2O2 accumulation, and stomatal resistance (SR), malondialdehyde (MDA), membrane permeability (MP) and the concentrations of sodium (Na), chloride (Cl) and boron (B) of lettuce were investigated. Boron toxicity and salinity reduced growth of lettuce plants. Under B toxicity, B concentration of the plants was increased, but in the presence of NaCl, the concentration of B was significantly reduced. Sodium and Cl concentrations were increased in B + NaCl and NaCl treatments. Membrane damage was more pronounced in NaCl and B + NaCl treatments. Stomatal resistance of the plants was significantly increased by salinity treatments. The accumulation of proline and ascorbic acid was the highest in the B + NaCl treatment. In general, stress conditions significantly increased H2O2 and antioxidant enzyme (SOD, CAT and APX) activities. The present results indicate that stomatal closure is an important response of lettuce against NaCl and B + NaCl stress. Furthermore NaCl and B + NaCl toxicity-induced oxidative stress in lettuce resulting in lipid peroxidation and membrane damage. Increased antioxidant enzyme activities and also accumulation of ascorbic acid and proline are involved in order to overcome B- and NaCl-induced oxidative stress.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Scientia Horticulturae - Volume 114, Issue 1, 11 September 2007, Pages 5–10
نویسندگان
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