کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2057331 | 1075877 | 2008 | 11 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Ultraviolet-B-induced oxidative stress and antioxidant defense system responses in ascorbate-deficient vtc1 mutants of Arabidopsis thaliana Ultraviolet-B-induced oxidative stress and antioxidant defense system responses in ascorbate-deficient vtc1 mutants of Arabidopsis thaliana](/preview/png/2057331.png)
SummaryUltraviolet-B (UV-B) radiation has a negative impact on plant cells, and results in the generation of reactive oxygen species (ROS). In order to increase our understanding of the effects of UV-B on antioxidant processes, we investigated the response of an ascorbate-deficient Arabidopsis thaliana mutant vtc1 to short-term increased UV-B exposure. After UV-B supplementation, vtc1 mutants exhibited oxidative damage. Evidence for damage included an increase in H2O2 content and the production of thiobarbituric acid reactive substances (TBARS); a decrease in chlorophyll content and chlorophyll fluorescence parameters were also reported. The vtc1 mutants had higher total glutathione than the wild type (WT) during the first day of UV-B treatment. We found reduced ratio of glutathione/total glutathione and increased ratio of dehydroascorbate/total ascorbate in the vtc1 mutants, compared to the WT plants. In addition, the enzymes responsible for ROS scavenging, including superoxide dismutase, catalase, and ascorbate peroxidase, had insufficient activity in the vtc1 mutants, compared to the WT plants. The same reduced activity in the vtc1 mutants was reported for the enzymes responsible for the regeneration of ascorbate and glutathione (including monodehydroascorbate reductase, dehydroascorbate reductase, and glutathione reductase). These results suggest that the ascorbate-deficient mutant vtc1 is more sensitive to supplementary UV-B treatment than WT plants and ascorbate can be considered an important antioxidant for UV-B radiation.
Journal: Journal of Plant Physiology - Volume 165, Issue 2, 1 February 2008, Pages 138–148