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抗坏血酸缺乏型拟南芥突变体vtc1中的L-抗坏血酸代谢

L-ascorbic acid metabolism in the ascorbate-deficient arabidopsis mutant vtc1.

作者信息

Conklin P L, Pallanca J E, Last R L, Smirnoff N

机构信息

Boyce Thompson Institute for Plant Research, Cornell University, Ithaca, New York 14853-1801, USA.

出版信息

Plant Physiol. 1997 Nov;115(3):1277-85. doi: 10.1104/pp.115.3.1277.

Abstract

The biosynthesis of L-ascorbic acid (vitamin C) is not well understood in plants. The ozone-sensitive Arabidopsis thaliana mutant vitamin c-1 (vtc1; formerly known as soz1) is deficient in ascorbic acid, accumulating approximately 30% of wild-type levels. This deficiency could result from elevated catabolism or decreased biosynthesis. No differences that could account for the deficiency were found in the activities of enzymes that catalyze the oxidation or reduction of ascorbic acid. The absolute rate of ascorbic acid turnover is actually less in vtc1 than in wild type; however, the turnover rate relative to the pool of ascorbic acid is not significantly different. The results from [U-14C]Glc labeling experiments suggest that the deficiency is the result of a biosynthetic defect: less L-[14C]ascorbic acid as a percentage of total soluble 14C accumulates in vtc1 than in wild type. The feeding of two putative biosynthetic intermediates, D-glucosone and L-sorbosone, had no positive effect on ascorbic acid levels in either genotype. The vtc1 defect does not appear to be the result of a deficiency in L-galactono-1,4-lactone dehydrogenase, an enzyme able to convert L-galactono-1,4-lactone to ascorbic acid.

摘要

植物中L-抗坏血酸(维生素C)的生物合成尚未完全明确。对臭氧敏感的拟南芥突变体维生素c-1(vtc1;以前称为soz1)缺乏抗坏血酸,其积累量约为野生型水平的30%。这种缺乏可能是由于分解代谢增加或生物合成减少所致。在催化抗坏血酸氧化或还原的酶活性方面,未发现能解释这种缺乏的差异。实际上,vtc1中抗坏血酸周转的绝对速率低于野生型;然而,相对于抗坏血酸池的周转率并无显著差异。[U-14C]葡萄糖标记实验结果表明,这种缺乏是生物合成缺陷的结果:与野生型相比,vtc1中L-[14C]抗坏血酸占总可溶性14C的百分比更低。添加两种假定的生物合成中间体D-葡糖酮和L-山梨糖对两种基因型的抗坏血酸水平均无积极影响。vtc1的缺陷似乎不是由于L-半乳糖-1,4-内酯脱氢酶缺乏所致,该酶能够将L-半乳糖-1,4-内酯转化为抗坏血酸。

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