Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama, Japan.
Plant & Microbial Research Unit (PMRU), Research, Technology & Value Creation Division, Nagase Viita Co. Ltd., Naka-ku, Okayama, Japan.
Biosci Biotechnol Biochem. 2024 Sep 20;88(10):1164-1171. doi: 10.1093/bbb/zbae092.
SO2/H2SO3 can damage plants. However, its toxic mechanism has still been controversial. Two models have been proposed, cytosolic acidification model and cellular oxidation model. Here, we assessed the toxic mechanism of H2SO3 in three cell types of Arabidopsis thaliana, mesophyll cells, guard cells (GCs), and petal cells. The sensitivity of GCs of Chloride channel a (CLCa)-knockout mutants to H2SO3 was significantly lower than those of wildtype plants. Expression of other CLC genes in mesophyll cells and petal cells were different from GCs. Treatment with antioxidant, disodium 4,5-dihydroxy-1,3-benzenedisulfonate (tiron), increased the median lethal concentration (LC50) of H2SO3 in GCs indicating the involvement of cellular oxidation, while the effect was negligible in mesophyll cells and petal cells. These results indicate that there are two toxic mechanisms of SO2 to Arabidopsis cells: cytosolic acidification and cellular oxidation, and the toxic mechanism may vary among cell types.
SO2/H2SO3 会对植物造成损害。然而，其毒性机制仍存在争议。目前已经提出了两种模型，即细胞质酸化模型和细胞氧化模型。在这里，我们评估了 H2SO3 在拟南芥三种细胞类型（叶肉细胞、保卫细胞和花瓣细胞）中的毒性机制。氯离子通道 a（CLCa）敲除突变体保卫细胞对 H2SO3 的敏感性明显低于野生型植物。叶肉细胞和花瓣细胞中其他 CLC 基因的表达与保卫细胞不同。抗氧化剂二钠 4,5-二羟基-1,3-苯二磺酸钠（tiron）的处理增加了 H2SO3 在保卫细胞中的半数致死浓度（LC50），表明细胞氧化的参与，而在叶肉细胞和花瓣细胞中，这种作用可以忽略不计。这些结果表明，SO2 对拟南芥细胞有两种毒性机制：细胞质酸化和细胞氧化，并且毒性机制可能因细胞类型而异。
