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臭氧对烟草线粒体肿胀的影响。

Effect of ozone on swelling of tobacco mitochondria.

作者信息

Lee T T

机构信息

Canada Department of Agriculture, Research Branch, Research Station, Delhi, Ontario, Canada.

出版信息

Plant Physiol. 1968 Feb;43(2):133-9. doi: 10.1104/pp.43.2.133.

Abstract

The swelling of mitochondria isolated from leaves, roots, and callus tissues of Nicotiana tabacum, L, var. White Gold, was measured by following changes in optical density at 520 mmu in buffered 0.25 m sucrose or 0.125 m KCl. Ozone induced rapid swelling of the isolated mitochondria and increased the permeability of mitochondrial membranes. The extent of mitochondrial swelling and the amount of soluble proteins and other substances absorbing at 260 and 280 mmu released from mitochondria into the suspending medium were positively correlated with the length of exposure to O(3). The correlation between the extent of mitochondrial swelling and the loss of intramitochondrial materials was also highly significant.Protocatechuic acid, when initially present in the suspending medium, completely prevented O(3)-induced swelling. Reduced glutathione, ascorbate, and l-cysteine partially prevented O(3)-induced swelling. But these reducing substances failed to reverse mitochondrial swelling when added after O(3) treatment.Polyvinylpyrrolidone (PVP) and bovine serum albumin (BSA) induced contraction of tobacco mitochondria in the absence of O(3), but did not reverse swelling of O(3)-treated mitochondria. PVP and BSA only stopped O(3)-induced swelling. Evidently O(3)-induced swelling was osmotically irreversible. Hypertonic solutions of sucrose neither induced contraction of tobacco mitochondria nor prevented O(3)-induced swelling.Contraction of tobacco mitochondria occurred rapidly at acid pH, but the contracting state affected by acid pH did not protect mitochondria from O(3)-induced swelling. Although O(3) induced greater swelling at acid pH, the O(3)-treated mitochondria were still responsive to acid-induced contraction.

摘要

对烟草(Nicotiana tabacum, L, var. White Gold)叶片、根和愈伤组织中分离出的线粒体肿胀情况进行了测定,方法是跟踪在缓冲的0.25m蔗糖溶液或0.125m氯化钾溶液中520毫微米处光密度的变化。臭氧可使分离出的线粒体迅速肿胀,并增加线粒体膜的通透性。线粒体肿胀的程度以及从线粒体释放到悬浮介质中、在260和280毫微米处有吸收的可溶性蛋白质及其他物质的量,与暴露于臭氧的时间长短呈正相关。线粒体肿胀程度与线粒体内物质损失之间的相关性也非常显著。原儿茶酸若最初存在于悬浮介质中,可完全阻止臭氧诱导的肿胀。还原型谷胱甘肽、抗坏血酸和L-半胱氨酸可部分阻止臭氧诱导的肿胀。但这些还原性物质在臭氧处理后添加时,无法使线粒体肿胀逆转。聚乙烯吡咯烷酮(PVP)和牛血清白蛋白(BSA)在无臭氧的情况下可诱导烟草线粒体收缩,但不能使经臭氧处理的线粒体肿胀逆转。PVP和BSA仅能阻止臭氧诱导的肿胀。显然,臭氧诱导的肿胀在渗透方面是不可逆的。高渗蔗糖溶液既不能诱导烟草线粒体收缩,也不能阻止臭氧诱导的肿胀。烟草线粒体在酸性pH条件下迅速发生收缩,但酸性pH影响的收缩状态并不能保护线粒体免受臭氧诱导的肿胀。尽管臭氧在酸性pH条件下诱导的肿胀更大,但经臭氧处理的线粒体仍对酸诱导的收缩有反应。

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