Cadmium induces senescence symptoms in leaf peroxisomes of pea plants
The effect of growing pea (Pisum sativum L.) plants with a toxic CdCl2 concentration (50 µm) on the metabolism and proteolytic activity of leaf peroxisomes was studied. In peroxisomes purified from plants treated with cadmium, an increase in the total protein concentration and in the activity and pr...
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Published in | Plant, cell and environment Vol. 24; no. 10; pp. 1065 - 1073 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Science, Ltd
01.10.2001
Blackwell Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | The effect of growing pea (Pisum sativum L.) plants with a toxic CdCl2 concentration (50 µm) on the metabolism and proteolytic activity of leaf peroxisomes was studied. In peroxisomes purified from plants treated with cadmium, an increase in the total protein concentration and in the activity and protein level of the photorespiratory enzyme glycolate oxidase was found. The glyoxylate cycle enzymes, malate synthase and isocitrate lyase, whose activity is normally very low in leaf peroxisomes, were enhanced by Cd treatment. The activity of the endogenous proteases of leaf peroxisomes was determined. Two leucine‐aminopeptidase isozymes (AP1‐AP2) were detected, and their activity was slightly higher in Cd‐treated plants. Five endopeptidases (EP1‐EP5) were present in pea leaf peroxisomes, and in plants grown with Cd the activity of isozymes EP1‐EP4 was increased. The ultrastructural analysis of pea leaves showed that Cd produced a disorganization of the chloroplast structure, with an increase in the number of plastoglobuli, and the formation of vesicles in the vacuoles. Taken together, these results indicate that Cd induces senescence symptoms in leaf peroxisomes, and probably a metabolic transition of leaf peroxisomes into glyoxysomes, and suggest that the peroxisomal proteases could participate in the metabolic changes produced by Cd. |
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ISSN: | 0140-7791 1365-3040 |
DOI: | 10.1046/j.1365-3040.2001.00750.x |