RESEARCH ARTICLE
Rapid Accumulation of Cadmium and Antioxidative Response in Tobacco Leaves
Inna M. Buzduga1, Ivan Salamon2, Roman A. Volkov1, Irina I. Pаnchuk1, *
Article Information
Identifiers and Pagination:
Year: 2022Volume: 16
Issue: Suppl-1, M4
E-location ID: e187433152206271
Publisher ID: e187433152206271
DOI: 10.2174/18743315-v16-e2206271
Article History:
Received Date: 3/11/2021Revision Received Date: 9/2/2022
Acceptance Date: 19/4/2022
Electronic publication date: 22/09/2022
Collection year: 2022
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background:
Cadmium (Cd) is one of the most dangerous environmental pollutants. Plant damage caused by oxidative stress during long-term Cd accumulation is well documented, while the primary response to Cd uptake is poorly understood.
Objective:
We assess the short-term injury and the primary reaction of the antioxidant system to the rapid accumulation of Cd in tobacco leaves.
Methods:
Leaf rosettes of the 5-week-old plants without roots were exposed to 100, 500 and 5000 μM Cd chloride for 2 and 12 hours. Cd accumulation, oxidation levels of proteins and lipids, content of reduced (Asc) and oxidized (DHA) ascorbate and activity of CAT, APX and POD were determined.
Results:
An accumulation of Cd in high concentration, but only a relatively small increase in the oxidation of proteins and lipids was found in the leaves after 2 hours of treatment. These effects were transient and disappeared after 12 hours. No visible damage to plants was observed. After 12 hours, the total ascorbate content (Asc + DHA) decreased by 18%, remained unchanged or increased by 85% after the application of 100, 500 and 5000 µM Cd chloride. The increase in the ascorbate pool, which should be considered as a component of the protective response, was caused by the accumulation of DHA. The activity of APX and POD remained unchanged, while that of CAT decreased, indicating that antioxidant enzymes activation is not involved in the primary response to Cd.
Conclusions:
The primary generation of ROS induced by Cd does not appear to be a deleterious manifestation of Cd toxicity, but rather a component of stress signaling that causes activation of the protective response. Uptake of Cd caused severe damage to the plant after long-term, but not after short-term treatment, suggesting that the damage is the result of secondary effects of Cd toxicity.
