Response of Tradescantia plants to oxidative stress induced by heavy metal pollution of soils from industrial areas
2019
Šiukšta, Raimondas | Bondzinskaitė, Skaistė | Kleizaitė, Violeta | Žvingila, Donatas | Taraškevičius, Ričardas | Mockeliūnas, Laurynas | Stapulionytė, Asta | Mak, Kristina | Čėsnienė, Tatjana
Numerous investigations have demonstrated that even soil in which concentrations of individual elements do not exceed permissible limits can cause harmful effects in living organisms. In the present study, polluted-soil-induced oxidative stress was evaluated using Tradescantia clone 4430, which is widely used for genotoxicity evaluations, employing biochemical (superoxide dismutase (SOD), contents of ascorbic acid (AA), carotenoids (Car), hydrogen peroxide (H₂O₂), chlorophyll (Chl) a/b ratio), and molecular (RAPD and differential display (DD-PCR)) markers after long-term exposure. The activity (staining intensity) of SOD isoforms in Tradescantia leaves was higher in plants grown in all heavy-metal-polluted test soils compared to the control. No direct link between the soil pollution category and the contents of AA, Car, Chl a/b in Tradescantia leaves was revealed, but the concentration of H₂O₂ was shown to be a sensitive biochemical indicator that may appropriately reflect the soil contamination level. Both short-term (treatment of cuttings with H₂O extracts of soil) and long-term (0.5 and 1.0 year) exposure increased MN frequencies, but the coincidence of the MN induction and the soil pollution level was observed only in some cases of long-term exposure. Soil (geno)toxin-induced polymorphism in the RAPD profile was determined with two primers in plants after long-term exposure to soils of an extremely hazard category. Transcript profiling of plants after long-term cultivation in test soils using DD-PCR showed that the majority of differentially expressed transcript-derived fragments (TDFs) were homologous to genes directly or indirectly participating in photosynthesis, the abiotic stress response, and signal transduction cascades.
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