AI Summary & Key Takeaways
AI InsightOur element analysis results show that β-estradiol did not prevent lead uptake by roots, even it did stimulate the accumulation there.
📌 3 Key Takeaways
Abstract
In the present study, to determine the effects of β-estradiol on the ability of plants to tolerate lead toxicity, β-estradiol (10 μM) and lead (1.75 mM), singly or in combination, were exogenously applied to wheat seeds. Although lead resulted in a marked increase in the activities of antioxidant enzymes, including superoxide dismutase, guaiacol peroxidase, ascorbate peroxidase, and glutathione reductase (but not catalase), as well as an increase in the level of antioxidant compounds such as ascorbic acid and glutathione, this was insufficient to ameliorate the lead-induced oxidative injury or the superoxide anion, hydrogen peroxide, and malondialdehyde levels. However, β-estradiol was able to reduce the lead-induced oxidative damage and improved the antioxidant system. Similarly, β-estradiol reduced lead-induced α-amylase activity. The effects of lead toxicity on genetic material were also determined using the randomly amplified polymorphic DNA technique. While lead led to DNA damage in wheat seedlings, β-estradiol significantly mitigated this damage. Our element analysis results show that β-estradiol did not prevent lead uptake by roots, even it did stimulate the accumulation there. Taken together, our data demonstrate for the first time that β-estradiol-induced lead tolerance is associated with many biochemical and molecular mechanisms, including the antioxidant system, detoxification of reactive oxygen species, modulation of uptake and accumulation of lead, and protection of genetic material.
Özet
In the present study, to determine the effects of β-estradiol on the ability of plants to tolerate lead toxicity, β-estradiol (10 μM) and lead (1.75 mM), singly or in combination, were exogenously applied to wheat seeds. Although lead resulted in a marked increase in the activities of antioxidant enzymes, including superoxide dismutase, guaiacol peroxidase, ascorbate peroxidase, and glutathione reductase (but not catalase), as well as an increase in the level of antioxidant compounds such as ascorbic acid and glutathione, this was insufficient to ameliorate the lead-induced oxidative injury or the superoxide anion, hydrogen peroxide, and malondialdehyde levels. However, β-estradiol was able to reduce the lead-induced oxidative damage and improved the antioxidant system. Similarly, β-estradiol reduced lead-induced α-amylase activity. The effects of lead toxicity on genetic material were also determined using the randomly amplified polymorphic DNA technique. While lead led to DNA damage in wheat seedlings, β-estradiol significantly mitigated this damage. Our element analysis results show that β-estradiol did not prevent lead uptake by roots, even it did stimulate the accumulation there. Taken together, our data demonstrate for the first time that β-estradiol-induced lead tolerance is associated with many biochemical and molecular mechanisms, including the antioxidant system, detoxification of reactive oxygen species, modulation of uptake and accumulation of lead, and protection of genetic material.