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<p>The aim of this study was to determine the tolerance-enhancing effect of <i>Lavandula stoechas</i> L. (LSE) against prometryn herbicide using <i>Allium cepa</i>. Six treatment groups were established to assess whether LSE could mitigate prometryn-induced stress: control, LSE (200 and 400&#xa0;mg/L), prometryn (6000&#xa0;mg/L), and prometryn combined with LSE (200 and 400&#xa0;mg/L). Alterations in physiological, genotoxic, biochemical, and root meristematic tissues of <i>A. cepa</i> were systematically evaluated. Prometryn exposure led to substantial physiological deterioration in <i>A. cepa</i>, as evidenced by reductions of 57% in rooting percentage, 83% in root elongation, and 69% in weight gain compared to the control group. Moreover, the mitotic index showed a significant reduction of 26%, while the frequency of chromosomal aberrations, micronuclei formation, and tail DNA percentage demonstrated a pronounced increase, indicating a major genotoxic effect induced by prometryn treatment. In the prometryn-treated group, the most prevalent chromosomal abnormalities included fragment, followed by sticky chromosomes, vagrant chromosomes, chromosomal bridges, unequal chromatin distribution, vacuolated nuclei, and reverse polarization. In the group treated with prometryn, malondialdehyde content increased by 2.7-fold, catalase and superoxide dismutase activities rose by 2.1-fold each, whereas chlorophyll a and chlorophyll b levels declined by 55.4% and 75.5%, respectively, compared to the control. Prometryn treatment also provoked structural changes in the root meristem, including epidermal cell damage, cortex cell damage, thickening of cortex cell walls, flattened cell nucleus, and thickening of conduction tissue. The interaction of prometryn with key macromolecules was further investigated through molecular docking to elucidate its toxicity mechanism. Conversely, co-application of increasing concentrations of LSE alongside prometryn significantly alleviated the physiological, biochemical, and cytogenetic alterations induced by prometryn toxicity. LC–MS/MS analysis revealed that rosmarinic acid, caffeic acid, <i>p</i>-coumaric acid, protocatechualdehyde, sesamol, 4-hydroxybenzoic acid, salicylic acid, vanillin, gentisic acid, taxifolin, quercetin, rutin, naringenin, and syringaldehyde were identified as the predominant phenolic constituents. The findings indicate that LSE has a protective effect in <i>A. cepa</i> against prometryn-induced phytotoxicity, genotoxicity, and oxidative stress. This protective capacity is attributed to the potent antioxidant and antigenotoxic properties of LSE, which are likely associated with its rich phenolic composition. The results demonstrated that LSE alone did not exhibit any toxic effects at the tested concentrations, while co-treatment with prometryn significantly alleviated prometryn-induced physiological, cytogenetic, and biochemical alterations. These findings provide the first experimental evidence that LSE exerts a dose-dependent protective role against prometryn toxicity in <i>A. cepa</i>, likely due to its rich phenolic composition and antioxidant capacity.</p>

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The role of Lavandula stoechas L. extract in enhancing tolerance to prometryn toxicity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月29日

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  • Oksal Macar,
  • Tuğçe Kalefetoğlu Macar,
  • Kültiğin Çavuşoğlu,
  • Emine Yalçın,
  • Ali Acar

摘要

The aim of this study was to determine the tolerance-enhancing effect of Lavandula stoechas L. (LSE) against prometryn herbicide using Allium cepa. Six treatment groups were established to assess whether LSE could mitigate prometryn-induced stress: control, LSE (200 and 400 mg/L), prometryn (6000 mg/L), and prometryn combined with LSE (200 and 400 mg/L). Alterations in physiological, genotoxic, biochemical, and root meristematic tissues of A. cepa were systematically evaluated. Prometryn exposure led to substantial physiological deterioration in A. cepa, as evidenced by reductions of 57% in rooting percentage, 83% in root elongation, and 69% in weight gain compared to the control group. Moreover, the mitotic index showed a significant reduction of 26%, while the frequency of chromosomal aberrations, micronuclei formation, and tail DNA percentage demonstrated a pronounced increase, indicating a major genotoxic effect induced by prometryn treatment. In the prometryn-treated group, the most prevalent chromosomal abnormalities included fragment, followed by sticky chromosomes, vagrant chromosomes, chromosomal bridges, unequal chromatin distribution, vacuolated nuclei, and reverse polarization. In the group treated with prometryn, malondialdehyde content increased by 2.7-fold, catalase and superoxide dismutase activities rose by 2.1-fold each, whereas chlorophyll a and chlorophyll b levels declined by 55.4% and 75.5%, respectively, compared to the control. Prometryn treatment also provoked structural changes in the root meristem, including epidermal cell damage, cortex cell damage, thickening of cortex cell walls, flattened cell nucleus, and thickening of conduction tissue. The interaction of prometryn with key macromolecules was further investigated through molecular docking to elucidate its toxicity mechanism. Conversely, co-application of increasing concentrations of LSE alongside prometryn significantly alleviated the physiological, biochemical, and cytogenetic alterations induced by prometryn toxicity. LC–MS/MS analysis revealed that rosmarinic acid, caffeic acid, p-coumaric acid, protocatechualdehyde, sesamol, 4-hydroxybenzoic acid, salicylic acid, vanillin, gentisic acid, taxifolin, quercetin, rutin, naringenin, and syringaldehyde were identified as the predominant phenolic constituents. The findings indicate that LSE has a protective effect in A. cepa against prometryn-induced phytotoxicity, genotoxicity, and oxidative stress. This protective capacity is attributed to the potent antioxidant and antigenotoxic properties of LSE, which are likely associated with its rich phenolic composition. The results demonstrated that LSE alone did not exhibit any toxic effects at the tested concentrations, while co-treatment with prometryn significantly alleviated prometryn-induced physiological, cytogenetic, and biochemical alterations. These findings provide the first experimental evidence that LSE exerts a dose-dependent protective role against prometryn toxicity in A. cepa, likely due to its rich phenolic composition and antioxidant capacity.