Increased urbanization detrimentally affects crop plants. Heavy metals pollution sharply threatens food security. However, greenly synthesized nanoparticles were recently proposed as growth bioregulators. To investigate the evolved mechanisms by which sulfur nanoparticles (SNPs) could improve cellular defense against manganese toxicity, the present experiment was applied on Helianthus annuus (L.) seedlings. The experimental design was based on priming of sunflower seeds for 18 h in different (12.5–200 μM) SNPs, while 100 mM manganese sulfate (MnSO4) was implemented as irrigation treatment. The 14-day-old seedlings manifested Mn noxiousness and oxidative stress indications such as increased reactive oxygen species (O2·− and H2O2) and lipid peroxidation. Manganese exposure severely lowered the activity of some antioxidant enzymes like superoxide dismutase (SOD) and catalase (CAT), while induced ascorbate peroxidase (APX), guaiacol peroxidase (POX), polyphenol oxidase (PPO), and glutathione reductase (GR) activities. An evident decline in the pool of antioxidant compounds, such as ascorbic acid (ASA), glutathione (GSH), and total flavonoids content (TFC), was attained with Mn stress. Priming with SNPs significantly stimulated CAT and SOD activities and enhanced the antioxidant compounds (ASA, TFC, and total phenolic compounds) level in Mn-stressed seedlings. Consequently, SNPs caused a significant decrease in O2·−, H2O2, and lipid peroxidation and their oxidative damage. However, a significant reduction in GSH was detected with SNPs that might be consumed and incorporated into biosynthesis of other chelating ligands. Therefore, SNPs manifested a vital role in Mn detoxification through counterbalancing oxidative damage and elevating the antioxidant defense machinery.

中文翻译：

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用绿色合成的硫纳米粒子引发种子增强抗氧化防御机制并限制锰胁迫下向日葵 (L.) 幼苗的氧化损伤

城市化进程的加快对农作物产生不利影响。重金属污染严重威胁粮食安全。然而，最近提出了绿色合成的纳米颗粒作为生长生物调节剂。为了研究硫纳米粒子 (SNP) 可以改善细胞对锰毒性的防御的进化机制，本实验应用于向日葵 (L.) 幼苗。实验设计基于向日葵种子在不同 (12.5–200 μM) SNP 中引发 18 小时，同时使用 100 mM 硫酸锰 (MnSO4) 作为灌溉处理。14 天龄的幼苗表现出锰毒性和氧化应激迹象，例如活性氧（O2·-和 H2O2）增加和脂质过氧化。锰暴露严重降低了一些抗氧化酶的活性，如超氧化物歧化酶 (SOD) 和过氧化氢酶 (CAT)，同时诱导抗坏血酸过氧化物酶 (APX)、愈创木酚过氧化物酶 (POX)、多酚氧化酶 (PPO) 和谷胱甘肽还原酶 (GR) 活性。在锰胁迫下，抗氧化化合物（如抗坏血酸 (ASA)、谷胱甘肽 (GSH) 和总黄酮含量 (TFC)）明显下降。用 SNP 启动显着刺激了 CAT 和 SOD 活性，并提高了 Mn 胁迫幼苗中的抗氧化化合物（ASA、TFC 和总酚类化合物）水平。因此，SNP 导致 O2·-、H2O2 和脂质过氧化及其氧化损伤显着减少。然而，用 SNP 检测到 GSH 的显着减少，这些 SNP 可能被消耗并结合到其他螯合配体的生物合成中。因此，SNPs 通过平衡氧化损伤和提升抗氧化防御机制，在锰解毒中发挥重要作用。