Nicosulfuron stress on the glyoxalase system and endogenous hormone content in sweet maize seedlings.

To reduce the harmful effects of nicosulfuron on sweet corn, the physiological regulation mechanism of sweet corn detoxification was studied. This study analyzed the effects of nicosulfuron stress on the glyoxalase system, hormone content, and key gene expression of nicosulfuron-tolerant "HK301" and nicosulfuron-sensitive "HK320" sweet corn seedling sister lines. After spraying nicosulfuron, the methylglyoxal (MG) content in HK301 increased first and then decreased. Glyoxalase I (GlyI) and glyoxalase II (GlyII) activities, non-enzymatic glutathione (GSH), and the glutathione redox state glutathione/(glutathione + glutathione disulfide) (GSH/(GSH + GSSG)) showed a similar trend as the MG content. Abscisic acid (ABA), gibberellin (GA), and zeatin nucleoside (ZR) also increased first and then decreased, whereas the auxin (IAA) increased continuously. In HK301, all indices after spraying nicosulfuron were significantly greater than those of the control. In HK320, MG accumulation continued to increase after nicosulfuron spraying and GlyI and GlyII activities, and GSH first increased and then decreased after 1 day of stress. The indicators above were significantly greater than the control. The GSH/(GSH + GSSG) ratio showed a decreasing trend and was significantly smaller than the control. Furthermore, ABA and IAA continued to increase, and the GA and ZR first increased and then decreased. Compared with HK320, HK301 significantly upregulated the transcription levels of GlyI and GlyII genes in roots, stems, and leaves. Comprehensive analysis showed that sweet maize seedlings improved their herbicide resistance by changing the glyoxalase system and regulating endogenous hormones. The results provide a theoretical basis for further understanding the response mechanism of the glyoxalase system and the regulation characteristics of endogenous hormones in maize under nicosulfuron stress.

Responses of photosynthesis, antioxidant enzymes, and related gene expression to nicosulfuron stress in sweet maize (Zea mays L.).

Weed control in maize (Zea mays L.) crops is usually undertaken using the postemergence herbicide nicosulfuron. The toxicity of nicosulfuron on maize, especially sweet maize, has been widely reported. In order to examine the effect of nicosulfuron on seedling photosynthetic characteristics, chlorophyll fluorescence, reactive oxygen species production, antioxidant enzyme activities, and gene expressions on sweet maize, nicosulfuron-tolerant "HK310" and nicosulfuron-sensitive "HK320" were studied. All experiment samples were subjected to a water or 80 mg kg-1 of nicosulfuron treatment when sweet maize seedlings grow to the stage of four leaves. After treatment with nicosulfuron, results for HK301 were significantly higher than those for HK320 for net photosynthetic rate, transpiration rate, stomatal conductance, leaf maximum photochemical efficiency of PSII, photochemical quenching of chlorophyll fluorescence, and the electron transport rate. These results were contrary to nonphotochemical quenching and intercellular CO2 concentration. As exposure time increased, associated effects also increased. Both O2·- and H2O2 detoxification is modulated by antioxidant enzymes. Compared to HK301, SOD, POD, and CAT activities of HK320 were significantly reduced as exposure time increase. Compared to HK320, the gene expression for the majority of SOD genes, except for SOD2, increased due to inducement by nicosulfuron, and it significantly upregulated the gene expression of CAT in HK301. Results from this study indicate that plants can improve photosynthesis, scavenging capabilities of ROS, and protective mechanisms to alleviate phytotoxic effect of nicosulfuron. Future research is needed to further elucidate the important role antioxidant systems and gene regulation play in herbicide detoxification in sweet maize.