Physiological response of Conyza Canadensis to cadmium stress monitored by Fourier transform infrared spectroscopy and cadmium accumulation.

The cadmium(Cd) pollution of soil causes serious environmental problems. Cd is a high toxic and high water soluble element without biological function, and it is easily taken in by plants owing to its high bioavailability. Thus it easily entered the food chain and threaten people's health. Here，different concentrations of Cd solutions were used to study the physiological response and Cd accumulation characteristics of Conyza Canadensis (L.) Cronq. The physiological response was characterized by Fourier Transform Infrared (FTIR) spectroscopy, and Cd accumulation in plant and distribution were tested by Atomic absorption spectroscopy (AAS) under different concentrations Cd stress. When Cd concentrations toxicity <3 mg·L-1, the C. Canadensis (L.) Cronq. could grow normally without any symptoms, and the Cd concentrations increased to 7 mg·L-1, the C. Canadensis (L.) Cronq. had a little lower biomass, but there was no significant difference in the biomass among treatment concentrations. The peak shape of each component remained unchanged before and after Cd treatment. Only the absorption peak of some functional groups involved in Cd adsorption shifted with different degrees, such as hydroxy groups (3417-3429 cm-1), carboxyl groups (1380-1386 cm-1), and acid amide groups (1631-1637 cm -1). The characteristic peak absorption intensity of root, stem and leaf was different with the increase of heavy metal concentration. The absorbance of the roots with high Cd concentration was higher than that with medium-low Cd concentration. This shows that high concentration of Cd could induce C. Canadensis (L.) Cronq. seedlings to produce a large number of protein, amino acid and other substances, and through osmotic regulation to enhance stress resistance, provide nitrogen source, reduce heavy metal toxicity, and stabilize the internal environment. After Cd treatment, the characteristic peaks of stem and leaf were higher than or close to the control. This is due to the high tolerance of C. Canadensis (L.) Cronq. seedlings to heavy metals. The Cd accumulation in the shoots (stems and leaves) of C. Canadensis (L.) Cronq. was obviously lower than that in roots and the Cd content in the shoots usually increased with increasing Cd concentration. The maximum accumulation of Cd in shoots was 1898.07 mg·kg-1 after 11 days grown in the water spiked with 7 mg·L-1 Cd concentration. The study suggests that C. Canadensis (L.) Cronq. has some remediation effect and endurance ability against heavy metal polluted contaminated soil and has potential utilization value in the technical field of phytoremediation of Cd polluted soil.

Physiological response of Arundo donax to cadmium stress by Fourier transform infrared spectroscopy.

The present paper deals with the physiological response of the changes in chemical contents of the root, stem and leaf of Arundo donax seedlings stressed by excess cadmium using Fourier transform infrared spectroscopy technique, cadmium accumulation in plant by atomic absorption spectroscopy were tested after different concentrations cadmium stress. The results showed that low cadmium concentrations (<1.0mg/L) the root tissue of Arundo donax uses osmosis of organic substances (e.g. carbohydrates and amino acids) to improve cadmium tolerance. Organic substances (e.g. carbohydrates) that contain a lot of OH in leaf were transported to the root firstly and then could chelate cadmium, but no obvious changes in stems were noted. The cadmium in the shoots (stem and leaf) usually increased with increasing cadmium concentration. These studies demonstrate the potential of Fourier transform infrared spectroscopy technique for the non-invasive and rapid monitoring of the plants stressed with heavy metals, Arundo donax is suitable for phytoremediation of cadmium -contaminated wetland.

[Effect of Coupling Process of Wetting-Drying Cycles and Seasonal Temperature Increasing on Sediment Nitrogen Minerization in the Water Level Fluctuating Zone].

To reveal the effect of coupling process of wetting-drying and seasonal temperature on sediment nitrogen (N) minerization, surface sediment samples were collected from the water level fluctuating zone(WLFZ) of Pengxi River crossing two hydrological sections. The sediment samples were incubated under drying and submerging conditions at the controlled temperature. The result showed that NO3--N and sand% in the sediment of higher altitude of water level (170 m) were higher than those in low altitudes (150 and 160 m), whereas contents of TN, NH4+-N and clay% and silt% in low altitudes were much higher. Generally, Net N mineralization rate and cumulation were lower in higher altitude of water level during the drying period and submerging period. The ammonification rate decreased rapidly at the initial stage of incubation (0-7 d), and then had no obvious change, and no significant differences among altitudes was observed. The nitrification rate at low altitude decreased with incubation time, while it had only a little change at higher altitude; The nitrification contributed a higher fraction of net N mineralization than ammonification. Net N mineralization rate and its cumulation were significantly higher in the drying period than in the submerging period, while net N mineralization rate decreased with incubation time at all altitudes. Net N mineralization cumulation tended to rise first and then declined at all altitudes of the drying period, whereas it was continuously decreasing at the low water level altitude during the submerging period. Net N nitrogen mineralization rate of the drying period was positively correlate to both the sediment organic matter content and its C:N ratio, while it showed a negative correlation in the submerging period(P<0.001). Net N mineralization was sensitive to temperature increase (Q10>1) in the drying period, while it was insensitive during the submerging period of low altitude (Q10<1). Thus, the impact of temperature on Net N mineralization was relatively low in submerging period of winter and N was accumulated with low releasing rate. In contrast to winter, summer exhibited warmer and drying period, this two factors would lead to higher N mineralization rate and further induce the potential risk of eutrophication as N releasing into water body.

Transmissions of serotonin, dopamine, and glutamate are required for the formation of neurotoxicity from Al2O3-NPs in nematode Caenorhabditis elegans.

In this study, we investigated genetic mechanisms of neurotransmitters in regulating the formation of adverse effects on locomotion behavior in Al2O3 nanoparticles (NPs)-exposed Caenorhabditis elegans. Al2O3-NPs exposure caused the decrease of locomotion behavior with head thrash and body bend as endpoints. Interestingly, the neurotransmitters of glutamate, serotonin, and dopamine were required for the adverse effects of Al2O3-NPs on locomotion behavior in nematodes. Glutamate transporter EAT-4, serotonin transporter MOD-5, and dopamine transporter DAT-1 might serve as the molecular targets of Al2O3-NPs for neurotoxicity formation. Moreover, the behavioral response of nematodes to Al2O3-NPs exposure was primarily mediated by non-NMDA glutamate receptors GLR-2 and GLR-6, ionotropic serotonin receptor MOD-1, and D1-like dopamine receptor DOP-1. Therefore, Al2O3-NPs exposure influences locomotion behavior of nematodes primarily by impinging on their glutamatergic, serotoninergic, and dopaminergic systems. Our data will shed light on questions surrounding the involvement of neurotransmitters in mediating the adverse behavioral effects from Al2O3-NPs.

Chronic Al2O3-nanoparticle exposure causes neurotoxic effects on locomotion behaviors by inducing severe ROS production and disruption of ROS defense mechanisms in nematode Caenorhabditis elegans.

To date, knowledge on mechanisms regarding the chronic nanotoxicity is still largely minimal. In the present study, the effect of chronic (10-day) Al(2)O(3)-nanoparticles (NPs) toxicity on locomotion behavior was investigated in the nematode Caenorhabditis elegans. Exposure to 0.01-23.1 mg/L of Al(2)O(3)-NPs induced a decrease in locomotion behavior, a severe stress response, and a severe oxidative stress; however, these effects were only detected in nematodes exposed to 23.1 mg/L of bulk Al(2)O(3). Formation of significant oxidative stress in nematodes exposed to Al(2)O(3)-NPs was due to both the increase in ROS production and the suppression of ROS defense mechanisms. More pronounced increases in ROS, decreases in SOD activity, and decrease in expression of genes encoding Mn-SODs (sod-2 and sod-3) were detected in nematodes exposed to Al(2)O(3)-NPs compared with bulk Al(2)O(3). Moreover, treatment with antioxidants or SOD-3 overexpression not only suppressed oxidative stress but also prevented adverse effects on locomotion behaviors from Al(2)O(3)-NPs exposure. Thus, chronic exposure to Al(2)O(3)-NPs may have adverse effects on locomotion behaviors by both induction of ROS production and disruption of ROS defense mechanisms. Furthermore, sod-2 and sod-3 mutants were more susceptible than the wild-type to chronic Al(2)O(3)-NPs-induced neurotoxicity inhibition.

Close association of intestinal autofluorescence with the formation of severe oxidative damage in intestine of nematodes chronically exposed to Al(2)O(3)-nanoparticle.

In nematodes, acute exposure (24-h) to 8.1-30.6 mg/L Al(2)O(3)-nanoparticles (NPs) or Al(2)O(3) did not influence intestinal autofluorescence, whereas chronic exposure (10-d) to Al(2)O(3)-NPs at concentrations of 8.1-30.6 mg/L or Al(2)O(3) at concentrations of 23.1-30.6 mg/L induced significant increases of intestinal lipofuscin accumulation, and formation of severe stress response and oxidative damage in intestines. Moreover, significant differences of intestinal autofluorescence, stress response and oxidative damage in intestines of Al(2)O(3)-NPs exposed nematodes from those in Al(2)O(3) exposed nematodes were detected at examined concentrations. Oxidative damage in intestine was significantly correlated with intestinal autofluorescence in exposed nematodes, and oxidative damage in intestine was more closely associated with intestinal autofluorescence in nematodes exposed to Al(2)O(3)-NPs than exposed to Al(2)O(3). Thus, chronic exposure to Al(2)O(3)-NPs may cause adverse effects on intestinal lipofuscin accumulation by inducing the formation of more severe oxidative stress in intestines than exposure to Al(2)O(3) in nematodes.

Aluminum nanoparticle exposure in L1 larvae results in more severe lethality toxicity than in L4 larvae or young adults by strengthening the formation of stress response and intestinal lipofuscin accumulation in nematodes.

Toxicity of Al(2)O(3)-NPs, as compared to that of Al(2)O(3), to L1-larval, L4-larval or young adult nematodes was evaluated. When exposure was performed at L1-larval stage, the significant increases of lethality, stress response, and intestinal lipofuscin autofluorescence were observed in 6.3-203.9 mg/L of Al(2)O(3)-NPs exposed nematodes. In contrast, when exposure was performed at L4-larval or young adult stage, the significant increases of lethality and intestinal lipofuscin autofluorescence were observed in 12.7-203.9 mg/L of Al(2)O(3)-NPs exposed nematodes, and the significant inductions of stress response were detected in 25.5-203.9 mg/L of Al(2)O(3)-NPs exposed nematodes. Moreover, the lethality was significantly correlated with the stress response and the intestinal lipofuscin autofluorescence in Al(2)O(3)-NPs exposed nematodes. These data imply that Al(2)O(3)-NPs exposure in L1 larvae causes more severe lethality toxicity than in L4 larvae or young adults by strengthening the formation of stress response and intestinal lipofuscin accumulation in nematodes.

Four anthraquinones from Hedyotis diffusa.

A new anthraquinone has been isolated from the 95% EtOH extract of Hedyotis diffusa and characterized as 2-hydroxy-3-methoxy-6-methyl-9,10-anthraquinone (1) by extensive spectral analysis. The known compounds isolated for the first time from this plant have been identified as 2-hydroxy-3-methoxy-7-methyl-9,10-anthraquinone (2), 2-hydroxy-6-methylanthraquinone (3), and 1,3-dimethoxy-2-hydroxy-9,10-anthraquinone (4).