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Industrial polluted water has become an important water source for irrigation in the majority of constructed wetlands or even natural wetlands in China. The shortage of clean water resources has raised concerns about the potential accumulation of heavy metals, such as cadmium. Plants stressed by high levels of cadmium can increase the activity of superoxide dismutase. We have identified a positive correlation between the superoxide dismutase activity and the cadmium content of reed leaves in the wetland. Regression analysis confirmed that the superoxide dismutase activities fit a logistic curve. The logistic model was then applied to describe the superoxide dismutase activity, estimating parameters under different levels of cadmium stress. According to the findings, higher cadmium concentrations would cause the superoxide dismutase activity to increase at a higher intrinsic rate, have a lower environmental capacity k, and have lower inflection points. The dynamic model predicted an acceptable cadmium concentration of less than 3mg.kg-1. At this concentration, reeds could develop and grow satisfactorily in the presence of cadmium. Therefore, the concentration of cadmium in the irrigated water of polluted water in mine sites, papermaking wastewater, or other industrial wastewater should be less than or equal to 3mg.kg-1 to ensure the normal growth of reeds in related wetlands.

Normal aging is characterized with a decline in hippocampal memory functions that is associated with changes in long-term potentiation ( LTP) of the CA3-to- CA1 synapse. Age-related deficit of the dopaminergic system may contribute to impairment of CA1 LTP. Here we assessed how the modulation of CA1 LTP by dopamine is affected by aging and how it is dependent on the Ca2+ source. In slices from adult mice, the initial slope of the field potential showed strong LTP, but in slices from aged mice LTP was impaired. Dopamine did not affect LTP in adult slices, but enhanced LTP in aged slices. The dopamine D1/D5 receptor (D1R/D5R) agonist SKF-81297 did not affect LTP in adult but caused a relative small increase in LTP in aged slices; however, although there was no difference in dopamine D4 receptor (D4R) expression, the D4R agonist PD168077 increased LTP in aged slices to a magnitude similar to that in adult slices. The N-Methyl-D-aspartate receptor antagonist D- AP5 reduced LTP in adult slices, but not in aged slices. However, in the presence of D- AP5, PD168077 completely blocked LTP in aged slices. The voltage-dependent calcium channel ( VDCC) blocker nifedipine reduced LTP in adult slices, but surprisingly enhanced LTP in aged slices. Furthermore, in the presence of nifedipine, PD168077 caused a strong enhancement of LTP in aged slices to a magnitude exceeding LTP in adult slices. Our results indicate that the full rescue of impaired LTP in aging by the selective D4R activation and that a large potentiation role on LTP by co-application of D4R agonist and VDCC blocker may provide novel strategies for the intervention of cognitive decline of aging and age-related diseases. [ABSTRACT FROM AUTHOR]

The roles of nicotine on Ca(2+) oscillations [intracellular Ca(2+) ([Ca(2+)]i) oscillation] in rat primary cultured cortical neurons were studied. The spontaneous [Ca(2+)]i oscillations (SCO) were recorded in a portion of the neurons (65%) cultured for 7-10 days in vitro. Application of nicotine enhanced [Ca(2+)]i oscillation frequency and amplitude, which were reduced by the selective α4β2-nicotinic acetylcholine receptors (nAChRs) antagonist dihydro-β-erythroidine (DHβE) hydrobromide, and the selective α7-nAChRs antagonist methyllycaconitine citrate (MLA, 20 nM). DHβE reduced SCO frequency and prevented the nicotinic increase in the frequency. DHβE somewhat enhanced SCO amplitude and prevented nicotinic increase in the amplitude. MLA (20 nM) itself reduced SCO frequency without affecting the amplitude but blocked nicotinic increase in [Ca(2+)]i oscillation frequency and amplitude. Furthermore, coadministration of both α4β2- and α7-nAChRs antagonists completely prevented nicotinic increment in [Ca(2+)]i oscillation frequency and amplitude. Thus, our results indicate that both α4β2- and α7-nAChRs mediated nicotine-induced [Ca(2+)]i oscillations, and two nAChR subtypes differentially regulated SCO., (Copyright © 2016 the American Physiological Society.)