The potential of tourmaline as a natural adsorbent for toxic metals, such as Pb(II), from acidic water was investigated. Batch experiments were conducted to study the effects of pH, temperature, particle size, and dose of absorbents. Results indicated that the adsorption of Pb(II) depended significantly on all the above-mentioned parameters except pH: no significant differences in adsorption mass were noted between pH 4.0 and pH 5.0. This independence from pH was in contrast to heavy metal adsorption by the conventional materials in acidic conditions. Furthermore, Fourier transform infrared spectroscopy (FTIR) and scanning electron microscopy (SEM) analyses elucidated the adsorption mechanisms of tourmaline of different particle sizes for Pb(II). FTIR analyses revealed that the bands originating from tourmaline particles of the spectra of 0.5–50 μm differed from those of 60–180 μm before and after interaction with aqueous Pb(II). SEM showed the evidence that Pb(II) aggregates were formed on tourmaline surfaces of 0.5–50 μm size particles. These results indicated differences in Pb(II) adsorption between 0.5–50 and 60–180 μm particle sizes, which were attributed to their differing extent of adjusting the pH of the solution. Hence, Pb(II) adsorption on the 0.5–50 μm tourmaline particles at 25 °C was the result of electropolar adsorption and chemisorption processes. Langmuir, Freundlich, and Langmuir–Freundlich isotherms all indicated good fits to the experimental data. The maximum mass of Pb(II) adsorbed (q m), as evaluated by a Langmuir–Freundlich isotherm, was 108 mg/g on tourmaline of 0.5–50 μm at an initial pH 5.0, which was much greater than that obtained for previously reported materials. Thus, this study shows that tourmaline may be explored as a new material for removing pollutants from the environment.

Autophagy has been implicated as a cellular protein degradation process that is used to recycle cytoplasmic components under biotic and abiotic stresses and so restrict programmed cell death (PCD). In this study, we report a novel regulatory mechanism by which NADPH oxidase respiratory burst oxidase homolog D (RBOHD) regulated pathogeninduced autophagy and hypersensitive (HR) cell death. We found that the Pseudomonas syringae pv tomato bacteria DC3000 expressing avrRps4 (Pst-avrRps4) induction of RBOHD-dependent reactive oxygen species (ROS) production promoted the onset of autophagy, whereas a pretreatment with an NADPH oxidase RBOHD inhibitor reversed this trend. The inhibitor significantly blocked pathogen-induced autophagosome formation and ROS increase. Moreover, we also show that in the wild-type and atrbohF mutant, Pst-avrRps4-induced cell death was limited, whereas in the case of the atrbohD mutant, the infection triggered a spreading-type necrosis. Our results demonstrate that the RBOHDdependent ROS accumulation stimulated autophagosome formation and limited HR cell death.