1.
Arsenic speciation in the phloem exudates of rice and its role in arsenic accumulation in rice grains.
Ye, W, Zhang, J, Fan, T, Lu, H, Chen, H, Li, X, Hua, R
Ecotoxicology and environmental safety. 2017;:87-91
Abstract
Arsenic (As) speciation in the phloem sap of rice plants and its role in As accumulation in rice grains remain largely uncharacterized. In the present study, we tested As chemical species in the phloem exudates of rice treated with arsenate [As(V)], arsenite [As(III)], monomethylarsonic acid [MMA(V)], or dimethylarsinic acid [DMA(V)]. As(V) was the main species (58%) in the phloem exudates of As(V)-exposed rice, whereas As(III) predominated (69%) in As(III)-exposed rice. A large proportion of As(V) (41-45%) was observed in the phloem exudates when rice was treated with methylated As species. High concentrations of phytochelatins were detected in the phloem exudates when the As(V) treatment level was increased. The role of phloem transport was analyzed by applying a ±stem-girdling treatment to the rice plants, limiting phloem transport to the grain in rice pulsed with As(III), As(V), MMA(V), or DMA(V). The findings of the present study indicate that organic As is more mobile than inorganic As during phloem transport. Phloem transport accounted for 54% of As(III), 56% of As(V), 100% of MMA(V), and 89% of DMA(V) transport to the grain. The total As concentration and As(III) percentage in rice phloem and grain were significantly affected by increasing the phosphate concentration in the medium.
2.
[Effect of arsenic trioxide combined with adriamycin on the proliferation and apoptosis of human lymphoma cells].
Huang, R, Li, X, Huang, X, Yang, X, Li, W
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences. 2009;(6):515-22
Abstract
OBJECTIVE To determine the effect of arsenic trioxide combined with adriamycin(ADM) on the proliferation and apoptosis of human lymphoma cells. METHODS Raji cells were divided into an experimental group and a control group, and the experimental group was further divided into 1 micromol/L As(2)O(3) group,2 micromol/L As(2)O(3) group, ADM group,1 micromol/L As(2)O(3) and ADM group,2 micromol/L As(2)O(3) and ADM group. Human lymphoma cells Raji were treated with As(2)O(3) combined with ADM. Wright-Giemsa dying assay was used to observe the apoptosis morphology of lymphoma cells. The proliferation of the cells treated with As(2)O(3) and adriamycin was detected by the method of 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT). Flow cytometry(FCM) was used to detect the apoptosis rate of lymphoma and the fluorescene density in the lymphocytes. Effect of arsenic trioxide and adriamycin on the mutant p53 expression in Raji cells was detected by semi-quantitive RT-PCR. RESULTS Evident apoptotic morphological changes of Raji cells were observed 24 hours after treatment with As(2)O(3) or ADM. Compared with As(2)O(3) or ADM alone, As(2)O(3) combined with ADM could increase the inhibition ratio significantly (P<0.05), and the inhibition rate was related to the concentration and action time of As(2)O(3) (P<0.05). Compared with As(2)O(3) or ADM alone, As(2)O(3) combined with ADM could increase the apoptosis rate of lymphoma cells with obvious difference (P<0.05). Semi-quantitive and RT-PCR showed that the expression of mutant p53 in As(2)O(3) and ADM alone and combined groups was obviously less than that in the control (P<0.05). After the treatment with 1 micromol/L and 2 micromol/L As(2)O(3), the fluorescene density in the Raji cells was 18.53 and 18.12, 0.056 and 0.023 times increase respectively.There was no difference (P>0.05). CONCLUSION As(2)O(3) and ADM alone or combined can inhibit the proliferation, induce cell apoptosis, and downregulate the expression of mutant p53 in vitro. As(2)O(3) combined with ADM has synergistic anti-lymphoma cell effect in vitro. As(2)O(3) has no significant effect on the concentration of ADM on the Raji cells, but can enhance the chemosensitivity of Raji cells, and its mechanism may be that it can downregulate the expression of mutant p53.