砷(As^(3+))胁迫对鄂尔多斯高原碱湖钝顶螺旋藻生理生化指标的影响

为提高钝顶螺旋藻的养殖质量,以鄂尔多斯高原碱湖钝顶螺旋藻为材料,用不同浓度的亚砷酸钠(As^(3+))培养液培养螺旋藻,研究了砷(As^(3+))胁迫对钝顶螺旋藻的生理生化指标的影响。结果表明:砷(As^(3+))胁迫会使叶绿素a和类胡萝卜素的波峰发生蓝移,藻胆蛋白的波峰发生红移。叶绿素a和类胡萝卜素含量在低浓度砷(As^(3+))胁迫下增加,高浓度砷(As^(3+))胁迫下降低。藻蓝蛋白和可溶性蛋白的含量则是在高浓度砷(As^(3+))和低浓度砷(As^(3+))胁迫下均会降低。

Valence variation of arsenic in bioleaching process of arsenic-bearing gold ore

The concentration and variational trend of As3 +and As 5+,the bacterial resistance for the As 3+and As 5+and converting conditions from As3 +to As 5+were analyzed.The additive was used to prompt the bacterial leaching efficiency by changing valence state of arsenic.The results show that the concentration of As 3+ is larger than that of As 5+ in the lag phase.The concentration of As 3+ decreases in the log phase,and is lower than that of As5 +.HQ-0211 typed bacteria express better resistance for As 3+and As 5+and remain growing when the concentrations of As3 +and As 5+are above 6.0 g/L and 12.0 g/L,respectively.It is found that Fe 3+cannot oxidize As3 +singly as strong oxidant in the leaching system,but can cooperate with pyrite or chalcopyrite to do that.The oxidation of As 3+ is prompted with addition of H2O2.The bacterial activity is improved in favor of bacterial leaching efficiency.NaClO restrains the bacterial growth to depress leaching efficiency because of the chloric compounds affecting bacterial activity.

Roles of SET7/9 and LSD1 in the Pathogenesis of Arsenicinduced Hepatocyte Apoptosis

Background and Aims:Multiple regulatory mechanisms play an important role in arsenic-induced liver injury.To investigate whether histone H3 lysine 4(H3K4)methyltransferase(SET7/9)and histone H3K4 demethyltransferase(LSD1/KDM1A)can regulate endoplasmic reticulum stress(ERS)-related apoptosis by modulating the changes of H3K4 methylations in liver cells treated with arsenic.Methods:Apoptosis,proliferation and cell cycles were quantified by flow cytometry and real-time cell analyzer.The expression of ERS-and epigenetic-related proteins was detected by Western blot analysis.The antisense SET7/9 expression vector and the overexpressed LSD1 plasmid were used for transient transfection of LO_(2) cells.The effects of NaAsO_(2) on the methylation of H3 in the promoter regions of 78 kDa glucose-regulated protein,activating transcription factor 4 and C/EBP-homologous protein were evaluated by chromatin immunoprecipitation assay.Results:The protein expression of LSD1(1.25±0.08 vs.1.77±0.08,p=0.02)was markedly decreased by treatment with 100μM NaAsO_(2),whereas the SET7/9(0.68±0.05 vs.1.10±0.13,p=0.002)expression level was notably increased,which resulted in increased H3K4me1/2(0.93±0.64,1.19±0.22 vs.0.71±0.13,0.84±0.13,p=0.03 and p=0.003).After silencing SET7/9 and overexpressing LSD1 by transfection,apoptosis rate(in percentage:3.26±0.34 vs.7.04±0.42,4.80±0.32 vs.7.52±0.38,p=0.004 and p=0.02)was significantly decreased and proliferation rate was notably increased,which is reversed after inhibiting LSD1(in percentage:9.31±0.40 vs.7.52±0.38,p=0.03).Furthermore,the methylation levels of H3 in the promoter regions of GRP78(20.80±2.40 vs.11.75±2.47,20.46±2.23 vs.14.37±0.91,p=0.03 and p=0.01)and CHOP(48.67±4.04 vs.16.67±7.02,59.33±4.51 vs.20.67±3.06,p=0.004 and p=0.001)were significantly increased in LO_(2) cells exposed to 100μM NaAsO_(2) for 24 h.Conclusions:Histone methyltransferase SET7/9 and histone demethyltransferase LSD1 jointly regulate the changes of H3K4me1/me2 levels in arsenic-induced apoptosis.NaAsO_(2) induces apoptosis in LO_(2) cells by activating the ERS-mediated apoptotic signaling pathway,at least partially by enhancing the methylation of H3 on the promoter regions of ERS-associated genes,including GRP78 and CHOP.