Fe^(2+) bio-oxidation influenced by toxic metal ions released from the dissolution of arsenic-bearing gold ores was investigated.Fe^(2+) bio-oxidation by moderately thermophilic microorganisms was studied under differ...Fe^(2+) bio-oxidation influenced by toxic metal ions released from the dissolution of arsenic-bearing gold ores was investigated.Fe^(2+) bio-oxidation by moderately thermophilic microorganisms was studied under different initial concentrations of Fe^(2+) and As(Ⅲ),and Monod equation was used to fit the Fe^(2+) bio-oxidation under different conditions.Results showed that the Fe^(2+) bio-oxidation rate increased as the initial Fe^(2+) concentration increased until it reached 12 g/L.As(Ⅲ)severely inhibited Fe^(2+) bio-oxidation.When the As(Ⅲ)concentration was 8 g/L,9 g/L Fe^(2+) was more than 200 h.The Monod equation fitted the Fe^(2+) bio-oxidation well.In the absence of As(Ⅲ),the maximum specific growth rate of the culture and the substrate affinity constant were 0.142 h^(−1) and 0.053 g/L,respectively.As(Ⅲ)inhibited Fe^(2+) bio-oxidation via competitive inhibition,and the inhibition constant was 0.0035 g/L.展开更多
Objective The selective loss of dopaminergic neurons in Parkinson＇s disease is suspected to correlate with the increase of cellular iron, which may be involved in the pathogenesis of PD by promotion of oxidative stre...Objective The selective loss of dopaminergic neurons in Parkinson＇s disease is suspected to correlate with the increase of cellular iron, which may be involved in the pathogenesis of PD by promotion of oxidative stress. This research investigated dopamine-induced oxidative stress toxicity contributed by iron and the production of dopamine-derived neurotoxins in dopaminergic SH-SYSY cells. Methods After the SH-SYSY cells were pre-incubated with dopamine and Fe^2＋ for 24 h, the cell viability, hydroxyl radical, melondialdehyde, cell apoptosis, and catechol isoquinolines were measured by lactate dehydrogenase assay, salicylic acid trapping method, thiobarbuteric acid assay, Hoechst 33258 staining and HPLC-electrochemical detection （HPLC-ECD）, respectively. Results （1） Optimal dopamine （150 μmol/L） and Fe^2＋ （40 or 80 μmol/L） significantly increased the concentrations of hydroxy radicals and melondialdehyde in SH-SYSY cells. （2） Induction with dopamine alone or dopamine and Fe^2＋ （dopamine/Fe^2＋） caused cell apoptosis. （3） Compared with untreated cells, the catechol isoquinolines, salsolinol and N-methyl-salsolinol in dopamine/Fe^2＋-induced cells were detected in increasing amounts. Conclusion Due to dopamine/Fe^2＋-induced oxidative stress similar to the state in the parkinsonian substantia nigra neurons, dopamine and Fe^2＋ impaired SH-SYSY cells could be used as the cell oxidative stress model of Parkinson＇s disease. The catechol isoquinolines detected in cells may be involved in the pathogenesis of Parkinson＇s disease as potential neurotoxins.展开更多
基金supported by the National Natural Science Foundation of China(No.51904339)the Collaborative Innovation Center for Clean and Efficient Utilization of Strategic Metal Mineral Resources,China.
文摘Fe^(2+) bio-oxidation influenced by toxic metal ions released from the dissolution of arsenic-bearing gold ores was investigated.Fe^(2+) bio-oxidation by moderately thermophilic microorganisms was studied under different initial concentrations of Fe^(2+) and As(Ⅲ),and Monod equation was used to fit the Fe^(2+) bio-oxidation under different conditions.Results showed that the Fe^(2+) bio-oxidation rate increased as the initial Fe^(2+) concentration increased until it reached 12 g/L.As(Ⅲ)severely inhibited Fe^(2+) bio-oxidation.When the As(Ⅲ)concentration was 8 g/L,9 g/L Fe^(2+) was more than 200 h.The Monod equation fitted the Fe^(2+) bio-oxidation well.In the absence of As(Ⅲ),the maximum specific growth rate of the culture and the substrate affinity constant were 0.142 h^(−1) and 0.053 g/L,respectively.As(Ⅲ)inhibited Fe^(2+) bio-oxidation via competitive inhibition,and the inhibition constant was 0.0035 g/L.
基金This work was supported by the National Natural Science Foundation of China （No. 20435020, No. 20275005, and No. 30670645）.
文摘Objective The selective loss of dopaminergic neurons in Parkinson＇s disease is suspected to correlate with the increase of cellular iron, which may be involved in the pathogenesis of PD by promotion of oxidative stress. This research investigated dopamine-induced oxidative stress toxicity contributed by iron and the production of dopamine-derived neurotoxins in dopaminergic SH-SYSY cells. Methods After the SH-SYSY cells were pre-incubated with dopamine and Fe^2＋ for 24 h, the cell viability, hydroxyl radical, melondialdehyde, cell apoptosis, and catechol isoquinolines were measured by lactate dehydrogenase assay, salicylic acid trapping method, thiobarbuteric acid assay, Hoechst 33258 staining and HPLC-electrochemical detection （HPLC-ECD）, respectively. Results （1） Optimal dopamine （150 μmol/L） and Fe^2＋ （40 or 80 μmol/L） significantly increased the concentrations of hydroxy radicals and melondialdehyde in SH-SYSY cells. （2） Induction with dopamine alone or dopamine and Fe^2＋ （dopamine/Fe^2＋） caused cell apoptosis. （3） Compared with untreated cells, the catechol isoquinolines, salsolinol and N-methyl-salsolinol in dopamine/Fe^2＋-induced cells were detected in increasing amounts. Conclusion Due to dopamine/Fe^2＋-induced oxidative stress similar to the state in the parkinsonian substantia nigra neurons, dopamine and Fe^2＋ impaired SH-SYSY cells could be used as the cell oxidative stress model of Parkinson＇s disease. The catechol isoquinolines detected in cells may be involved in the pathogenesis of Parkinson＇s disease as potential neurotoxins.
