This study demonstrates a concentration dependent inhibition of carbon fixation, O2 evolution, photosynthetic electron transport chain and ATP content of A. doliolum and C. vulgaris by Cu, Ni and Fe. Although the mode...This study demonstrates a concentration dependent inhibition of carbon fixation, O2 evolution, photosynthetic electron transport chain and ATP content of A. doliolum and C. vulgaris by Cu, Ni and Fe. Although the mode of inhibition of photosynthetic electron transport chain of both the algae was similar, PS II depicted greater sensitivity to the test metals used. The toxicity in both organisms was Cu > Ni > Fe. A. doliolum was, however, more sensitive to Cu and Ni, and C. vulgaris to Fe. Toxicity was generally dependent on metal uptake, which in turn was dependent on their concentrations in the external medium. A partial restoration of nutrient uptake, carbon fixation, and enzyme activities following supplementation of exogenous ATP suggests that ATP regulates toxicity through chelation.展开更多
Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms invo...Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain （ETC） as a potential source for reactive oxygen species （ROS）. Tobacco BY-2 cells after exposure to MC-RR （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.展开更多
Highly-efficient oxidation of 5-hydroxymethylfurtural(HMF) to 2,5-furandicarboxylic acid(FDCA) at low temperature with air as the oxidant is still challenging.Herein,inspired by the respirato ry electron transport cha...Highly-efficient oxidation of 5-hydroxymethylfurtural(HMF) to 2,5-furandicarboxylic acid(FDCA) at low temperature with air as the oxidant is still challenging.Herein,inspired by the respirato ry electron transport chain(ETC) of living cells mediated by electron carriers,we constructed artificial ETCs and transformed liquid flow fuel cells(LFFCs) to flexible reactors for efficient oxidation of HMF to produce FDCA under mild conditions.This LFFC reactor employed an electrodeposition modified nickel foam as an anode to promote HMF oxidation and(VO_(2))_(2)SO_(4) as a cathode electron carrier to facilitate the electron transfer to air.The reaction rate could be easily controlled by selecting the anode catalyst,adjusting the external loading and changing the cathodic electron carrier or oxidants.A maximal power density of 44.9 mW cm^(-2) at room temperature was achieved,while for FDCA production,short-circuit condition was preferred to achieve quick transfer of electrons.For a single batch operation with 0.1 M initial HMF,FDCA yield reached 97.1%.By fed-batch operation,FDCA concentration reached 144.5 g L^(-1) with a total yield of 96%.Ni^(2+)/Ni^(3+) redox couple was the active species mediating the electron transfer,while both experimental and DFT calculation results indicated that HMFCA pathway was the preferred reaction mechanism.展开更多
目的观察慢性低氧时大鼠线粒体呼吸链复合体Ⅰ、Ⅱ、Ⅲ、Ⅴ蛋白表达变化并讨论其病理生理学意义。方法成年雄性Wistar大鼠随机分为慢性低氧(4500m,30d)组和对照组,取双侧腓肠肌,分离线粒体,用Clark氧电极法检测线粒体Ⅲ态呼吸(state3,S...目的观察慢性低氧时大鼠线粒体呼吸链复合体Ⅰ、Ⅱ、Ⅲ、Ⅴ蛋白表达变化并讨论其病理生理学意义。方法成年雄性Wistar大鼠随机分为慢性低氧(4500m,30d)组和对照组,取双侧腓肠肌,分离线粒体,用Clark氧电极法检测线粒体Ⅲ态呼吸(state3,ST3)、Ⅳ态呼吸(state4,ST4)和呼吸控制率(respiratory control ratio,RCR),用Western blot检测线粒体呼吸链复合体Ⅰ、Ⅱ、Ⅲ、Ⅴ蛋白的表达。结果慢性低氧组大鼠腓肠肌线粒体ST3和RCR显著低于对照组(P<0.05)。慢性低氧组大鼠腓肠肌线粒体复合体Ⅰ30×103亚基、复合体Ⅱ70×103亚基、复合体Ⅴα亚基蛋白表达量显著低对照组(P<0.05)。2组线粒体ST4和复合体Ⅲ核心亚基2蛋白表达无显著性差异(P>0.05)。结论低氧可调节大鼠骨骼机线粒体复合体蛋白非协同性表达,导致线粒体氧化磷酸化功能下降。展开更多
Hypobaric hypoxia can cause severe brain damage and mitochondrial dysfunction, and is involved in hypoxic brain injury. However, little is currently known about the mechanisms responsible for mi- tochondrial dysfuncti...Hypobaric hypoxia can cause severe brain damage and mitochondrial dysfunction, and is involved in hypoxic brain injury. However, little is currently known about the mechanisms responsible for mi- tochondrial dysfunction in hypobaric hypoxic brain damage. In this study, a rat model of hypobaric hypoxic brain injury was established to investigate the molecular mechanisms associated with mi- tochondrial dysfunction. As revealed by two-dimensional electrophoresis analysis, 16, 21, and 36 differential protein spots in cerebral mitochondria were observed at 6, 12, and 24 hours post-hypobaric hypoxia, respectively. Furthermore, ten protein spots selected from each hypobaric hypoxia subgroup were similarly regulated and were identified by mass spectrometry. These de- tected proteins included dihydropyrimidinase-related protein 2, creatine kinase B-type, is- ovaleryI-CoA dehydrogenase, elongation factor Ts, ATP synthase beta-subunit, 3-mercaptopyruvate sulfurtransferase, electron transfer flavoprotein alpha-subunit, Chain A of 2-enoyI-CoA hydratase, NADH dehydrogenase iron-sulfur protein 8 and tropomyosin beta chain. These ten proteins are all involved in the electron transport chain and the function of ATP synthase. Our findings indicate that hypobaric hypoxia can induce the differential expression of several cerebral mitochondrial proteins, which are involved in the regulation of mitochondrial energy production.展开更多
文摘This study demonstrates a concentration dependent inhibition of carbon fixation, O2 evolution, photosynthetic electron transport chain and ATP content of A. doliolum and C. vulgaris by Cu, Ni and Fe. Although the mode of inhibition of photosynthetic electron transport chain of both the algae was similar, PS II depicted greater sensitivity to the test metals used. The toxicity in both organisms was Cu > Ni > Fe. A. doliolum was, however, more sensitive to Cu and Ni, and C. vulgaris to Fe. Toxicity was generally dependent on metal uptake, which in turn was dependent on their concentrations in the external medium. A partial restoration of nutrient uptake, carbon fixation, and enzyme activities following supplementation of exogenous ATP suggests that ATP regulates toxicity through chelation.
基金supported by the National Natural Science Foundation of China (No.31100340)the Major Science and Technology Program for Water Pollution Control and Treatment (No.2012ZX07103-004-02)
文摘Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain （ETC） as a potential source for reactive oxygen species （ROS）. Tobacco BY-2 cells after exposure to MC-RR （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.
基金supported by the National Key R&D Program of China(2022YFA2105900)the National Natural Science Foundation of China(22178197)。
文摘Highly-efficient oxidation of 5-hydroxymethylfurtural(HMF) to 2,5-furandicarboxylic acid(FDCA) at low temperature with air as the oxidant is still challenging.Herein,inspired by the respirato ry electron transport chain(ETC) of living cells mediated by electron carriers,we constructed artificial ETCs and transformed liquid flow fuel cells(LFFCs) to flexible reactors for efficient oxidation of HMF to produce FDCA under mild conditions.This LFFC reactor employed an electrodeposition modified nickel foam as an anode to promote HMF oxidation and(VO_(2))_(2)SO_(4) as a cathode electron carrier to facilitate the electron transfer to air.The reaction rate could be easily controlled by selecting the anode catalyst,adjusting the external loading and changing the cathodic electron carrier or oxidants.A maximal power density of 44.9 mW cm^(-2) at room temperature was achieved,while for FDCA production,short-circuit condition was preferred to achieve quick transfer of electrons.For a single batch operation with 0.1 M initial HMF,FDCA yield reached 97.1%.By fed-batch operation,FDCA concentration reached 144.5 g L^(-1) with a total yield of 96%.Ni^(2+)/Ni^(3+) redox couple was the active species mediating the electron transfer,while both experimental and DFT calculation results indicated that HMFCA pathway was the preferred reaction mechanism.
文摘目的观察慢性低氧时大鼠线粒体呼吸链复合体Ⅰ、Ⅱ、Ⅲ、Ⅴ蛋白表达变化并讨论其病理生理学意义。方法成年雄性Wistar大鼠随机分为慢性低氧(4500m,30d)组和对照组,取双侧腓肠肌,分离线粒体,用Clark氧电极法检测线粒体Ⅲ态呼吸(state3,ST3)、Ⅳ态呼吸(state4,ST4)和呼吸控制率(respiratory control ratio,RCR),用Western blot检测线粒体呼吸链复合体Ⅰ、Ⅱ、Ⅲ、Ⅴ蛋白的表达。结果慢性低氧组大鼠腓肠肌线粒体ST3和RCR显著低于对照组(P<0.05)。慢性低氧组大鼠腓肠肌线粒体复合体Ⅰ30×103亚基、复合体Ⅱ70×103亚基、复合体Ⅴα亚基蛋白表达量显著低对照组(P<0.05)。2组线粒体ST4和复合体Ⅲ核心亚基2蛋白表达无显著性差异(P>0.05)。结论低氧可调节大鼠骨骼机线粒体复合体蛋白非协同性表达,导致线粒体氧化磷酸化功能下降。
基金supported by the National Natural Science Foundation of China,No.81073152the Key Science Foundation of Tianjin in China,No.10JCZDJC21100+1 种基金the Natural Science Foundation of Tianjin in China,No.10JCYBJC14700,No.13JCQNJC13200the Science Foundation of Tianjin Key Laboratory in China,No.WHTD 201303-2
文摘Hypobaric hypoxia can cause severe brain damage and mitochondrial dysfunction, and is involved in hypoxic brain injury. However, little is currently known about the mechanisms responsible for mi- tochondrial dysfunction in hypobaric hypoxic brain damage. In this study, a rat model of hypobaric hypoxic brain injury was established to investigate the molecular mechanisms associated with mi- tochondrial dysfunction. As revealed by two-dimensional electrophoresis analysis, 16, 21, and 36 differential protein spots in cerebral mitochondria were observed at 6, 12, and 24 hours post-hypobaric hypoxia, respectively. Furthermore, ten protein spots selected from each hypobaric hypoxia subgroup were similarly regulated and were identified by mass spectrometry. These de- tected proteins included dihydropyrimidinase-related protein 2, creatine kinase B-type, is- ovaleryI-CoA dehydrogenase, elongation factor Ts, ATP synthase beta-subunit, 3-mercaptopyruvate sulfurtransferase, electron transfer flavoprotein alpha-subunit, Chain A of 2-enoyI-CoA hydratase, NADH dehydrogenase iron-sulfur protein 8 and tropomyosin beta chain. These ten proteins are all involved in the electron transport chain and the function of ATP synthase. Our findings indicate that hypobaric hypoxia can induce the differential expression of several cerebral mitochondrial proteins, which are involved in the regulation of mitochondrial energy production.
