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Effects of dieback on the vegetative, chemical, and physiological status of mangrove forests, Iran
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作者 Vahid Farashi KAHNOUJ Marzieh REZAI +2 位作者 Rasool MAHDAVI maryam moslehi Saiedeh ESKANDARI 《Journal of Arid Land》 SCIE CSCD 2023年第11期1391-1404,共14页
Mangrove forests are valuable resources in tropical and subtropical regions,which have been faced dieback due to various human activities including rapid expansion of shrimp farming,urban development,and pollution,as ... Mangrove forests are valuable resources in tropical and subtropical regions,which have been faced dieback due to various human activities including rapid expansion of shrimp farming,urban development,and pollution,as well as natural factors such as rising sea level,increasing air temperature,drought,and sharp decrease in rainfall.However,the mechanisms of dieback of mangrove forests are not well understood.Therefore,this research aimed to assess the vegetative,chemical,and physiological status of grey mangrove(Avicennia marina(Forsk.)Vierh.)forests at different intensities of dieback in the Hormozgan Province,Iran.A total of 40 plots categorized into four dieback intensities(severe,medium,low,and control)were randomly selected for monitoring,and various parameters related to vegetative,chemical,and physiological status of grey mangrove forests were examined.The results revealed that the control group had the highest tree density,seedling density,vitality levels,aerial root density,and aerial root height.Generally,as dieback severity increased,a decrease in demographic and vegetative parameters of trees and seedlings was observed in the dieback treatments.The amounts of heavy metals(lead,cadmium,and nickel)in the sediment,roots,and leaves of grey mangrove trees at different dieback levels indicated that lead levels were the highest in the sediment,roots,and leaves in the severe dieback treatment.At the same time,the control had the lowest values.Cadmium concentrations in the sediment followed the pattern of severe dieback>moderate dieback>low dieback>control with no significant differences in the roots and leaves.Nickel amounts in all three parts,i.e.,sediment,roots,and leaves showed the highest levels in the severe dieback treatment.Furthermore,metal level analysis in the organs of grey mangrove trees at different dieback levels revealed that lead and nickel were more abundant in the root organ compared with the leaves.In contrast,the leaf organ exhibited the highest cadmium levels.Dieback significantly impacted water electrical conductivity(EC),soil organic carbon(SOC),and chlorophyll a,b,and total chlorophyll contents,with the highest values observed in the severe dieback treatment.However,no significant differences were observed in acidity and carotenoid levels.In conclusion,sediment erosion and heavy metal accumulation were critical contributors to dieback of grey mangrove trees,affecting their physiological,vegetative,and plant production characteristics.As the ability of these plants to rehabilitate has diminished,effective management planning is imperative in dieback-affected areas. 展开更多
关键词 NICKEL FORESTS GREY
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Erratum to: Effects of dieback on the vegetative, chemical, and physiological status of mangrove forests, Iran
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作者 Vahid Farashi KAHNOUJ Marzieh REZAI +2 位作者 Rasool MAHDAVI maryam moslehi Saeedeh ESKANDARI 《Journal of Arid Land》 SCIE CSCD 2023年第12期1544-1544,共1页
Published online:22 November 2023©Xinjiang Institute of Ecology and Geography,Chinese Academy of Sciences,Science Press and Springer-Verlag GmbH Germany,part of Springer Nature 2023 Erratum to:J Arid Land(2023)15... Published online:22 November 2023©Xinjiang Institute of Ecology and Geography,Chinese Academy of Sciences,Science Press and Springer-Verlag GmbH Germany,part of Springer Nature 2023 Erratum to:J Arid Land(2023)15(11):1391-1404 https://doi.org/10.1007/s40333-023-0031-6 In this Erratum,we correct the name of the last author that was incorrectly written as Saiedeh ESKANDARI and the correction is as follows:Saeedeh ESKANDARI. 展开更多
关键词 CORRECTION FORESTS XINJIANG
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Protective Effects of Flavonoid Baicalein against Menadione-Induced Damage in SK-N-MC Cells
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作者 maryam moslehi Razieh Yazdanparast 《CellBio》 2013年第2期35-44,共10页
Oxidative damage and redox metal homeostasis loss are two contributing factors in brain aging and widely distributed neurodegenerative diseases. Oxidative species in company with excessive amounts of intracellular fre... Oxidative damage and redox metal homeostasis loss are two contributing factors in brain aging and widely distributed neurodegenerative diseases. Oxidative species in company with excessive amounts of intracellular free iron result in Fenton-type reaction with subsequent production of highly reactive hydroxyl radicals which initiate peroxidation of biomolecules and further formation of non-degradable toxic pigments called lipofuscin that amasses in long-lived postmitotic cells such as neurons. Dietary flavonoid baicalein can counteract the detrimental consequences through exertion of a multiplicity of protective actions within the brain including direct ROS scavenging activity and iron chelation. In this study, we evaluated the neuroprotective effects of baicalein in menadione (superoxide radical generator)-treated SK-N-MC neuroblastoma cell line. Our results showed that treatment of cells with menadione led to lipofuscin formation due to elevated intracellular iron contents and accumulation of oxidative products such as MDA and PCO. Also, menadione caused apoptotic cell death in SK-N-MC cells. However, pretreatment with baicalein (40 μM) reversed the harmful effects by chelating free iron and preventing biomolecules peroxidations. Moreover, baicalein prevented cell death through modulation of key molecules in apoptotic pathways including suppression of Bax and caspase-9 activities and induction of bcl2 expression. Key structural features such as presence of hydroxyl groups and iron-binding motifs in baicalein make it the appropriate candidate in antioxidant-based therapy in age-related neurodegenerative diseases. 展开更多
关键词 AGING BAICALEIN LIPOFUSCIN MENADIONE NEURODEGENERATIVE Disease OXIDATIVE Stress
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