Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.14279/22682
DC FieldValueLanguage
dc.contributor.authorSingh, Samiksha-
dc.contributor.authorHusain, Tajammul-
dc.contributor.authorKushwaha, Bishwajit Kumar-
dc.contributor.authorSuhel, Mohammad-
dc.contributor.authorFatima, Abreeq-
dc.contributor.authorMishra, Vipul-
dc.contributor.authorSingh, Sani Kumar-
dc.contributor.authorBhatt, Javaid Akhtar-
dc.contributor.authorRai, Meena-
dc.contributor.authorPrasad, Sheo Mohan-
dc.contributor.authorDubey, Nawal Kishore-
dc.contributor.authorChauhan, Devendra Kumar-
dc.contributor.authorTripathi, Durgesh Kumar-
dc.contributor.authorFotopoulos, Vasileios-
dc.contributor.authorSingh, Vijay Pratap-
dc.date.accessioned2021-06-10T08:18:28Z-
dc.date.available2021-06-10T08:18:28Z-
dc.date.issued2021-05-05-
dc.identifier.citationJournal of Hazardous Materials, 2021, vol. 409, aticl. no. 123686en_US
dc.identifier.issn03043894-
dc.identifier.urihttps://hdl.handle.net/20.500.14279/22682-
dc.description.abstractThe role of nitric oxide (NO) and hydrogen peroxide (H2O2) is well known for regulating plant abiotic stress responses. However, underlying mechanisms are still poorly understood. Therefore, the present study investigated the involvement of NO and H2O2 signalling in the regulation of arsenate toxicity (AsV) in soybean roots employing a pharmacological approach. Results show that AsV toxicity declined root length and biomass due to greater As accumulation in the cell wall and cellular organelles. Arsenate induced cell death due to enhanced levels of reactive oxygen species, lipid and protein oxidation and down-regulation in ascorbate-glutathione cycle and redox states of ascorbate and glutathione. These results correlate with lower endogenous level of NO. Interestingly, addition of L-NAME increased AsV toxicity. However, addition of SNP reverses effect of L-NAME, suggesting that endogenous NO has a role in mitigating AsV toxicity. Exogenous H2O2 also demonstrated capability of alleviating AsV stress, while NAC reversed the protective effect of H2O2. Furthermore, DPI application further increased AsV toxicity, suggesting that endogenous H2O2 is also implicated in mitigating AsV stress. SNP was not able to mitigate AsV toxicity in the presence of DPI, suggesting that H2O2 might have acted downstream of NO in accomplishing amelioration of AsV toxicity.en_US
dc.formatpdfen_US
dc.language.isoenen_US
dc.relation.ispartofJournal of Hazardous Materialsen_US
dc.rights© Elsevieren_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAscorbate-glutathione cycleen_US
dc.subjectCell deathen_US
dc.subjectOxidative stressen_US
dc.subjectRoot growthen_US
dc.subjectSequestrationen_US
dc.subjectVacuolaren_US
dc.titleRegulation of ascorbate-glutathione cycle by exogenous nitric oxide and hydrogen peroxide in soybean roots under arsenate stressen_US
dc.typeArticleen_US
dc.collaborationUniversity of Allahabaden_US
dc.collaborationNanjing Agricultural Universityen_US
dc.collaborationBanaras Hindu Universityen_US
dc.collaborationAmity University Noidaen_US
dc.collaborationCyprus University of Technologyen_US
dc.subject.categoryAgriculture Forestry and Fisheriesen_US
dc.journalsSubscriptionen_US
dc.countryIndiaen_US
dc.countryChinaen_US
dc.countryCyprusen_US
dc.subject.fieldAgricultural Sciencesen_US
dc.publicationPeer Revieweden_US
dc.identifier.doi10.1016/j.jhazmat.2020.123686en_US
dc.relation.volume409en_US
cut.common.academicyear2020-2021en_US
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_6501-
item.cerifentitytypePublications-
item.openairetypearticle-
crisitem.journal.journalissn0304-3894-
crisitem.journal.publisherElsevier-
crisitem.author.deptDepartment of Agricultural Sciences, Biotechnology and Food Science-
crisitem.author.facultyFaculty of Geotechnical Sciences and Environmental Management-
crisitem.author.orcid0000-0003-1205-2070-
crisitem.author.parentorgFaculty of Geotechnical Sciences and Environmental Management-
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