Differential sensitivities of plant and animal mitochondria to the herbicide paraquat

Detalhes bibliográficos
Autor(a) principal: Vicente, Joaquim A. F.
Data de Publicação: 2001
Outros Autores: Peixoto, Francisco, Lopes, M. Ludovina, Madeira, Vítor M. C.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/8148
https://doi.org/10.1002/jbt.10010
Resumo: Paraquat herbicide is toxic to animals, including humans, via putative toxicity mechanisms associated to microsomal and mitochondrial redox systems. It is also believed to act in plants by generating highly reactive oxygen free radicals from electrons of photosystem I on exposure to light. Paraquat also acts on non-chlorophyllous plant tissues, where mitochondria are candidate targets, as in animal tissues. Therefore, we compared the interaction of paraquat with the mitochondrial bioenergetics of potato tuber, using rat liver mitochondria as a reference. Paraquat depressed succinate-dependent mitochondrial Deltapsi, with simultaneous stimulation of state 4 O2 consumption. It also induced a slow time-dependent effect for respiration of succinate, exogenous NADH, and N,N,N',N'-tetramethyl-p-phenylenediamine (TMPD)/ascorbate, which was more pronounced in rat than in potato mitochondria. However, with potato tuber mitochondria, the Deltapsi promoted by complex-I-dependent respiration is insensitive to this effect, indicating a protection against paraquat radical afforded by complex I redox activity, which was just the reverse of to the findings for rat liver mitochondria. The experimental set up with the tetraphenyl phosphonium (TPP+)-electrode also indivated production of the paraquat radical in mitochondria, also suggesting its accessibility to the outside space. The different activities of protective antioxidant agents can contribute to explain the different sensitivities of both kinds of mitochondria. Values of SOD activity and alpha-tocopherol detected in potato mitochondria were significantly higher than in rat mitochondria, which, in turn, revealed higher values of lipid peroxidation induced by paraquat. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:322-330, 2001
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spelling Differential sensitivities of plant and animal mitochondria to the herbicide paraquatParaquat herbicide is toxic to animals, including humans, via putative toxicity mechanisms associated to microsomal and mitochondrial redox systems. It is also believed to act in plants by generating highly reactive oxygen free radicals from electrons of photosystem I on exposure to light. Paraquat also acts on non-chlorophyllous plant tissues, where mitochondria are candidate targets, as in animal tissues. Therefore, we compared the interaction of paraquat with the mitochondrial bioenergetics of potato tuber, using rat liver mitochondria as a reference. Paraquat depressed succinate-dependent mitochondrial Deltapsi, with simultaneous stimulation of state 4 O2 consumption. It also induced a slow time-dependent effect for respiration of succinate, exogenous NADH, and N,N,N',N'-tetramethyl-p-phenylenediamine (TMPD)/ascorbate, which was more pronounced in rat than in potato mitochondria. However, with potato tuber mitochondria, the Deltapsi promoted by complex-I-dependent respiration is insensitive to this effect, indicating a protection against paraquat radical afforded by complex I redox activity, which was just the reverse of to the findings for rat liver mitochondria. The experimental set up with the tetraphenyl phosphonium (TPP+)-electrode also indivated production of the paraquat radical in mitochondria, also suggesting its accessibility to the outside space. The different activities of protective antioxidant agents can contribute to explain the different sensitivities of both kinds of mitochondria. Values of SOD activity and alpha-tocopherol detected in potato mitochondria were significantly higher than in rat mitochondria, which, in turn, revealed higher values of lipid peroxidation induced by paraquat. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:322-330, 20012001info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/8148http://hdl.handle.net/10316/8148https://doi.org/10.1002/jbt.10010engJournal of Biochemical and Molecular Toxicology. 15:6 (2001) 322-330Vicente, Joaquim A. F.Peixoto, FranciscoLopes, M. LudovinaMadeira, Vítor M. C.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2019-06-02T09:08:47Zoai:estudogeral.uc.pt:10316/8148Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:51.883960Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
title Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
spellingShingle Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
Vicente, Joaquim A. F.
title_short Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
title_full Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
title_fullStr Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
title_full_unstemmed Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
title_sort Differential sensitivities of plant and animal mitochondria to the herbicide paraquat
author Vicente, Joaquim A. F.
author_facet Vicente, Joaquim A. F.
Peixoto, Francisco
Lopes, M. Ludovina
Madeira, Vítor M. C.
author_role author
author2 Peixoto, Francisco
Lopes, M. Ludovina
Madeira, Vítor M. C.
author2_role author
author
author
dc.contributor.author.fl_str_mv Vicente, Joaquim A. F.
Peixoto, Francisco
Lopes, M. Ludovina
Madeira, Vítor M. C.
description Paraquat herbicide is toxic to animals, including humans, via putative toxicity mechanisms associated to microsomal and mitochondrial redox systems. It is also believed to act in plants by generating highly reactive oxygen free radicals from electrons of photosystem I on exposure to light. Paraquat also acts on non-chlorophyllous plant tissues, where mitochondria are candidate targets, as in animal tissues. Therefore, we compared the interaction of paraquat with the mitochondrial bioenergetics of potato tuber, using rat liver mitochondria as a reference. Paraquat depressed succinate-dependent mitochondrial Deltapsi, with simultaneous stimulation of state 4 O2 consumption. It also induced a slow time-dependent effect for respiration of succinate, exogenous NADH, and N,N,N',N'-tetramethyl-p-phenylenediamine (TMPD)/ascorbate, which was more pronounced in rat than in potato mitochondria. However, with potato tuber mitochondria, the Deltapsi promoted by complex-I-dependent respiration is insensitive to this effect, indicating a protection against paraquat radical afforded by complex I redox activity, which was just the reverse of to the findings for rat liver mitochondria. The experimental set up with the tetraphenyl phosphonium (TPP+)-electrode also indivated production of the paraquat radical in mitochondria, also suggesting its accessibility to the outside space. The different activities of protective antioxidant agents can contribute to explain the different sensitivities of both kinds of mitochondria. Values of SOD activity and alpha-tocopherol detected in potato mitochondria were significantly higher than in rat mitochondria, which, in turn, revealed higher values of lipid peroxidation induced by paraquat. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:322-330, 2001
publishDate 2001
dc.date.none.fl_str_mv 2001
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dc.identifier.uri.fl_str_mv http://hdl.handle.net/10316/8148
http://hdl.handle.net/10316/8148
https://doi.org/10.1002/jbt.10010
url http://hdl.handle.net/10316/8148
https://doi.org/10.1002/jbt.10010
dc.language.iso.fl_str_mv eng
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dc.relation.none.fl_str_mv Journal of Biochemical and Molecular Toxicology. 15:6 (2001) 322-330
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