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Inhibitory effects and oxidative target site of dibutyl phthalate on Karenia brevis.

•Dibutyl phthalate triggered an oxidative response in the algae Karenia brevis.•Different SOD isoforms showed different activity under DBP exposure.•Mitochondria could be the main target sites of DBP in Karenia brevis. The inhibitory action and possible damage mechanism of dibutyl phthalate (DBP) on... Full description

Journal Title: Chemosphere August 2015, Vol.132, pp.32-39
Main Author: Li, Feng-Min
Other Authors: Wu, Miao , Yao, Yuan , Zheng, Xiang , Zhao, Jian , Wang, Zhen-Yu , Xing, Bao-Shan
Format: Electronic Article Electronic Article
Language: English
Subjects:
DBP
ID: E-ISSN: 1879-1298 ; DOI: 10.1016/j.chemosphere.2015.01.051
Link: http://search.proquest.com/docview/1681911818/?pq-origsite=primo
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title: Inhibitory effects and oxidative target site of dibutyl phthalate on Karenia brevis.
format: Article
creator:
  • Li, Feng-Min
  • Wu, Miao
  • Yao, Yuan
  • Zheng, Xiang
  • Zhao, Jian
  • Wang, Zhen-Yu
  • Xing, Bao-Shan
subjects:
  • Dibutyl Phthalate–Metabolism
  • Dinoflagellida–Drug Effects
  • Harmful Algal Bloom–Drug Effects
  • Hydrogen Peroxide–Metabolism
  • Malondialdehyde–Metabolism
  • Oxidation-Reduction–Drug Effects
  • Oxidative Stress–Metabolism
  • Reactive Oxygen Species–Metabolism
  • Superoxide Dismutase–Metabolism
  • Reactive Oxygen Species
  • Dibutyl Phthalate
  • Malondialdehyde
  • Hydrogen Peroxide
  • Superoxide Dismutase
  • Superoxide Dismutase 2
  • DBP
  • Karenia Brevis
  • Oxidative Stress
  • Toxicity Mechanism
ispartof: Chemosphere, August 2015, Vol.132, pp.32-39
description: •Dibutyl phthalate triggered an oxidative response in the algae Karenia brevis.•Different SOD isoforms showed different activity under DBP exposure.•Mitochondria could be the main target sites of DBP in Karenia brevis. The inhibitory action and possible damage mechanism of dibutyl phthalate (DBP) on the red tide algae Karenia brevis were investigated. The results showed that the algae experienced oxidative stress after exposure to 5mgL−1 DBP. Malondialdehyde (MDA) peaked after 72h, with a value approximately 2.3 times higher than that observed for untreated cells. The superoxide dismutase (SOD) and catalase (CAT) activities significantly increased as an adaptive reaction after 48h. DBP induced the overproduction of reactive oxygen species (ROS), the OH concentration showed a peak of 33UmL−1 at 48h, and the highest H2O2 content was approximately 250nmol/107 cells at 72h; these latter two values were 2.5 and 4.4 times higher than observed for the control, respectively. TEM images showed that a number of small vacuoles or apical tubers were commonly found around the cell membrane, and the membrane structure was ultimately disintegrated. Further experiments were carried out to locate the original ROS production sites following DBP exposure. The activity of CuZn-SOD (a mainly cytosolic isoform, with some also found in chloroplasts) under DBP exposure was approximately 2.5 times higher than the control, whereas the Mn-SOD (mitochondrial isoform) activity was significantly inhibited. No significant difference was observed in the activity of Fe-SOD (chloroplastic isoform). In addition, dicumarol (an inhibitor of the electron transport chain in the plasma membrane) stimulated DBP-induced ROS production, whereas rotenone (an inhibitor of the mitochondria electron transport chain complex I) decreased DBP-induced ROS production. These results suggested that mitochondria could be the main target sites for DBP attack.
language: eng
source:
identifier: E-ISSN: 1879-1298 ; DOI: 10.1016/j.chemosphere.2015.01.051
fulltext: no_fulltext
issn:
  • 18791298
  • 1879-1298
url: Link


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titleInhibitory effects and oxidative target site of dibutyl phthalate on Karenia brevis.
creatorLi, Feng-Min ; Wu, Miao ; Yao, Yuan ; Zheng, Xiang ; Zhao, Jian ; Wang, Zhen-Yu ; Xing, Bao-Shan
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identifierE-ISSN: 1879-1298 ; DOI: 10.1016/j.chemosphere.2015.01.051
subjectDibutyl Phthalate–Metabolism ; Dinoflagellida–Drug Effects ; Harmful Algal Bloom–Drug Effects ; Hydrogen Peroxide–Metabolism ; Malondialdehyde–Metabolism ; Oxidation-Reduction–Drug Effects ; Oxidative Stress–Metabolism ; Reactive Oxygen Species–Metabolism ; Superoxide Dismutase–Metabolism ; Reactive Oxygen Species ; Dibutyl Phthalate ; Malondialdehyde ; Hydrogen Peroxide ; Superoxide Dismutase ; Superoxide Dismutase 2 ; DBP ; Karenia Brevis ; Oxidative Stress ; Toxicity Mechanism
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description•Dibutyl phthalate triggered an oxidative response in the algae Karenia brevis.•Different SOD isoforms showed different activity under DBP exposure.•Mitochondria could be the main target sites of DBP in Karenia brevis. The inhibitory action and possible damage mechanism of dibutyl phthalate (DBP) on the red tide algae Karenia brevis were investigated. The results showed that the algae experienced oxidative stress after exposure to 5mgL−1 DBP. Malondialdehyde (MDA) peaked after 72h, with a value approximately 2.3 times higher than that observed for untreated cells. The superoxide dismutase (SOD) and catalase (CAT) activities significantly increased as an adaptive reaction after 48h. DBP induced the overproduction of reactive oxygen species (ROS), the OH concentration showed a peak of 33UmL−1 at 48h, and the highest H2O2 content was approximately 250nmol/107 cells at 72h; these latter two values were 2.5 and 4.4 times higher than observed for the control, respectively. TEM images showed that a number of small vacuoles or apical tubers were commonly found around the cell membrane, and the membrane structure was ultimately disintegrated. Further experiments were carried out to locate the original ROS production sites following DBP exposure. The activity of CuZn-SOD (a mainly cytosolic isoform, with some also found in chloroplasts) under DBP exposure was approximately 2.5 times higher than the control, whereas the Mn-SOD (mitochondrial isoform) activity was significantly inhibited. No significant difference was observed in the activity of Fe-SOD (chloroplastic isoform). In addition, dicumarol (an inhibitor of the electron transport chain in the plasma membrane) stimulated DBP-induced ROS production, whereas rotenone (an inhibitor of the mitochondria electron transport chain complex I) decreased DBP-induced ROS production. These results suggested that mitochondria could be the main target sites for DBP attack.
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titleInhibitory effects and oxidative target site of dibutyl phthalate on Karenia brevis.
authorLi, Feng-Min ; Wu, Miao ; Yao, Yuan ; Zheng, Xiang ; Zhao, Jian ; Wang, Zhen-Yu ; Xing, Bao-Shan
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