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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-4-1
pubmed:abstractText
This study investigated the effects of N-phenyl-2-naphthylamine, an effective allelochemical on aquatic unicellular algae Chlorella vulgaris at physiological gene transcription level. Exposure to 2.5 mg L(-1) of N-phenyl-2-naphthylamine increased the activities of the antioxidant enzymes, superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), which were 2.47, 3.24, and 4.27 times higher than that of the control, however, exposure to 4.0 mg L(-1) N-phenyl-2-naphthylamine decreased the activities of these antioxidant enzymes. An increase in malondialdehyde content and a decrease in chlorophyll content following exposure to N-phenyl-2-naphthylamine suggested that the alga was severely damaged and that cell growth was greatly inhibited. Electron microscopy showed that the plasma membrane was detached from the cell wall, the nucleus was condensed, and the structure of chloroplasts was disrupted, in response to N-phenyl-2-naphthylamine exposure. Real-time PCR showed that N-phenyl-2-naphthylamine reduced the transcript abundance of psaB and psbC to 3% and 1% of the control, respectively. These results demonstrated that N-phenyl-2-naphthylamine not only inhibited photosynthesis, but also triggered the synthesis of reactive oxygen species (ROS) to disrupt the subcellular structure of this aquatic organism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1879-1298
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
368-75
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Allelochemical stress causes oxidative damage and inhibition of photosynthesis in Chlorella vulgaris.
pubmed:affiliation
College of Biological and Environmental Engineering, Zhejiang University of Technology, Hangzhou 310032, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't