Effects of naphthalene on gene transcription in Calanus finmarchicus (Crustacea: Copepoda)
The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene tr...
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| Vydáno v: | Aquatic toxicology Ročník 86; číslo 2; s. 157 - 165 |
|---|---|
| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
Amsterdam
Elsevier B.V
31.01.2008
Elsevier Science |
| Témata: | |
| ISSN: | 0166-445X, 1879-1514 |
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| Abstract | The planktonic copepod
Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC
50 concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to
C. finmarchicus was found to cause glutathione
S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of
C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species. |
|---|---|
| AbstractList | The planktonic copepod
Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC
50 concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to
C. finmarchicus was found to cause glutathione
S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of
C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species. The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC sub(5) sub(0) concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to C. finmarchicus was found to cause glutathione S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species. Effects of naphthalene on gene transcription in Calanus finmarchicus were investigated. The Graphical Prism 4 was used to conduct statistical analyses and graph plotting for Windows. It was naphthalene exposure to C. finmarchicus caused glutathione S-transferase (GST) mRNA to be induced, possibly as part of a defense against naphthalene-induced lipid peroxidation. Decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration might indicate an effect on ecdysteroidogenesis. The defense against naphthalene-mediated stress did not appear to involve antioxidants other than GST, since very few experimental groups had elevated levels of superoxide dismutase (SOD) and catalase (CAT) mRNA. Analysis of the naphthalene stock solution in the exposure experiments indicated a concentration of 14 mg L super(-1). The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC(50) concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to C. finmarchicus was found to cause glutathione S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species.The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC(50) concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to C. finmarchicus was found to cause glutathione S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species. The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC₅₀ concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to C. finmarchicus was found to cause glutathione S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species. The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is one of the major constituents of produced water and water soluble fractions of petrogenic oils. This study investigates the effects on gene transcription of a short term exposure to naphthalene at levels well below LC(50) concentrations. This was done in order to establish a molecular basis of naphthalene toxicity in a species which has previously been subject only to very limited studies at the molecular level. Naphthalene exposure to C. finmarchicus was found to cause glutathione S-transferase (GST) induction, indicating lipid peroxidation as the major mode of naphthalene toxicity. There is no clear evidence that the putative cytochrome P450 enzymes CYP1A2 and CYP330A1 mRNAs are parts of a detoxification enzyme system. Instead, an observed decrease in CYP330A1 mRNA levels at the highest naphthalene exposure concentration may indicate an effect on ecdysteroidogenesis. Only the lowest naphthalene concentration lead to increased mRNA levels of antioxidants SOD and CAT, indicating no clear evidence for general cellular oxidative stress following exposure. Small and insignificant changes in the HSP-70, HSP-90 and ubiquitin mRNA levels indicate a small degree of protein damage owing to naphthalene exposure. The established culture of C. finmarchicus at the SINTEF/NTNU Sealab, and the use of gene transcription analyses provide excellent tools for improving the understanding of biochemical mechanisms involved in the defense against environmental impacts and the molecular modes of toxicity in this species. |
| Author | Hansen, Bjørn Henrik Altin, Dag Olsen, Anders J. Vang, Siv-Hege Nordtug, Trond |
| Author_xml | – sequence: 1 givenname: Bjørn Henrik surname: Hansen fullname: Hansen, Bjørn Henrik email: bjorn.h.hansen@sintef.no organization: SINTEF Materials and Chemistry, Marine Environmental Technology, N-7465 Trondheim, Norway – sequence: 2 givenname: Dag surname: Altin fullname: Altin, Dag organization: BioTrix, N-7022 Trondheim, Norway – sequence: 3 givenname: Siv-Hege surname: Vang fullname: Vang, Siv-Hege organization: Norwegian University of Science and Technology, Department of Biology, N-7491 Trondheim, Norway – sequence: 4 givenname: Trond surname: Nordtug fullname: Nordtug, Trond organization: SINTEF Materials and Chemistry, Marine Environmental Technology, N-7465 Trondheim, Norway – sequence: 5 givenname: Anders J. surname: Olsen fullname: Olsen, Anders J. organization: Norwegian University of Science and Technology, Department of Biology, N-7491 Trondheim, Norway |
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| Keywords | Calanus finmarchicus Organic pollution Biotransformation Detoxification Antioxidant Protein turnover Petroleum Ecotoxicology Transcription Protein Crustacea Aquatic environment Pollution Naphthalene Arthropoda Copepoda Aromatic compound Invertebrata |
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| Snippet | The planktonic copepod
Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is... The planktonic copepod Calanus finmarchicus is a key species in the Northern Atlantic food web; an oceanic area with extensive oil production. Naphthalene is... Effects of naphthalene on gene transcription in Calanus finmarchicus were investigated. The Graphical Prism 4 was used to conduct statistical analyses and... |
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| StartPage | 157 |
| SubjectTerms | Animal, plant and microbial ecology Animals Antioxidant antioxidant activity Applied ecology Biological and medical sciences Biotransformation Calanus finmarchicus Copepoda Copepoda - drug effects Crustacea Detoxification DNA Primers - chemistry Ecotoxicology, biological effects of pollution Enzymes - analysis Enzymes - biosynthesis Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects gene induction General aspects glutathione transferase Invertebrates lethal concentration 50 lipid peroxidation Marine messenger RNA metabolic detoxification naphthalene Naphthalenes - analysis Naphthalenes - toxicity Organic pollution Petroleum plankton Polymerase Chain Reaction - veterinary Protein turnover Proteins - analysis RNA, Messenger - analysis Time Factors toxicity transcriptional activation Water Pollutants, Chemical - toxicity water pollution |
| Title | Effects of naphthalene on gene transcription in Calanus finmarchicus (Crustacea: Copepoda) |
| URI | https://dx.doi.org/10.1016/j.aquatox.2007.10.009 https://www.ncbi.nlm.nih.gov/pubmed/18054806 https://www.proquest.com/docview/14850008 https://www.proquest.com/docview/20205616 https://www.proquest.com/docview/47692688 https://www.proquest.com/docview/70248075 |
| Volume | 86 |
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