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50bp deletion in the promoter for superoxide dismutase 1 (SOD1) reduces SOD1 expression in vitro and may correlate with increased age of onset of sporadic amyotrophic lateral sclerosis.

https://arctichealth.org/en/permalink/ahliterature156293
Source
Amyotroph Lateral Scler. 2008 Aug;9(4):229-37
Publication Type
Article
Date
Aug-2008
Author
Wendy J Broom
Matthew Greenway
Ghazaleh Sadri-Vakili
Carsten Russ
Kristen E Auwarter
Kelly E Glajch
Nicolas Dupre
Robert J Swingler
Shaun Purcell
Caroline Hayward
Peter C Sapp
Diane McKenna-Yasek
Paul N Valdmanis
Jean-Pierre Bouchard
Vincent Meininger
Betsy A Hosler
Jonathan D Glass
Meraida Polack
Guy A Rouleau
Jang-Ho J Cha
Orla Hardiman
Robert H Brown
Author Affiliation
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA. wendy.broom@gmail.com
Source
Amyotroph Lateral Scler. 2008 Aug;9(4):229-37
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Age of Onset
Amyotrophic Lateral Sclerosis - enzymology - epidemiology - genetics
Base Sequence
DNA Mutational Analysis
Female
Gene Expression
Genetic Predisposition to Disease
Genotype
Homozygote
Humans
Ireland - epidemiology
Male
Middle Aged
Phenotype
Polymorphism, Genetic
Promoter Regions, Genetic
Quebec - epidemiology
Risk factors
Scotland - epidemiology
Sequence Deletion
Sp1 Transcription Factor - metabolism
Superoxide Dismutase - genetics - metabolism
United States - epidemiology
Abstract
The objective was to test the hypothesis that a described association between homozygosity for a 50bp deletion in the SOD1 promoter 1684bp upstream of the SOD1 ATG and an increased age of onset in SALS can be replicated in additional SALS and control sample sets from other populations. Our second objective was to examine whether this deletion attenuates expression of the SOD1 gene. Genomic DNA from more than 1200 SALS cases from Ireland, Scotland, Quebec and the USA was genotyped for the 50bp SOD1 promoter deletion. Reporter gene expression analysis, electrophoretic mobility shift assays and chromatin immunoprecipitation studies were utilized to examine the functional effects of the deletion. The genetic association for homozygosity for the promoter deletion with an increased age of symptom onset was confirmed overall in this further study (p=0.032), although it was only statistically significant in the Irish subset, and remained highly significant in the combined set of all cohorts (p=0.001). Functional studies demonstrated that this polymorphism reduces the activity of the SOD1 promoter by approximately 50%. In addition we revealed that the transcription factor SP1 binds within the 50bp deletion region in vitro and in vivo. Our findings suggest the hypothesis that this deletion reduces expression of the SOD1 gene and that levels of the SOD1 protein may modify the phenotype of SALS within selected populations.
PubMed ID
18608091 View in PubMed
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Aging and susceptibility to toluene in rats: a pharmacokinetic, biomarker, and physiological approach.

https://arctichealth.org/en/permalink/ahliterature98359
Source
J Toxicol Environ Health A. 2010;73(4):301-18
Publication Type
Article
Date
2010
Author
Christopher J Gordon
Reddy R Gottipolu
Elaina M Kenyon
Ronald Thomas
Mette C Schladweiler
Cina M Mack
Jonathan H Shannahan
J Grace Wallenborn
Abraham Nyska
Robert C MacPhail
Judy E Richards
Mike Devito
Urmila P Kodavanti
Author Affiliation
National Health and Environmental Effects Research Laboratory, ORD, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA. Gordon.christopher@epa.gov
Source
J Toxicol Environ Health A. 2010;73(4):301-18
Date
2010
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Biological Markers
Brain - metabolism
Dose-Response Relationship, Drug
Gene Expression Regulation - drug effects
Glutathione Peroxidase - genetics - metabolism
Glutathione Transferase - genetics - metabolism
Heart - drug effects
Male
Myocardium - metabolism
Rats
Superoxide Dismutase - genetics - metabolism
Toluene - blood - pharmacokinetics - toxicity
Abstract
Aging adults are a growing segment of the U.S. population and are likely to exhibit increased susceptibility to many environmental toxicants. However, there is little information on the susceptibility of the aged to toxicants. The toxicity of toluene has been well characterized in young adult rodents but there is little information in the aged. Three approaches were used: (1) pharmacokinetic (PK), (2) cardiac biomarkers, and (3) whole-animal physiology to assess whether aging increases susceptibility to toluene in the Brown Norway (BN) rat. Three life stages, young adult, middle aged, and aged (4, 12, and 24 mo, respectively), were administered toluene orally at doses of 0, 0.3, 0.65, or 1 g/kg and subjected to the following: terminated at 45 min or 4 h post dosing, and blood and brain toluene concentration were measured; terminated at 4 h post dosing, and biomarkers of cardiac function were measured; or monitor heart rate (HR), core temperature (Tc), and motor activity (MA) by radiotelemetry before and after dosing. Brain toluene concentration was significantly elevated in aged rats at 4 h after dosing with either 0.3 or 1 g/kg. Blood toluene concentrations were unaffected by age. There were various interactions between aging and toluene-induced effects on cardiac biomarkers. Most notably, toluene exposure led to reductions in mRNA markers for oxidative stress in aged but not younger animals. Toluene also produced a reduction in cardiac endothelin-1 in aged rats. Higher doses of toluene led to tachycardia, hypothermia, and a transient elevation in MA. Aged rats were less sensitive to the tachycardic effects of toluene but showed a prolonged hypothermic response. Elevated brain levels of toluene in aged rats may be attributed to their suppressed cardiovascular and respiratory responses. The expression of several cardiac biochemical markers of toluene exposure in the aged may also reflect differential susceptibility to this toxicant.
PubMed ID
20077299 View in PubMed
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Aging and the brown Norway rat leydig cell antioxidant defense system.

https://arctichealth.org/en/permalink/ahliterature83080
Source
J Androl. 2006 Mar-Apr;27(2):240-7
Publication Type
Article
Author
Luo Lindi
Chen Haolin
Trush Michael A
Show Matthew D
Anway Matthew D
Zirkin Barry R
Author Affiliation
Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205, USA. lluo@jhsph.edu
Source
J Androl. 2006 Mar-Apr;27(2):240-7
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Antioxidants - metabolism
Glutathione Peroxidase - genetics - metabolism
Leydig Cells - enzymology
Male
RNA, Messenger - genetics
Rats
Rats, Inbred BN
Superoxide Dismutase - genetics - metabolism
Testis - growth & development
Transcription, Genetic
Abstract
Previous studies have shown that testosterone production by the Leydig cells of aged Brown Norway rats is reduced from the relatively high levels produced by Leydig cells of young rats and that this reduction is not secondary to decreased serum luteinizing hormone concentration. The free radical theory of aging proposes that imbalance between pro-oxidants and the antioxidant defense system ultimately results in oxidative damage to cellular processes. With this in mind, we hypothesized herein that age-related reductions in steroidogenesis by Brown Norway rat Leydig cells may be associated with the impairment of the antioxidant defense system of these cells. To begin to test this hypothesis, we compared the activities and steady-state mRNA and protein levels of the antioxidant enzymes copper zinc (CuZn) superoxide dismutase (CuZnSOD, SOD1), manganese (Mn) superoxide dismutase (MnSOD, SOD2), and glutathione peroxidase (GPx) and the levels of reduced and oxidized glutathione in Leydig cells isolated from the testes of young (4-month-old) and aged (20-month-old) Brown Norway rats. For some studies, Leydig cells were isolated separately from aged testes that either had regressed because of age-related losses of germ cells or that were nonregressed. SOD (total) and GPx activities were found to decrease significantly with age whether or not the testes were regressed. CuZnSOD and MnSOD mRNA levels decreased with aging, though the magnitude of the decreases were considerably lower than the respective decreases in enzyme activities. GPx mRNA levels also decreased, which is consistent with the decreases seen in enzyme activity. MnSOD protein expression declined with age, and to a lesser extent, CuZnSOD did as well. Reduced and oxidized glutathione also exhibited age-related reductions in cells from both normal and regressed aged testes. The age-related decreases in Leydig cell antioxidant enzyme activities, gene expression, and protein levels and in glutathione were consistent with the hypothesis that the loss of steroidogenic function that accompanies Leydig cell aging may result in part from a decrease in the fidelity of the cellular antioxidant defense system.
PubMed ID
16304208 View in PubMed
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An association between manganese superoxide dismutase polymorphism and outcome of chemotherapy in acute myeloid leukemia.

https://arctichealth.org/en/permalink/ahliterature81872
Source
Haematologica. 2006 Jun;91(6):829-32
Publication Type
Article
Date
Jun-2006
Author
Koistinen Pirjo
Ruuska Satu
Saily Marjaana
Kakko Sakari
Siitonen Pauliina
Siitonen Timo
Savolainen Markku J
Kinnula Vuokko L
Savolainen Eeva-Riitta
Author Affiliation
Department of Internal Medicine, University of Oulu, Finland. pirjo.koistinen@oulu.fi
Source
Haematologica. 2006 Jun;91(6):829-32
Date
Jun-2006
Language
English
Publication Type
Article
Keywords
Acute Disease
Base Sequence
Catalase - genetics
DNA Primers
Glutathione Peroxidase - genetics
Humans
Kinetics
Leukemia, Myeloid - drug therapy - enzymology - mortality
Mitochondria - enzymology
Oxidation-Reduction
Polymorphism, Single Nucleotide
Prognosis
Superoxide Dismutase - genetics - metabolism
Survival Analysis
Treatment Outcome
Abstract
Manganese superoxide dismutase (MnSOD) protects cells against oxidative stress by eliminating superoxides. Hypothetically, decreased MnSOD levels in cancer might lead to increased oxidative stress and, thus, to increased sensitivity of cells to chemotherapy agents. Eighty-nine patients with acute myeloid leukemia (AML) were analyzed for a functional C to T polymorphism of MnSOD, which could potentially lead to decreased enzyme concentrations inside mitochondria. A significant survival advantage (p=0.02) was observed for those AML patients carrying T-containing alleles of MnSOD compared to the patients with the CC genotype. These preliminary results may indicate an important role for genetic factors regulating the cellular redox state in determining the outcome of leukemia chemotherapy.
PubMed ID
16769586 View in PubMed
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Antioxidant defense mechanisms of human mesothelioma and lung adenocarcinoma cells.

https://arctichealth.org/en/permalink/ahliterature20527
Source
Am J Physiol Lung Cell Mol Physiol. 2000 Apr;278(4):L696-702
Publication Type
Article
Date
Apr-2000
Author
K. Järvinen
P. Pietarinen-Runtti
K. Linnainmaa
K O Raivio
C M Krejsa
T. Kavanagh
V L Kinnula
Author Affiliation
Childrens Hospital, University of Helsinki, 00029 Helsinki, 90220 Oulu Finland.
Source
Am J Physiol Lung Cell Mol Physiol. 2000 Apr;278(4):L696-702
Date
Apr-2000
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - metabolism - pathology
Antioxidants - metabolism
Catalase - metabolism
Glutamate-Cysteine Ligase - metabolism
Glutathione - metabolism
Humans
Hydrogen Peroxide - pharmacology
Lung Neoplasms - metabolism - pathology
Mesothelioma - metabolism - pathology
Oxidants - pharmacology
RNA, Messenger - metabolism
Research Support, Non-U.S. Gov't
Superoxide Dismutase - genetics - metabolism
Tumor Cells, Cultured
Vitamin K - pharmacology
Abstract
The development of drug resistance of tumors is multifactorial and still poorly understood. Some cytotoxic drugs generate free radicals, and, therefore, antioxidant enzymes may contribute to drug resistance. We investigated the levels of manganese superoxide dismutase (Mn SOD), its inducibility, and its protective role against tumor necrosis factor-alpha and cytotoxic drugs (cisplatin, epirubicin, methotrexate, and vindesin) in human pleural mesothelioma (M14K) and pulmonary adenocarcinoma (A549) cells. We also studied other major antioxidant mechanisms in relation to oxidant and drug resistance of these cells. A549 cells were more resistant than M14K cells toward both oxidants (hydrogen peroxide and menadione) and all the cytotoxic drugs tested. M14K cells contained higher basal Mn SOD activity than A549 cells (28.3 +/- 3.4 vs. 1.8 +/- 0.3 U/mg protein), and Mn SOD activity was significantly induced by tumor necrosis factor-alpha only in A549 cells (+524%), but the induction did not offer any protection during subsequent oxidant or drug exposure. Mn SOD was not induced significantly in either of these cell lines by any of the cytotoxic drugs (0.007-2 microM, 48 h) tested when assessed by Northern blotting, Western blotting, or specific activity. A549 cells contained higher catalase activity than M14K cells (7.6 +/- 1.3 vs. 3.6 +/- 0.5 nmol O(2). min(-1). mg protein(-1)). They also contained twofold higher levels of glutathione and higher immunoreactivity of the heavy subunit of gamma-glutamylcysteine synthetase than M14K cells. Experiments with inhibitors of gamma-glutamylcysteine synthetase and catalase supported our conclusion that mechanisms associated with glutathione contribute to the drug resistance of these cells.
PubMed ID
10749746 View in PubMed
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Antioxidative stress proteins and their gene expression in brown trout (Salmo trutta) from three rivers with different heavy metal levels.

https://arctichealth.org/en/permalink/ahliterature82460
Source
Comp Biochem Physiol C Toxicol Pharmacol. 2006 Jul;143(3):263-74
Publication Type
Article
Date
Jul-2006
Author
Hansen B H
Rømma S.
Garmo Ø A
Olsvik P A
Andersen R A
Author Affiliation
Norwegian University of Science and Technology (NTNU), Department of Biology, Høgskoleringen 5, N-7491 Trondheim, Norway. bjorn.henrik.hansen@bio.ntnu.no
Source
Comp Biochem Physiol C Toxicol Pharmacol. 2006 Jul;143(3):263-74
Date
Jul-2006
Language
English
Publication Type
Article
Keywords
Animals
Antioxidants - metabolism
Cadmium - analysis - toxicity
Catalase - genetics - metabolism
Copper - analysis - toxicity
Environmental monitoring
Female
Gene Expression
Gills - chemistry - drug effects - metabolism
Glutathione Peroxidase - genetics - metabolism
Kidney - drug effects - metabolism
Liver - drug effects - metabolism
Male
Metallothionein - genetics - metabolism
Norway
Oxidative Stress
RNA, Messenger - metabolism
Rivers
Superoxide Dismutase - genetics - metabolism
Trout - metabolism
Water Pollutants, Chemical - analysis - toxicity
Zinc - analysis - toxicity
Abstract
Three populations of brown trout (Salmo trutta) exposed to different metal levels in their natural environments, were studied with respect to antioxidants metallothionein (MT), superoxide dismutase (SOD) and catalase (CAT) as well as for corresponding mRNA levels. In addition, mRNA levels were studied for glutathione peroxidase (GPx) and glutathione reductase (GR). The Cd/Zn-exposed trout (Naustebekken River) had higher accumulated levels of Cd, Cu and Zn in gills, and higher levels of MT (both protein and mRNA) in liver and kidney as well as in gills compared to the Cu-exposed trout (Rugla River) and trout from an uncontaminated reference river (Stribekken River). Less MT found in the Cu-exposed trout may increase susceptibility to oxidative stress, but no higher levels of antioxidant mRNAs were found in gills of these trouts. The data indicated that chronic exposures of brown trout to Cd, Zn and/or Cu did not involve maintenance of high activities of SOD and CAT enzymes in gills, although SOD mRNA levels were higher in the Cd/Zn-exposed trout. In livers, mRNA levels of SOD, CAT and GPx were higher in the metal-exposed trout, but in the case of GR this was only seen in kidneys of Cd/Zn-exposed trout. However, both metal-exposed groups had higher activities of SOD enzyme in liver compared to the unexposed reference trout, and CAT activity was found to be higher in kidneys of Cu-exposed trout. The Cu-exposed trout did not seem to rely on MT production to avoid Cu toxicity in gills, but rather by keeping the Cu uptake at a low level. A coordinated expression of different stress genes may also be important in chronic metal exposure. It may be concluded that the observed metal effects relies on acclimation rather than on genetic adaptation in the metal exposed populations.
PubMed ID
16616685 View in PubMed
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Expression and developmental profile of antioxidant enzymes in human lung and liver.

https://arctichealth.org/en/permalink/ahliterature58929
Source
Am J Respir Cell Mol Biol. 1998 Dec;19(6):942-9
Publication Type
Article
Date
Dec-1998
Author
T M Asikainen
K O Raivio
M. Saksela
V L Kinnula
Author Affiliation
Hospital for Children and Adolescents, University of Helsinki, Helsinki; and Department of Internal Medicine, University of Oulu, Oulu, Finland. tmasikai@cc.helsinki.fi
Source
Am J Respir Cell Mol Biol. 1998 Dec;19(6):942-9
Date
Dec-1998
Language
English
Publication Type
Article
Keywords
Adult
Antioxidants
Catalase - genetics - metabolism
Gene Expression
Glutathione Peroxidase - genetics - metabolism
Humans
Infant, Newborn
Liver - embryology - enzymology - growth & development
Lung - embryology - enzymology - growth & development
Lung Transplantation
RNA, Messenger - metabolism
Research Support, Non-U.S. Gov't
Smoking
Superoxide Dismutase - genetics - metabolism
Abstract
Air breathing, especially oxygen therapy, exposes the lung to reactive oxygen species (ROS). Antioxidant enzymes (AOEs) may protect the lung from ROS-mediated injury. Because expression of the key AOEs increases in several animal species during gestation, we investigated (1) the messenger RNA (mRNA) and activity levels of the key AOEs manganese and copper-zinc superoxide dismutases (MnSOD and CuZnSOD, respectively), catalase (CAT), and glutathione peroxidase (GPx) in adult lung samples and during ontogenesis; and (2) the difference in AOE expression between lung and liver. In the lung, the mRNA expression of MnSOD, CuZnSOD, and CAT increased toward adulthood, and GPx was unchanged. Pulmonary activities of MnSOD and CuZnSOD were unchanged, whereas CAT increased 3-fold from fetuses to adults. In the liver, the mRNA expression of MnSOD, CuZnSOD, and GPx increased, whereas that of CAT decreased toward adulthood. Hepatic activities of MnSOD and CuZnSOD increased 2-fold and 4-fold, respectively, whereas CAT was similar in fetuses and adults. Neonatal GPx activity was 2-fold higher in the lung and 6-fold higher in the liver compared with adults. The mRNA levels of MnSOD correlated positively with those of CuZnSOD and CAT in the lung, and GPx with those of MnSOD and CuZnSOD in the liver. Activities of MnSOD and CuZnSOD correlated positively in the liver. We conclude that the regulation of AOEs differs between human lung and liver, and is not tightly coordinated in either tissue.
PubMed ID
9843929 View in PubMed
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Genetically Low Antioxidant Protection and Risk of Cardiovascular Disease and Heart Failure in Diabetic Subjects.

https://arctichealth.org/en/permalink/ahliterature277172
Source
EBioMedicine. 2015 Dec;2(12):2010-5
Publication Type
Article
Date
Dec-2015
Author
Camilla J Kobylecki
Shoaib Afzal
Børge G Nordestgaard
Source
EBioMedicine. 2015 Dec;2(12):2010-5
Date
Dec-2015
Language
English
Publication Type
Article
Keywords
Aged
Antioxidants - metabolism
Cardiovascular Diseases - epidemiology - etiology
Denmark - epidemiology
Diabetes Complications - epidemiology
Diabetes Mellitus - epidemiology
Female
Genetic Predisposition to Disease
Heart Failure - epidemiology - etiology
Humans
Incidence
Male
Middle Aged
Proportional Hazards Models
Risk
Superoxide Dismutase - genetics - metabolism
Abstract
Hyperglycemia-induced oxidative stress is one mechanism believed to underlie diabetic vascular disease. We tested the hypothesis that diabetic subjects heterozygous for extracellular superoxide dismutase (SOD3) R213G, which entails lower antioxidant capacity in tissues, have increased risk of cardiovascular disease and heart failure.
We used the prospective Copenhagen General Population Study and Copenhagen City Heart Study and genotyped 95,871 individuals for the rs1799895 R213G variation in the SOD3 gene, of which 4498 had diabetes. We used national hospitalization and death registers to assess cardiovascular disease and heart failure.
Out of 95,871 individuals, we identified 93,521 R213G non-carriers (213RR, 97.5%), 2336 heterozygotes (213RG, 2.4%) and 14 homozygotes (213GG, 0.01%). In diabetic subjects, the hazard ratio for cardiovascular disease in R213G heterozygotes compared to non-carriers was 2.32 (95% CI 1·44-3.75), with a corresponding hazard ratio in non-diabetic subjects of 0.97 (0·80-1.19) (p for interaction 0.002). For heart failure, the hazard ratios in R213G heterozygotes compared to non-carriers were 2.19 (1.28-3.76) in diabetic and 0.68 (0.49-0.92) in non-diabetic subjects (p for interaction
Notes
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Comment In: EBioMedicine. 2015 Dec;2(12):1864-526844262
PubMed ID
26844281 View in PubMed
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Genetic tags applied to the European hake, Merluccius merluccius (L.).

https://arctichealth.org/en/permalink/ahliterature51471
Source
Anim Blood Groups Biochem Genet. 1979;10(1):39-48
Publication Type
Article
Date
1979
Author
G. Mangaly
A. Jamieson
Source
Anim Blood Groups Biochem Genet. 1979;10(1):39-48
Date
1979
Language
English
Publication Type
Article
Keywords
Alleles
Animals
Comparative Study
Esterases - genetics - metabolism
Fishes - genetics
Gene Frequency
Liver - enzymology
Polymorphism, Genetic
Superoxide Dismutase - genetics - metabolism
Transferrin - genetics
Vitreous Body - enzymology
Abstract
Three biochemical gene markers test the hypothesis that the European hake, Merluccius merluccius (L.), along the west European continental shelf are one race. The three polymorphic loci were serum transferrin (Tf), eye vitreous fluid butyric esterase (Es) and liver superoxide dismutase (Sod). Five transferrin alleles, three esterase alleles and two superoxide dismutase alleles were identified. Heterogeneity tests on genotype frequency distribution for twelve areas ranging from Norway to Biscay revealed no significant variation. The results using these genetic tags are consistent with the unit race hypothesis for hake throughout the sea areas sampled.
PubMed ID
507470 View in PubMed
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Gill metal binding and stress gene transcription in brown trout (Salmo trutta) exposed to metal environments: the effect of pre-exposure in natural populations.

https://arctichealth.org/en/permalink/ahliterature77611
Source
Environ Toxicol Chem. 2007 May;26(5):944-53
Publication Type
Article
Date
May-2007
Author
Hansen Bjørn Henrik
Garmo Oyvind A
Olsvik Pål A
Andersen Rolf A
Author Affiliation
Department of Biology, Norwegian University of Science and Technology. bjorn.h.hansen@sinetef.no
Source
Environ Toxicol Chem. 2007 May;26(5):944-53
Date
May-2007
Language
English
Publication Type
Article
Keywords
Animals
Cadmium - toxicity
Catalase - genetics - metabolism
Copper - toxicity
Gills - drug effects - metabolism
Glutathione Peroxidase - genetics - metabolism
Glutathione Reductase - genetics - metabolism
HSP70 Heat-Shock Proteins - genetics - metabolism
Metallothionein - genetics - metabolism
Metals - toxicity
Norway
Oxidative Stress - drug effects - physiology
Superoxide Dismutase - genetics - metabolism
Transcription, Genetic - drug effects - physiology
Trout
Water Pollutants, Chemical - toxicity
Zinc - toxicity
Abstract
Brown trout (Salmo trutta) from two native populations from the Røros area in Central Norway, acclimated in mining-affected habitats to different levels of Cd/Zn and Cu, together with trout from a nearby unaffected river (reference) were transferred to a nearby lake with higher levels of Cu, Cd, and Zn than those in their respective native rivers. This experiment was conducted to gain information about the underlying resistance mechanisms developed in fish exposed to metal environments. The focus was on gill metal accumulation and transcription of the metal-responsive stress genes metallothionein-A (MT-A), Cu/Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and heat shock protein 70 (HSP-70). The only shared response shown between the three groups after transfer were Cu accumulation and MT-A induction. The Cu-acclimated trout produced mucus to reduce the uptake of Cu into the gills. The MT-A levels were highest in the Cd/Zn-acclimated trout both before and after transfer. Before transfer, antioxidant transcription (SOD and GPx) was higher in gills of Cu-acclimated compared to the Cd/Zn-acclimated trout, but increased transcription of antioxidant stress genes was observed after transfer in both metal-acclimated groups. The metal-acclimated trout groups also showed an increase in the transcription of HSP-70. Compared to the reference population not previously exposed to metals, stress gene transcription increased faster in the metal-acclimated populations. The exception was induction of CAT, which appeared to be depressed after transfer in Cd/Zn-acclimated trout. The data indicate that acclimation to chronic metal exposure involves different strategies to cope with different metals and that these strategies involve both physiological mechanisms (mucus production) as well as metal-related stress gene transcription.
PubMed ID
17521141 View in PubMed
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16 records – page 1 of 2.