Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions
Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contri...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Noremberg, Simone [verfasserIn] Bohrer, Denise [verfasserIn] Schetinger, Maria R. C. [verfasserIn] Bairros, André V. [verfasserIn] Gutierres, Jessié [verfasserIn] Gonçalves, Jamile F. [verfasserIn] Veiga, Marlei [verfasserIn] Santos, Francielli W. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Biological trace element research - [S.l.] : Springer US, 1979, 169(2015), 1 vom: 07. Juni, Seite 77-85 |
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| Übergeordnetes Werk: |
volume:169 ; year:2015 ; number:1 ; day:07 ; month:06 ; pages:77-85 |
| Links: |
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| DOI / URN: |
10.1007/s12011-015-0392-6 |
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| Katalog-ID: |
SPR023634278 |
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| 245 | 1 | 0 | |a Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions |
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| 520 | |a Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. | ||
| 650 | 4 | |a Silicon |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Aluminum |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Hydroxyaluminosilicates |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Rat |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Brain |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Blood |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Bohrer, Denise |e verfasserin |4 aut | |
| 700 | 1 | |a Schetinger, Maria R. C. |e verfasserin |4 aut | |
| 700 | 1 | |a Bairros, André V. |e verfasserin |4 aut | |
| 700 | 1 | |a Gutierres, Jessié |e verfasserin |4 aut | |
| 700 | 1 | |a Gonçalves, Jamile F. |e verfasserin |4 aut | |
| 700 | 1 | |a Veiga, Marlei |e verfasserin |4 aut | |
| 700 | 1 | |a Santos, Francielli W. |e verfasserin |4 aut | |
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10.1007/s12011-015-0392-6 doi (DE-627)SPR023634278 (SPR)s12011-015-0392-6-e DE-627 ger DE-627 rakwb eng 570 ASE Noremberg, Simone verfasserin aut Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. Silicon (dpeaa)DE-He213 Aluminum (dpeaa)DE-He213 Hydroxyaluminosilicates (dpeaa)DE-He213 Rat (dpeaa)DE-He213 Brain (dpeaa)DE-He213 Blood (dpeaa)DE-He213 Bohrer, Denise verfasserin aut Schetinger, Maria R. C. verfasserin aut Bairros, André V. verfasserin aut Gutierres, Jessié verfasserin aut Gonçalves, Jamile F. verfasserin aut Veiga, Marlei verfasserin aut Santos, Francielli W. verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 169(2015), 1 vom: 07. Juni, Seite 77-85 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:169 year:2015 number:1 day:07 month:06 pages:77-85 https://dx.doi.org/10.1007/s12011-015-0392-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 169 2015 1 07 06 77-85 |
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10.1007/s12011-015-0392-6 doi (DE-627)SPR023634278 (SPR)s12011-015-0392-6-e DE-627 ger DE-627 rakwb eng 570 ASE Noremberg, Simone verfasserin aut Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. Silicon (dpeaa)DE-He213 Aluminum (dpeaa)DE-He213 Hydroxyaluminosilicates (dpeaa)DE-He213 Rat (dpeaa)DE-He213 Brain (dpeaa)DE-He213 Blood (dpeaa)DE-He213 Bohrer, Denise verfasserin aut Schetinger, Maria R. C. verfasserin aut Bairros, André V. verfasserin aut Gutierres, Jessié verfasserin aut Gonçalves, Jamile F. verfasserin aut Veiga, Marlei verfasserin aut Santos, Francielli W. verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 169(2015), 1 vom: 07. Juni, Seite 77-85 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:169 year:2015 number:1 day:07 month:06 pages:77-85 https://dx.doi.org/10.1007/s12011-015-0392-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 169 2015 1 07 06 77-85 |
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10.1007/s12011-015-0392-6 doi (DE-627)SPR023634278 (SPR)s12011-015-0392-6-e DE-627 ger DE-627 rakwb eng 570 ASE Noremberg, Simone verfasserin aut Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. Silicon (dpeaa)DE-He213 Aluminum (dpeaa)DE-He213 Hydroxyaluminosilicates (dpeaa)DE-He213 Rat (dpeaa)DE-He213 Brain (dpeaa)DE-He213 Blood (dpeaa)DE-He213 Bohrer, Denise verfasserin aut Schetinger, Maria R. C. verfasserin aut Bairros, André V. verfasserin aut Gutierres, Jessié verfasserin aut Gonçalves, Jamile F. verfasserin aut Veiga, Marlei verfasserin aut Santos, Francielli W. verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 169(2015), 1 vom: 07. Juni, Seite 77-85 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:169 year:2015 number:1 day:07 month:06 pages:77-85 https://dx.doi.org/10.1007/s12011-015-0392-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 169 2015 1 07 06 77-85 |
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10.1007/s12011-015-0392-6 doi (DE-627)SPR023634278 (SPR)s12011-015-0392-6-e DE-627 ger DE-627 rakwb eng 570 ASE Noremberg, Simone verfasserin aut Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. Silicon (dpeaa)DE-He213 Aluminum (dpeaa)DE-He213 Hydroxyaluminosilicates (dpeaa)DE-He213 Rat (dpeaa)DE-He213 Brain (dpeaa)DE-He213 Blood (dpeaa)DE-He213 Bohrer, Denise verfasserin aut Schetinger, Maria R. C. verfasserin aut Bairros, André V. verfasserin aut Gutierres, Jessié verfasserin aut Gonçalves, Jamile F. verfasserin aut Veiga, Marlei verfasserin aut Santos, Francielli W. verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 169(2015), 1 vom: 07. Juni, Seite 77-85 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:169 year:2015 number:1 day:07 month:06 pages:77-85 https://dx.doi.org/10.1007/s12011-015-0392-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 169 2015 1 07 06 77-85 |
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10.1007/s12011-015-0392-6 doi (DE-627)SPR023634278 (SPR)s12011-015-0392-6-e DE-627 ger DE-627 rakwb eng 570 ASE Noremberg, Simone verfasserin aut Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. Silicon (dpeaa)DE-He213 Aluminum (dpeaa)DE-He213 Hydroxyaluminosilicates (dpeaa)DE-He213 Rat (dpeaa)DE-He213 Brain (dpeaa)DE-He213 Blood (dpeaa)DE-He213 Bohrer, Denise verfasserin aut Schetinger, Maria R. C. verfasserin aut Bairros, André V. verfasserin aut Gutierres, Jessié verfasserin aut Gonçalves, Jamile F. verfasserin aut Veiga, Marlei verfasserin aut Santos, Francielli W. verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 169(2015), 1 vom: 07. Juni, Seite 77-85 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:169 year:2015 number:1 day:07 month:06 pages:77-85 https://dx.doi.org/10.1007/s12011-015-0392-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 169 2015 1 07 06 77-85 |
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Enthalten in Biological trace element research 169(2015), 1 vom: 07. Juni, Seite 77-85 volume:169 year:2015 number:1 day:07 month:06 pages:77-85 |
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Enthalten in Biological trace element research 169(2015), 1 vom: 07. Juni, Seite 77-85 volume:169 year:2015 number:1 day:07 month:06 pages:77-85 |
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Silicon Aluminum Hydroxyaluminosilicates Rat Brain Blood |
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Noremberg, Simone @@aut@@ Bohrer, Denise @@aut@@ Schetinger, Maria R. C. @@aut@@ Bairros, André V. @@aut@@ Gutierres, Jessié @@aut@@ Gonçalves, Jamile F. @@aut@@ Veiga, Marlei @@aut@@ Santos, Francielli W. @@aut@@ |
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Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. 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Noremberg, Simone |
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570 ASE Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions Silicon (dpeaa)DE-He213 Aluminum (dpeaa)DE-He213 Hydroxyaluminosilicates (dpeaa)DE-He213 Rat (dpeaa)DE-He213 Brain (dpeaa)DE-He213 Blood (dpeaa)DE-He213 |
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Noremberg, Simone Bohrer, Denise Schetinger, Maria R. C. Bairros, André V. Gutierres, Jessié Gonçalves, Jamile F. Veiga, Marlei Santos, Francielli W. |
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Elektronische Aufsätze |
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Noremberg, Simone |
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10.1007/s12011-015-0392-6 |
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silicon reverses lipid peroxidation but not acetylcholinesterase activity induced by long-term exposure to low aluminum levels in rat brain regions |
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Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions |
| abstract |
Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. |
| abstractGer |
Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. |
| abstract_unstemmed |
Abstract Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon ($ SiO_{2} $) with $ Al^{3+} $ to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. $ Al^{3+} $ increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas $ SiO_{2} $ reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. $ SiO_{2} $ showed a protective effect in the hippocampus and cerebellum against cellular damage caused by $ Al^{3+} $-induced lipid peroxidation. Thus, $ SiO_{2} $ may be considered an important protector in LPO induced by $ Al^{3+} $. |
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Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions |
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| score |
7.399987 |