Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes
Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short d...
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| Autor*in: |
M’Bemba-Meka, Prosper [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2006 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer-Verlag 2006 |
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| Übergeordnetes Werk: |
Enthalten in: Archives of toxicology - Berlin : Springer, 1930, 81(2006), 2 vom: 07. Juli, Seite 89-99 |
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| Übergeordnetes Werk: |
volume:81 ; year:2006 ; number:2 ; day:07 ; month:07 ; pages:89-99 |
| Links: |
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| DOI / URN: |
10.1007/s00204-006-0128-7 |
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| Katalog-ID: |
SPR001821113 |
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| 100 | 1 | |a M’Bemba-Meka, Prosper |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes |
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| 520 | |a Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. | ||
| 650 | 4 | |a Human blood lymphocytes |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Nickel carbonate hydroxide |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Sister-chromatid exchange |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Replication index |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mitotic index |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Oxidative stress |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Calcium homeostasis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Lemieux, Nicole |4 aut | |
| 700 | 1 | |a Chakrabarti, Saroj K. |4 aut | |
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10.1007/s00204-006-0128-7 doi (DE-627)SPR001821113 (SPR)s00204-006-0128-7-e DE-627 ger DE-627 rakwb eng M’Bemba-Meka, Prosper verfasserin aut Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. Human blood lymphocytes (dpeaa)DE-He213 Nickel carbonate hydroxide (dpeaa)DE-He213 Sister-chromatid exchange (dpeaa)DE-He213 Replication index (dpeaa)DE-He213 Mitotic index (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Calcium homeostasis (dpeaa)DE-He213 Lemieux, Nicole aut Chakrabarti, Saroj K. aut Enthalten in Archives of toxicology Berlin : Springer, 1930 81(2006), 2 vom: 07. Juli, Seite 89-99 (DE-627)25339015X (DE-600)1458459-1 1432-0738 nnns volume:81 year:2006 number:2 day:07 month:07 pages:89-99 https://dx.doi.org/10.1007/s00204-006-0128-7 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_267 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_2360 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 81 2006 2 07 07 89-99 |
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10.1007/s00204-006-0128-7 doi (DE-627)SPR001821113 (SPR)s00204-006-0128-7-e DE-627 ger DE-627 rakwb eng M’Bemba-Meka, Prosper verfasserin aut Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. Human blood lymphocytes (dpeaa)DE-He213 Nickel carbonate hydroxide (dpeaa)DE-He213 Sister-chromatid exchange (dpeaa)DE-He213 Replication index (dpeaa)DE-He213 Mitotic index (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Calcium homeostasis (dpeaa)DE-He213 Lemieux, Nicole aut Chakrabarti, Saroj K. aut Enthalten in Archives of toxicology Berlin : Springer, 1930 81(2006), 2 vom: 07. Juli, Seite 89-99 (DE-627)25339015X (DE-600)1458459-1 1432-0738 nnns volume:81 year:2006 number:2 day:07 month:07 pages:89-99 https://dx.doi.org/10.1007/s00204-006-0128-7 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_267 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_2360 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 81 2006 2 07 07 89-99 |
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10.1007/s00204-006-0128-7 doi (DE-627)SPR001821113 (SPR)s00204-006-0128-7-e DE-627 ger DE-627 rakwb eng M’Bemba-Meka, Prosper verfasserin aut Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. Human blood lymphocytes (dpeaa)DE-He213 Nickel carbonate hydroxide (dpeaa)DE-He213 Sister-chromatid exchange (dpeaa)DE-He213 Replication index (dpeaa)DE-He213 Mitotic index (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Calcium homeostasis (dpeaa)DE-He213 Lemieux, Nicole aut Chakrabarti, Saroj K. aut Enthalten in Archives of toxicology Berlin : Springer, 1930 81(2006), 2 vom: 07. Juli, Seite 89-99 (DE-627)25339015X (DE-600)1458459-1 1432-0738 nnns volume:81 year:2006 number:2 day:07 month:07 pages:89-99 https://dx.doi.org/10.1007/s00204-006-0128-7 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_267 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_2360 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 81 2006 2 07 07 89-99 |
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10.1007/s00204-006-0128-7 doi (DE-627)SPR001821113 (SPR)s00204-006-0128-7-e DE-627 ger DE-627 rakwb eng M’Bemba-Meka, Prosper verfasserin aut Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. Human blood lymphocytes (dpeaa)DE-He213 Nickel carbonate hydroxide (dpeaa)DE-He213 Sister-chromatid exchange (dpeaa)DE-He213 Replication index (dpeaa)DE-He213 Mitotic index (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Calcium homeostasis (dpeaa)DE-He213 Lemieux, Nicole aut Chakrabarti, Saroj K. aut Enthalten in Archives of toxicology Berlin : Springer, 1930 81(2006), 2 vom: 07. Juli, Seite 89-99 (DE-627)25339015X (DE-600)1458459-1 1432-0738 nnns volume:81 year:2006 number:2 day:07 month:07 pages:89-99 https://dx.doi.org/10.1007/s00204-006-0128-7 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_267 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_2360 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 81 2006 2 07 07 89-99 |
| allfieldsSound |
10.1007/s00204-006-0128-7 doi (DE-627)SPR001821113 (SPR)s00204-006-0128-7-e DE-627 ger DE-627 rakwb eng M’Bemba-Meka, Prosper verfasserin aut Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. Human blood lymphocytes (dpeaa)DE-He213 Nickel carbonate hydroxide (dpeaa)DE-He213 Sister-chromatid exchange (dpeaa)DE-He213 Replication index (dpeaa)DE-He213 Mitotic index (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Calcium homeostasis (dpeaa)DE-He213 Lemieux, Nicole aut Chakrabarti, Saroj K. aut Enthalten in Archives of toxicology Berlin : Springer, 1930 81(2006), 2 vom: 07. Juli, Seite 89-99 (DE-627)25339015X (DE-600)1458459-1 1432-0738 nnns volume:81 year:2006 number:2 day:07 month:07 pages:89-99 https://dx.doi.org/10.1007/s00204-006-0128-7 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_267 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_2360 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 81 2006 2 07 07 89-99 |
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English |
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Enthalten in Archives of toxicology 81(2006), 2 vom: 07. Juli, Seite 89-99 volume:81 year:2006 number:2 day:07 month:07 pages:89-99 |
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Enthalten in Archives of toxicology 81(2006), 2 vom: 07. Juli, Seite 89-99 volume:81 year:2006 number:2 day:07 month:07 pages:89-99 |
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Human blood lymphocytes Nickel carbonate hydroxide Sister-chromatid exchange Replication index Mitotic index Oxidative stress Calcium homeostasis |
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M’Bemba-Meka, Prosper @@aut@@ Lemieux, Nicole @@aut@@ Chakrabarti, Saroj K. @@aut@@ |
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The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. 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M’Bemba-Meka, Prosper |
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M’Bemba-Meka, Prosper misc Human blood lymphocytes misc Nickel carbonate hydroxide misc Sister-chromatid exchange misc Replication index misc Mitotic index misc Oxidative stress misc Calcium homeostasis Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes |
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Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes Human blood lymphocytes (dpeaa)DE-He213 Nickel carbonate hydroxide (dpeaa)DE-He213 Sister-chromatid exchange (dpeaa)DE-He213 Replication index (dpeaa)DE-He213 Mitotic index (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Calcium homeostasis (dpeaa)DE-He213 |
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M’Bemba-Meka, Prosper Lemieux, Nicole Chakrabarti, Saroj K. |
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Elektronische Aufsätze |
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M’Bemba-Meka, Prosper |
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10.1007/s00204-006-0128-7 |
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role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes |
| title_auth |
Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes |
| abstract |
Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. © Springer-Verlag 2006 |
| abstractGer |
Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. © Springer-Verlag 2006 |
| abstract_unstemmed |
Abstract Human peripheral lymphocytes from whole blood cultures were exposed to either soluble form of nickel carbonate hydroxide (NiCH) (0–60 μM), or of nickel subsulfide ($ Ni_{3} %$ S_{2} $) (0–120 μM), or of nickel oxide (NiO) (0–120 μM), or nickel sulfate ($ NiSO_{4} $) (0–120 μM) for a short duration of 2 h. The treatments occurred 46 h after the beginning of the cultures. The cultures were harvested after a total incubation of 72 h, and sister-chromatid exchange (SCE), replication index (RI), and mitotic index (MI) were measured for each nickel compound. The soluble form of NiCH at 30 μM but those of $ Ni_{3} %$ S_{2} $ and NiO at 120 μM produced significant increase in the SCE per cell compared to the control value, whereas $ NiSO_{4} $ failed to produce any such significant increase. Except $ NiSO_{4} $, the soluble forms of NiCH, $ Ni_{3} %$ S_{2} $, and NiO produced significant cell-cycle delay (as measured by the inhibition of RI) as well as significant inhibition of the MI at respective similar concentrations as mentioned above. Pretreatment of human blood lymphocytes with catalase ($ H_{2} %$ O_{2} $ scavenger), or superoxide dismutase (superoxide anion scavenger), or dimethylthiourea (hydroxyl radical scavenger), or deferoxamine (iron chelator), or N-acetylcysteine (general antioxidant) inhibited NiCH-induced SCE, and changes in RI and MI. This suggests the participation of oxidative stress involving $ H_{2} %$ O_{2} $, the superoxide anion radical, the hydroxyl radical, and iron in the NiCH-induced genotoxic responses. Cotreatment of NiCH with either verapamil (inhibitor of intracellular calcium ion ([$ Ca^{2+} $]i) movement through plasma membranes), or dantrolene (inhibitor of [$ Ca^{2+} $]i release from sarcoplasmic reticulum), or BAPTA ($ Ca^{2+} $ chelator) also inhibited the NiCH-induced responses. These results suggest that [$ Ca^{2+} $]i is also implicated in the genotoxicity of NiCH. Overall these data indicate that various types of oxidative stress including iron-mediated oxidative stress involving the Fenton–Haber/Weiss reaction, and alterations in calcium homeostasis are involved in the genetic damage produced by the soluble form of NiCH. © Springer-Verlag 2006 |
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Role of oxidative stress and intracellular calcium in nickel carbonate hydroxide-induced sister-chromatid exchange, and alterations in replication index and mitotic index in cultured human peripheral blood lymphocytes |
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| score |
7.399661 |