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Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin

Received: 18 September 2016     Accepted: 19 October 2016     Published: 17 December 2016
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Abstract

Potassium dichromate (K2Cr2O7), a Cr (VI) compound, is the most toxic form of Cr (VI) and has been demonstrated to induce toxicity associated with oxidative stress in humans and animals. The wide environmental distribution of chromium leads to an increased interest of its toxicity and biological effects. Mitochondria provide most of the cellular energy (ATP) and yield many intermediate compounds involved in normal cellular metabolism. Therefore, perturbations of mitochondrial function may result in severe consequences for general metabolism and all the energy transducing processes that require ATP. The present study was designed to investigate the Cr (VI) -induced oxidative stress on mitochondria in liver and lungs. Male albino rats of Wistar strain (80-100 g) were used for the present study. Rats were divided into two groups of almost equal average body weight. The animals of one group were injected (i.p.) K2Cr2O7 at a dose of 0.8 mg per 100 g body weight per day for 28 days. The animals of the remaining group received only the vehicle (0.9% NaCl), served as control. Measurement of oxidative stress biomarkers like lipid peroxidation (MDA), conjugated dienes and nitric oxide contents were increased in both liver and lungs mitochondria. The decreased antioxidant marker enzymes like the activities of glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione-S-transferase (G-S-T), superoxide dismutase (SOD) and catalase (CAT) of Cr (VI) treated rats were accompanied by a significant decrease in the level of glutathione’s (GSH and GSSG) in liver and lungs mitochondria. The results of the present study demonstrates that the exposure of Cr (VI) at the present dose and duration caused reduction in LPO and antioxidant enzyme activities in rat’s liver and lungs mitochondria.

Published in American Journal of Applied Scientific Research (Volume 2, Issue 6)
DOI 10.11648/j.ajasr.20160206.15
Page(s) 59-64
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2016. Published by Science Publishing Group

Keywords

Chromium, Mitochondria, Oxidative Stress, Tissues

References
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    Durga Pada Dolai, Sankar Kumar Dey, Sandeep Kumar Dash, Somenath Roy. (2016). Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin. American Journal of Applied Scientific Research, 2(6), 59-64. https://doi.org/10.11648/j.ajasr.20160206.15

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    ACS Style

    Durga Pada Dolai; Sankar Kumar Dey; Sandeep Kumar Dash; Somenath Roy. Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin. Am. J. Appl. Sci. Res. 2016, 2(6), 59-64. doi: 10.11648/j.ajasr.20160206.15

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    AMA Style

    Durga Pada Dolai, Sankar Kumar Dey, Sandeep Kumar Dash, Somenath Roy. Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin. Am J Appl Sci Res. 2016;2(6):59-64. doi: 10.11648/j.ajasr.20160206.15

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  • @article{10.11648/j.ajasr.20160206.15,
      author = {Durga Pada Dolai and Sankar Kumar Dey and Sandeep Kumar Dash and Somenath Roy},
      title = {Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin},
      journal = {American Journal of Applied Scientific Research},
      volume = {2},
      number = {6},
      pages = {59-64},
      doi = {10.11648/j.ajasr.20160206.15},
      url = {https://doi.org/10.11648/j.ajasr.20160206.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajasr.20160206.15},
      abstract = {Potassium dichromate (K2Cr2O7), a Cr (VI) compound, is the most toxic form of Cr (VI) and has been demonstrated to induce toxicity associated with oxidative stress in humans and animals. The wide environmental distribution of chromium leads to an increased interest of its toxicity and biological effects. Mitochondria provide most of the cellular energy (ATP) and yield many intermediate compounds involved in normal cellular metabolism. Therefore, perturbations of mitochondrial function may result in severe consequences for general metabolism and all the energy transducing processes that require ATP. The present study was designed to investigate the Cr (VI) -induced oxidative stress on mitochondria in liver and lungs. Male albino rats of Wistar strain (80-100 g) were used for the present study. Rats were divided into two groups of almost equal average body weight. The animals of one group were injected (i.p.) K2Cr2O7 at a dose of 0.8 mg per 100 g body weight per day for 28 days. The animals of the remaining group received only the vehicle (0.9% NaCl), served as control. Measurement of oxidative stress biomarkers like lipid peroxidation (MDA), conjugated dienes and nitric oxide contents were increased in both liver and lungs mitochondria. The decreased antioxidant marker enzymes like the activities of glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione-S-transferase (G-S-T), superoxide dismutase (SOD) and catalase (CAT) of Cr (VI) treated rats were accompanied by a significant decrease in the level of glutathione’s (GSH and GSSG) in liver and lungs mitochondria. The results of the present study demonstrates that the exposure of Cr (VI) at the present dose and duration caused reduction in LPO and antioxidant enzyme activities in rat’s liver and lungs mitochondria.},
     year = {2016}
    }
    

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  • TY  - JOUR
    T1  - Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin
    AU  - Durga Pada Dolai
    AU  - Sankar Kumar Dey
    AU  - Sandeep Kumar Dash
    AU  - Somenath Roy
    Y1  - 2016/12/17
    PY  - 2016
    N1  - https://doi.org/10.11648/j.ajasr.20160206.15
    DO  - 10.11648/j.ajasr.20160206.15
    T2  - American Journal of Applied Scientific Research
    JF  - American Journal of Applied Scientific Research
    JO  - American Journal of Applied Scientific Research
    SP  - 59
    EP  - 64
    PB  - Science Publishing Group
    SN  - 2471-9730
    UR  - https://doi.org/10.11648/j.ajasr.20160206.15
    AB  - Potassium dichromate (K2Cr2O7), a Cr (VI) compound, is the most toxic form of Cr (VI) and has been demonstrated to induce toxicity associated with oxidative stress in humans and animals. The wide environmental distribution of chromium leads to an increased interest of its toxicity and biological effects. Mitochondria provide most of the cellular energy (ATP) and yield many intermediate compounds involved in normal cellular metabolism. Therefore, perturbations of mitochondrial function may result in severe consequences for general metabolism and all the energy transducing processes that require ATP. The present study was designed to investigate the Cr (VI) -induced oxidative stress on mitochondria in liver and lungs. Male albino rats of Wistar strain (80-100 g) were used for the present study. Rats were divided into two groups of almost equal average body weight. The animals of one group were injected (i.p.) K2Cr2O7 at a dose of 0.8 mg per 100 g body weight per day for 28 days. The animals of the remaining group received only the vehicle (0.9% NaCl), served as control. Measurement of oxidative stress biomarkers like lipid peroxidation (MDA), conjugated dienes and nitric oxide contents were increased in both liver and lungs mitochondria. The decreased antioxidant marker enzymes like the activities of glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione-S-transferase (G-S-T), superoxide dismutase (SOD) and catalase (CAT) of Cr (VI) treated rats were accompanied by a significant decrease in the level of glutathione’s (GSH and GSSG) in liver and lungs mitochondria. The results of the present study demonstrates that the exposure of Cr (VI) at the present dose and duration caused reduction in LPO and antioxidant enzyme activities in rat’s liver and lungs mitochondria.
    VL  - 2
    IS  - 6
    ER  - 

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Author Information
  • Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, India

  • Department of Physiology, S. B. S. S. Mahavidyalaya, Paschim Medinipur, India

  • Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, India

  • Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, India

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