Volume 2, Issue 6, November 2016, Page: 59-64
Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin
Durga Pada Dolai, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, India
Sankar Kumar Dey, Department of Physiology, S. B. S. S. Mahavidyalaya, Paschim Medinipur, India
Sandeep Kumar Dash, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, India
Somenath Roy, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, India
Received: Sep. 18, 2016;       Accepted: Oct. 19, 2016;       Published: Dec. 17, 2016
DOI: 10.11648/j.ajasr.20160206.15      View  3176      Downloads  73
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.
Keywords
Chromium, Mitochondria, Oxidative Stress, Tissues
To cite this article
Durga Pada Dolai, Sankar Kumar Dey, Sandeep Kumar Dash, Somenath Roy, Study the Chromium-Induced Oxidative Stress on Mitochondria from Liver and Lungs Origin, American Journal of Applied Scientific Research. Vol. 2, No. 6, 2016, pp. 59-64. doi: 10.11648/j.ajasr.20160206.15
Copyright
Copyright © 2016 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Reference
[1]
Barceloux, D (1999). Chromium. Clin. Toxicol., 37:173-194.
[2]
Wang, X. F.; Xing, M. L.; Shen, Y.; Zhu, X. and Xu, L. H. (2006). Oral administration of Cr (VI) induced oxidative stress, DNA damage and apoptotic cell death in mice. Toxicology, 228: 16-23.
[3]
Dolai, D.; Tripathy, S.; Dey, S. K. and Roy, S. (2016). Review on health effects of chromium exposure: reflection from oxidative stress towards carcinogenicity. Int. J. Pharm. Bio. Sci., 7(3): (B) 343–354.
[4]
Stohs, S. J. and Bagchi, D. (1995). Oxidative mechanisms in the toxicity of metal ions. Free Radical Biol. Med., 18 (2):321-336.
[5]
Bagchi, D.; Balmoori, J.; Bagchi, M.; Ye, X.; Williams, C. B. and Stohs, S. J. (2002a). Comparative effects of TCDD, endrin, naphthalene and chromium VI on oxidative stress and tissue damage in the liver and brain tissues of mice. Toxicology, 175: 73-82.
[6]
Bagchi, D.; Stohs, S. J.; Downs, B. W.; Bagchi, M. and Preuss, H. (2002b). Cytotoxicity and oxidative mechanisms of different forms of chromium. Toxicol., 180: 5-22.
[7]
Debetto, P.; Dal Toso, R.; Varotto, R.; Bianchi, V. and Luciani, S. (1982). Effects of potassium dichromate on ATP content of mammalian cells cultured in vitro. Chem. Biol. Interact., 41(1): 15-24.
[8]
Messer, R. L. and Lucas, L. C. (2000). Cytotoxicity of nickel-chromium alloys: Bulk alloys compared to multiple ion salt solutions. Dent. Mater., 16: 207-212.
[9]
Lazzarini, A.; Luciani, S.; Beltrami, M. and Arslan, P. (1985). Effects of Chromium (VI) and Chromium (III) on energy Charge and oxygen consumption in Rat thermosytes. Chem. Biol. Interact., 53(3): 273-281.
[10]
Ryberg, D. and Alexander, J. (1984). Inhibitory action of hexavalent chromium (Cr (VI)) on the mitochondrial respiration and a possible coupling to the reduction of Cr (VI). Biochem. Pharmacol., 33: 2461-2466.
[11]
Ryberg, D. and Alexandar, A. (1990). Mechanism of Chromium toxicity in mitochondria.. Chem. Biol. Interact., 75(2):141-151.
[12]
Bianchi, V.; Debetto, P.; Zantedeschi, A. and Levis, A. G. (1982). Effects of hexavalent chromium on the adenylate pool of hamster fibroblasts. Toxicology., 25(1):19-30.
[13]
Shi, X.; Dalal, N. S. and Vallyathan, V. (1991). One-electron reduction of carcinogen chromate by microsomes, mitochondria, and Escherichia coli: Identification of Cr (V) and OH radical. Arch. Biochem. Biophys., 290(2): 381-386.
[14]
Travacio, M.; María Polo, J. and Llesuy, S. (2000). Chromium (VI) induces oxidative stress in the mouse brain. Chromium (VI) induces oxidative stress in the mouse brain. Toxicology, 150(1-3):137-146.
[15]
Dey, S. K.; Nayak, P. and Roy, S. (2003). Alpha-tocopherol supplementation on chromium toxicity: a study on rat liver and kidney cell membrane. J. Environ. Sci., 15: 356-359.
[16]
Gazotti, P.; Malmstron, K. and Crompton, M. A. (1979). Laboratory manual on transport and bioenergetics. In: Carofoli E, Semanza G, editors. Membrane Biochemistry. New York: Springer-Verlag, 62-69.
[17]
Ohkawa. H,; Ohisi, N. and Yagi, K. (1979). Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal. Biochem., 95: 351-358.
[18]
Slater, T. I. (1980). Overview of methods used for detecting lipid peroxidation. Methods Enzymol., 105: 283-293.
[19]
Sanai, S.; Tomisato, M.; Shinsuka, N.; Mayoko, Y.; Mayoko, H. and Akio, N. (1998). Protective role of nitric oxide in S. aurues infection in mice. Infect. Immun. 66: 1017–1028. PMID: 9488390.
[20]
Griffith, O. W. (1980). Determination of glutathione and glutathione sulfide using glutathione reductase and 2-vinyl pyridine. Anal. Biochem., 106: 207-212.
[21]
Aebi, H. (1984). Catalase in vitro. Methods Enzymol, 105: 121–126.
[22]
Marklund, S. and Marklund, G. (1974). Involvement of superoxide anion radical in autoxidation of pyrogallol and a convenient assay of superoxide dismutase. Eur. J. Biochem., 47: 469-474.
[23]
Paglia, D. E. and Valentine, W. N. (1967). Studies on quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J. Lab. Clin. Med., 70: 158–169.
[24]
Miwa, S. (1972). Hematology, In: Modern Medical Techonology, 3: 306-310.
[25]
Habig, W. H.; Pabst, M. J. and Jakoby, W. B. (1974). Glutathone S-transferases, the first enzymatic step in mercapturic acid formation. J. Biol. Chem., 249: 7130-7139.
[26]
Lowry, O. H.; Roseborough, N. J.; Farr, A. L. and Randll, A. J. (1951). Protein measurement with Folin’s phenol reagent. J. Biol. Chem., 193: 265-275.
[27]
Bagchi, D.; Hossoun, E. A.; Bagchi, M. and Stohs, S. J. (1995). Chromium-induced excretion of urinary lipid metabolites, DNA damage, nitric oxide production and generation of reactive oxygen species in Sprague-Dawley rats. Comp. Biochem. Physiol. C Pharmacol. Toxicol. Endocrinol, 110(2): 177-187.
[28]
Nordbeg, J. and Arner, E. S. (2001). Reactive oxygen species, antioxidants, and the mammalian thioredoxin system. Free Radical Biol. Med., 31: 1287-1312.
[29]
Poderoso, J. J.; Carreras, M. C.; Lisdero, C.; Riobo, N.; Schopfer, F. and Boveris, A. (1996). Nitric oxide inhibits electron transfer and increases superoxide radical production in rat heart mitochondria and submitochondrial particles. Arch. Biochem. Biophys., 328: 85-92.
[30]
Cassina, A. and Radi, R. (1996). Differential inhibitory action of nitric oxide and peroxynitrite on mitochondrial electron transport. Arch. Biochem. Biophys., 328: 309-316.
[31]
Radi, R.; Cassina, A. and Hodara, R. (2002). Nitric oxide and peroxynitrite interactions with mitochondria. Biol. Chem., 383: 401-409.
[32]
Srinivasan, K.; Narayanan, S.; Ananthasadagopan, S. and Ganapasam, S. (2008). Chromium (VI)-induced oxidative stress and apoptosis is reduced by garlic and its derivative S-allylcysteine through the activation of Nrf2 in the hepatocytes of Wistar rats. J. Appl. Toxicol., 28:908-919.
[33]
Pedraza-Chaverri, J.; Barrera, D.; Medina-Campos, O.N.; Carvajal, R.C.; Hernandez-Pando, R.; Macias-Ruvalcaba, N.A. et al. (2005). Time course study of oxidative and nitrosative stress and antioxidant enzymes in K2Cr2O7-induced nephrotoxicity. BMC Nephrol., 26: 6-14.
[34]
Radi, R.; Turrens, J. F.; Chang, I. Y.; Bush. K. M.; Crapo, J. D. and Freeman, B. A. (1991). Detection of catalase in rat heart mitochondria. J. Biol. Chem., 266: 22028-22034.
[35]
Phung, C. D.; Ezieme, J. A. and Turrens, J. F. (1994). Hydrogen peroxide metabolism in skeletal muscle mitochondria. Arch. Biochem. Biophys., 315: 479-482.
[36]
Ueno, S.; Susa, N.; Furukawa, Y.; Aikawa, K.; Itagaki, I.; Komiyama, T. and Takashima, Y. (1988). Effect of chromium on lipid peroxidation in isolated rat hepatocytes, Japanese Journal of Veterinary Science, 50: 45-52.
[37]
Rao, A. V. and Shaha, C. (2001). Multiple glutathione S-transferase isoforms are present on male germ cell plasma membrane. FEBS Lett., 507:174-180.
[38]
Lu, S. C. (1999). Regulation of hepatic glutathione synthesis: current concepts and controversies. FASEB J., 13: 1169-1183.
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