The prophylactic effect of ethanolic extract of Irvingia gabonensis stem bark on cadmium-induced oxidative damage in male albino rats’ liver was investigated. Male Wistar rats were divided into control, cadmium, and treatment groups. In the prophylactic experiment, Irvingia gabonensis (200 and 400？mg/kg body weight) was administered by oral gavage for 21 days before exposure to cadmium. Antioxidant marker enzymes such as reduced glutathione (GSH) levels, catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and lipid peroxidation (LPO) were determined in the liver and heart alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were monitored and histological examination was carried out. Results indicate that cadmium-induced rats had significantly increased relative weight of liver and heart when compared to controls. Treatment with Irvingia gabonensis at 200 and 400？mg/kg caused a significant decrease in relative weight of the organs. In cadmium-induced rats, serum ALT and AST activities and levels of LPO were increased whereas hepatic and cardiac marker enzymes significantly decreased. Furthermore, histological alteration in liver and aorta was observed in cadmium untreated rats and was ameliorated in cadmium rats treated with Irvingia gabonensis. In conclusion, the extract indicates antioxidant and hepatoprotective properties that eliminate the deleterious effects of toxic metabolites of cadmium. 1. Introduction It has become obvious that humans have adjusted the global cycle of heavy metals and metalloids, including the toxic non-essential like cadmium. Thus there is enough opportunity for exposure to cadmium both inside and outside the workplace [1]. Cadmium (Cd) is one of the toxic hnavy metals and increased concentration of Cd in agricultural soils is to come from application of phosphate fertilizers, sewage sludge, waste water, and pesticides [2]. Further sources of cadmium drawn from mining at mines, smelting of ores, and industrial application of Cd in pigments, plastic stabilizers, and nickel cadmium batteries resulted in widespread agricultural soil pollution [3]. Cadmium is a risk reason for humans. It amasses in the body tissues, such as the liver, lungs, kidneys, bones, and reproductive organs [4, 5]. Liu et al. [6] reported that Cd creates reactive oxygen species (ROS) causing oxidative damage in various tissues. It is shown that exposure to Cd by different routes causes increased lipid peroxidation (LPO) in membranes of erythrocytes and tissues, where thiobarbituric acid reactive substances
References
[1]
P. Vinoth Kumar, A. Amala Bricey, V. Veera Thamari Selvi, C. Sudheer Kumar, and N. Ramesh, “Antioxidant effect of green tea extract in cadmium chloride intoxicated rats,” Advances in Applied Science Research, vol. 1, no. 2, pp. 9–13, 2010.
[2]
Z. Limei, L. Xiaoyong, C. Tongbin, et al., “Regional assessment of cadmium pollution in agricultural lands and the potential health risk related to intensive mining activities: a case study in Chenzhou City, China,” Journal of Environmental Sciences, vol. 20, no. 6, pp. 696–703, 2008.
[3]
X.-Y. Liao, T.-B. Chen, H. Xie, and Y.-R. Liu, “Soil As contamination and its risk assessment in areas near the industrial districts of Chenzhou City, Southern China,” Environment International, vol. 31, no. 6, pp. 791–798, 2005.
[4]
S. Thijssen, J. Maringwa, C. Faes, I. Lambrichts, and E. van Kerkhove, “Chronic exposure of mice to environmentally relevant, low doses of cadmium leads to early renal damage, not predicted by blood or urine cadmium levels,” Toxicology, vol. 229, no. 1-2, pp. 145–156, 2007.
[5]
S. M. Alvarez, N. N. Gómez, L. Scardapane, M. W. Fornés, and M. S. Giménez, “Effects of chronic exposure to cadmium on prostate lipids and morphology,” BioMetals, vol. 20, no. 5, pp. 727–741, 2007.
[6]
J. Liu, S. Y. Qian, Q. Guo et al., “Cadmium generates reactive oxygen- and carbon-centered radical species in rats: insights from in vivo spin-trapping studies,” Free Radical Biology and Medicine, vol. 45, no. 4, pp. 475–481, 2008.
[7]
T. Jahangir, T. H. Khan, L. Prasad, and S. Sultana, “Alleviation of free radical mediated oxidative and genotoxic effects of cadmium by farnesol in Swiss albino mice,” Redox Report, vol. 10, no. 6, pp. 303–310, 2005.
[8]
V. Eybl, D. Kotyzová, L. Le？eticky, M. Bludovská, and J. Koutensky, “The influence of curcumin and manganese complex of curcumin on cadmium-induced oxidative damage and trace elements status in tissues of mice,” Journal of Applied Toxicology, vol. 26, no. 3, pp. 207–212, 2006.
[9]
D. Swarup, R. Naresh, V. P. Varshney et al., “Changes in plasma hormones profile and liver function in cows naturally exposed to lead and cadmium around different industrial areas,” Research in Veterinary Science, vol. 82, no. 1, pp. 16–21, 2007.
[10]
M. Valko, H. Morris, and M. T. D. Cronin, “Metals, toxicity and oxidative stress,” Current Medicinal Chemistry, vol. 12, no. 10, pp. 1161–1208, 2005.
[11]
M. Abd-El-Baset and A. Abd El-reheem, “The roles of honeybee solution on the physiological parameters of rats exposed to cadmium chloride,” Australian Journal of Basic and Applied Sciences, vol. 2, pp. 1438–1453, 2008.
[12]
A. Abd-El-Reheem and S. Zaahkcuk, “Protective effect of Vitamin C and selenium against the toxicity induced by lead acetate on some physiological parameters in blood of male albino rats,” Bulletin of the Physiological Society of Egypt, vol. 27, pp. 59–76, 2007.
[13]
S. O. Asagba, G. E. Eriyamremu, M. A. Adaikpoh, and A. Ezeoma, “Levels of lipid peroxidation, superoxide dismutase, and Na +/K+ ATPase in some tissues of rats exposed to a Nigerian-like diet and cadmium,” Biological Trace Element Research, vol. 100, no. 1, pp. 75–86, 2004.
[14]
B. I. Ognjanovi？, S. D. Markovi？, N. Z. Ethordevi？, et al., “Cadmium-induced lipid peroxidation and changes in antioxidant defense system in the rat testes: protective role of coenzyme Q (10) and vitamin E,” Reproductive Toxicology, vol. 29, pp. 191–197, 2010.
[15]
J. R. Lee, S. J. Park, H.-S. Lee et al., “Hepatoprotective activity of licorice water extract against Cadmium-induced toxicity in rats,” Evidence-Based Complementary and Alternative Medicine, vol. 6, no. 2, pp. 195–201, 2009.
[16]
E. Kowalczyk, A. Kopff, P. Fija？kowski et al., “Effect of anthocyanins on selected biochemical parameters in rats exposed to cadmium,” Acta Biochimica Polonica, vol. 50, no. 2, pp. 543–548, 2003.
[17]
J. L. Reyes, M. Lamas, D. Martin et al., “The renal segmental distribution of claudins changes with development,” Kidney International, vol. 62, no. 2, pp. 476–487, 2002.
[18]
A. S. El-Sharaky, A. A. Newairy, M. M. Badreldeen, S. M. Eweda, and S. A. Sheweita, “Protective role of selenium against renal toxicity induced by cadmium in rats,” Toxicology, vol. 235, no. 3, pp. 185–193, 2007.
[19]
S. Satarug, S. H. Garrett, M. A. Sens, and D. A. Sens, “Cadmium, environmental exposure, and health outcomes,” Environmental Health Perspectives, vol. 118, no. 2, pp. 182–190, 2010.
[20]
R. E. Graham, A. C. Ahn, R. B. Davis, B. B. O'Connor, D. M. Eisenberg, and R. S. Phillips, “Use of complementary and alternative medical therapies among racial and ethnic minority adults: results from the 2002 national health interview survey,” Journal of the National Medical Association, vol. 97, no. 4, pp. 535–545, 2005.
[21]
E. Ernst, “When natural is not harmless,” International Journal of Clinical Practice, vol. 60, no. 4, p. 380, 2006.
[22]
A. A. Shati and F. G. Elsaid, “Effects of water extracts of thyme (Thymus vulgaris) and ginger (Zingiber officinale Roscoe) on alcohol abuse,” Food and Chemical Toxicology, vol. 47, no. 8, pp. 1945–1949, 2009.
[23]
T. J. Nangue, H. M. Womeni, F. T. Mbiapo, J. Fanni, and L. Michel, “Irvingia gabonensis fat: nutritional properties and effect of increasing amounts on the growth and lipid metabolism of young rats wistar sp,” Lipids in Health and Disease, vol. 10, article 43, 2011.
[24]
A. R. S. Dienagha and T. O. Miebi, “Energy requirments for cracking dika (Ogbono) nuts (Irvingia Gabonensis),” European Journal of Scientific Research, vol. 59, no. 2, pp. 208–215, 2011.
[25]
R. Srinivasan, M. J. N. Chandrasekar, M. J. Nanjan, and B. Suresh, “Antioxidant activity of Caesalpinia digyna root,” Journal of Ethnopharmacology, vol. 113, no. 2, pp. 284–291, 2007.
[26]
O. H. Lowry, N. J. Rosebrough, A. L. Farr, and R. J. Randall, “Protein measurement with the Folin phenol reagent,” The Journal of Biological Chemistry, vol. 193, no. 1, pp. 265–275, 1951.
[27]
A. F. Mohun and I. J. Cook, “Simple methods for measuring serum levels of the glutamic-oxalacetic and glutamic-pyruvic transaminases in routine laboratories.,” Journal of clinical pathology, vol. 10, no. 4, pp. 394–399, 1957.
[28]
S. Reitman and S. Frankel, “A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases,” The American Journal of Clinical Pathology, vol. 28, no. 1, pp. 56–63, 1957.
[29]
J. A. Buege and S. D. Aust, “Microsomal lipid peroxidation,” Methods in Enzymology, vol. 52, no. C, pp. 302–310, 1978.
[30]
J. M. McCord and I. Fridovich, “Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein),” Journal of Biological Chemistry, vol. 244, no. 22, pp. 6049–6055, 1969.
[31]
H. Aebi, “Catalase estimation,” in Methods of Enzymatic Analysis, H. V. Bergmeyer, Ed., pp. 673–684, Verlag Chemic, 1974.
[32]
E. Beutler, O. Duron, and B. M. Kellin, “Improved method for the determination of blood glutathione,” The Journal of Laboratory Clinical Medicine, vol. 61, pp. 882–888, 1963.
[33]
J. T. Rotruck, A. L. Pope, H. E. Ganther, A. B. Swanson, D. G. Hafeman, and W. G. Hoekstra, “Selenium: biochemical role as a component of glatathione peroxidase,” Science, vol. 179, no. 4073, pp. 588–590, 1973.
[34]
B. Fuhrman and M. Aviram, “Flavonoids protect LDL from oxidation and attenuate atherosclerosis,” Current Opinion in Lipidology, vol. 12, no. 1, pp. 41–48, 2001.
[35]
T. Sajeesh, K. Arunachalam, and T. Parimelazhagan, “Antioxidant and antipyretic studies on Pothos scandens L,” Asian Pacific Journal of Tropical Medicine, vol. 4, no. 11, pp. 889–899, 2011.
[36]
F. M. El-Demerdash, M. I. Yousef, and F. M. E. Radwan, “Ameliorating effect of curcumin on sodium arsenite-induced oxidative damage and lipid peroxidation in different rat organs,” Food and Chemical Toxicology, vol. 47, no. 1, pp. 249–254, 2009.
[37]
M. Rahman, M. Tondel, and S. A. Ahmad, “Diabetes mellitus associated with arsenic exposure in Bangladesh,” American Journal of Epidemiology, vol. 148, no. 2, pp. 198–203, 1998.
[38]
R. C. Kaltreider, A. M. Davis, J. P. Lariviere, and J. W. Hamilton, “Arsenic alters the function of the glucocorticoid receptor as a transcription factor,” Environmental Health Perspectives, vol. 109, no. 3, pp. 245–251, 2001.
[39]
S. J. Stohs and D. Bagchi, “Oxidative mechanisms in the toxicity of metal ions,” Free Radical Biology and Medicine, vol. 18, no. 2, pp. 321–336, 1995.
[40]
T. Koizumi and Z. G. Li, “Role of oxidative stress in single-dose, cadmium-induced testicular cancer,” Journal of Toxicology and Environmental Health, vol. 37, no. 1, pp. 25–36, 1992.
[41]
M. Waisberg, P. Joseph, B. Hale, and D. Beyersmann, “Molecular and cellular mechanisms of cadmium carcinogenesis,” Toxicology, vol. 192, no. 2-3, pp. 95–117, 2003.
[42]
S. J. Stohs, D. Bagchi, E. Hassoun, and M. Bagchi, “Oxidative mechanisms in the toxicity of chromium and cadmium ions,” Journal of Environmental Pathology, Toxicology and Oncology, vol. 19, no. 3, pp. 201–213, 2000.
[43]
S. Milton Prabu, J. Renugadevi, and T. Ramesh Kumar, “Ameliorative effect of selenium against cadmium induced biochemical alterations in Cirrhinus mrigala (Hamilton),” Asian Journal of Biosciences, vol. 2, pp. 143–148, 2007.
[44]
L. Chen, L. Liu, and S. Huang, “Cadmium activates the mitogen-activated protein kinase (MAPK) pathway via induction of reactive oxygen species and inhibition of protein phosphatases 2A and 5,” Free Radical Biology and Medicine, vol. 45, no. 7, pp. 1035–1044, 2008.
[45]
C. O. Ikediobi, V. L. Badisa, L. T. Ayuk-Takem, L. M. Latinwo, and J. West, “Response of antioxidant enzymes and redox metabolites to cadmium-induced oxidative stress in CRL-1439 normal rat liver cells.,” International journal of molecular medicine, vol. 14, no. 1, pp. 87–92, 2004.
[46]
M. Uchida, H. Teranishi, K. Aoshima, T. Katoh, M. Kasuya, and H. Inadera, “Reduction of erythrocyte catalase and superoxide dismutase activities in male inhabitants of a cadmium-polluted area in Jinzu river basin, Japan,” Toxicology Letters, vol. 151, no. 3, pp. 451–457, 2004.
[47]
J. Renugadevi and S. M. Prabu, “Cadmium-induced hepatotoxicity in rats and the protective effect of naringenin,” Experimental and Toxicologic Pathology, vol. 62, no. 2, pp. 171–181, 2010.
[48]
I. Messaoudi, J. El Heni, F. Hammouda, K. Sa？d, and A. Kerkeni, “Protective effects of selenium, zinc, or their combination on cadmium-induced oxidative stress in rat kidney,” Biological Trace Element Research, vol. 130, no. 2, pp. 152–161, 2009.
[49]
E. Casalino, G. Calzaretti, C. Sblano, and C. Landriscina, “Molecular inhibitory mechanisms of antioxidant enzymes in rat liver and kidney by cadmium,” Toxicology, vol. 179, no. 1-2, pp. 37–50, 2002.
