Effects of short term exposure of atrazine on the liver and kidney of normal and diabetic rats.
Numerous environmental chemicals (ECs) affecting the endocrine activity in humans are included under endocrine disrupting compounds (EDCs) (e.g., polychlorinated biphenyls, bisphenol A, methoxychlor, and atrazine) [1, 2] which are hazardous to the reproductive health of fish and amphibians wild life. But their impact on mammals, particularly humans, is less clear . Atrazine (2-chloro-4-ethylamino-6-isopropylamino-1,3,5-triazine) is a triazine herbicide that is widely used as a preemergence and postemergence herbicide for the control of weeds in maize, sorghum, pineapple, sugar cane, and cereals [4, 5]. Because of its widespread use, residues of atrazine, its metabolites deethylatrazine, and other derivatives contaminated both ground water and surface water for several years. Atrazine is resistant to degradation and has a half-life about 95-350 days . Atrazine exposure is associated with severe health problems such as cancer, neurologic diseases, dermatologic diseases, and respiratory disorders . So the researchers around the globe are mainly concerned and interested to study the adverse effects of atrazine .
Diabetes mellitus (DM) is a group of heterogeneous, hormonal, and metabolic disorders characterized by hyperglycemia and glucosuria, resulting from defects in insulin secretion, insulin action, or both . Hyperglycemia can induce the increased production of free radicals both reactive oxygen species (ROS) and reactive nitrogen species (RNS) by various means such as mitochondrial respiratory system, glucose autoxidation and activation of the polyol pathway, formation of advanced glycation end-products (AGEs), and antioxidant enzyme inactivation. At high concentration, free radicals damage major cellular components, including nucleic acids , proteins and amino acids , and lipids . The prevalence of diabetes varied from 9% to 16.6% in different regions of India, with the southern region having higher prevalence rates than other regions . The aspect of environmental pollution is of great importance, particularly in developing countries, like India, where environmental pollution and diabetes are rampant. Therefore, the present study aimed to investigate the effects of atrazine in normal and diabetic rats.
The primary target of atrazine in humans and animals is the endocrine (hormonal) system. Effects reported in adults (human and experimental animals) include shortening of estrous cycle length, attenuation of the LH (luteinizing hormone) surge, decreases in pituitary hormone levels, ovarian histopathology (changes in ovarian tissue), and liver effects including increased serum lipids and liver enzymes and liver histopathology. Other effects on the central nervous system, immune system, and cardiovascular function have been reported in adults. Exposure to atrazine may be associated with some types of non-Hodgkin's lymphoma in adult humans. Significantly increased risk of preterm delivery, intrauterine growth retardation, and decreased birth weight were associated with atrazine concentrations in drinking water .
Pesticides can suppress the expression of functional glucose transporter proteins in several organs, providing a hypothetical mechanism for the observed link between these chemicals and insulin resistance . Exposure to atrazine (ATZ) can cause mitochondrial toxicity and insulin resistance, with even more negative effects observed when animals were fed with high-fat diet .
Atrazine (ATZ) is an herbicide which binds irreversibly to the plastoquinone binding sites of photosystem complex II on thylakoid membranes in chloroplasts, thereby inhibiting electron transport. As mitochondrial electron transfer chain (ETC) complexes I and III also have similar Q binding sites, we hypothesized that ATZ might bind to these mitochondrial sites and cause mitochondrial dysfunction. Recently, scientific evidence supports a connection between environmental chemical exposures, which includes herbicides, and development of type 2 diabetes . Prevalence of diabetes among the human population and exposure to toxicants may further aggravate the disease like diabetes. However, there is limited information about the link between influences of atrazine on diabetes. Thus, the purpose of the study was to determine the effects of low concentrations of ATZ on diabetes in vivo.
2. Materials and Methods
2.1. Animals. Adult male Wistar rats, weighing about 120-180 g, were procured from an authorized vendor (Sri Raghavendra Enterprises, Bangalore, India). The animals were housed in plastic cages under standard conditions of 12 h light/12 h dark with an ambient temperature of 24[degrees]C [+ or -] 2[degrees]C. They were fed with normal pelletized chow as diet and water ad libitum. The experimental animals handled as per the guidelines of Committee for the Purpose of Control and Supervision on Experiments on Animals (CPCSEA) which were approved by the Institutional Animal Ethics Committee (IAEC approval number: PU/SLS/IAEC/2014/11, dated 20/02/2014) of Pondicherry University, Puducherry, India.
2.2. Experimental Plan. Animals were divided into four groups with four rats each. Groups I and II were normal (nondiabetic) rats and Groups III and IV were diabetic rats. Group I (normal control rats-NC): animals were given 300 [micro]L of safflower oil, orally; Group II (atrazine treated rats-NA): animals were given atrazine (300 [micro]g [kg.sup.-1] body weight/rat/day) (Sigma Aldrich, 98.8% purity) dissolved in safflower oil, orally; Group III (diabetic control rats-DC): diabetic animals were given safflower oil, orally; Group IV (atrazine treated diabetic rats-DA): diabetic animals were given atrazine (300 [micro]g [kg.sup.-1] body weight/rat/day) dissolved in safflower oil, orally. The treatment was continued to all the groups for a period of 15 days.
2.3. Induction of Diabetes. Diabetes was induced in Groups III and IV rats fed with high fat diet (HFD) for four weeks followed by the intraperitoneal injection of a single dose of streptozotocin (STZ: 35mg kg body weight). HFD (58% fat, 25% protein, and 17% carbohydrate) was freshly prepared daily in sterile condition with the composition of 365 g normal pelletized rat chow, 310 g lard oil, 250 g casein, 10 g cholesterol, 60 g vitamin, and mineralmix, 3 gmethionine, 1 g yeast, and 1 g sodium chloride. After 72 h of STZ induction, animals showing higher blood glucose levels (>140mg/dL) were considered as diabetic [17, 18].
At the end of the experimental period, the overnight fasted animals were euthanized by cervical dislocation. Blood was collected and allowed to clot, and then the blood samples were centrifuged at 1500 rpm for 15 min to collect the serum. Liver and kidneys were dissected out of rats, washed in ice-cold 1.15% potassium chloride (KCl) solution, and pat-dried and the wet weight was noted. The separated serum and tissues were stored at -80[degrees]C until analysis.
2.4. Biochemical Parameters. Tissues (liver and kidney) were homogenized in 1x phosphate buffered saline (PBS) pH 7.4 that contained 8 g of sodium chloride (NaCl), 0.2 g of KCl, 1.4 g of disodium hydrogen phosphate ([Na.sub.2][HPO.sub.4]), and 0.24 g of potassium dihydrogen phosphate ([KH.sub.2][PO.sub.4]), and the homogenate was centrifuged at 10 000 xg for 15 min at 4[degrees]C. The supernatant was collected for analyzing the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) by S. Marklund and G. Marklund method , Claiborne method , and Rotruck et al. method , respectively. The levels of lipid peroxidation (LPO) and reduced glutathione (GSH) content were analyzed by Ohkawa et al. method  and Ellman's  method, respectively. Serum parameters like alanine amino transferase (ALT), aspartate amino transferase (AST), alkaline phosphatase (ALP), urea, and creatinine were estimated by commercially available kits (Agappe Diagnostics, Kerala, India). Blood glucose levels were determined by the kit method (Agappe Diagnostics Ltd., Kerala, India). Values were expressed as mg/dL.
2.5. Statistical Analysis. Data were analyzed using SPSS software version 16 and one-way analysis of variance (ANOVA) followed by Tukey's test and the results were expressed as mean [+ or -] SD; P = 0.05 was considered significant.
3. Results and Discussion
3.1. Effect of Atrazine on Body Weight and Organ Weights. Pesticide exposure usually causes a decrease in body weight and organ weights of animals [23-26]. The changes in the body weight and organ weights of animals are shown in Table 1. In the present study, atrazine administration resulted in increased body weight in all experimental rats during the experimental period. An increase in liver weight and kidney weight was noted in atrazine treated rats compared to normal control rats, whereas increased liver weight but decreased kidney weight was observed in atrazine treated diabetic rats compared to diabetic control rats.
Unchanged or decreased body weights with the administration of atrazine were also reported [27-30]. The decreased body weight and organ weight (i.e., liver and kidney) after atrazine treatment could be due to reduced diet intake or due to necrotic changes in different body tissues . In contrast, in our study, an increased body weight was observed with the atrazine administration. The increase in body weight in our study, particularly in atrazine treated rats (Group II), might be due to increased insulin resistance and hence led to normal weight gain. Our results are similar to a previous study by Gojmerac et al.  who have reported increased body weights in rats with the chronic administration of atrazine at low concentrations (30 or 300 [micro]g [kg.sup.-1]).
3.2. Effect of Atrazine on Lipid Peroxidation. Atrazine administration resulted in a nonsignificant increase in MDA concentration in both liver and kidney of atrazine treated as well as atrazine treated diabetic rats compared to their respective control groups (Figure 1). Exposure to pesticides is known to induce lipid peroxidation which is responsible for adverse biological effects [14, 33, 34]. Mechanism of pesticide toxicity is usually associated with the increased lipid peroxidation in the liver . Reactive oxygen species such as superoxide anions, hydroxyl radicals, and hydrogen peroxide enhance the oxidative process and induce peroxidative damage to membrane lipids. Though nonsignificant, in the present study an increased LPO was observed in both liver and kidney which might be one of the molecular mechanisms involved in atrazine induced toxicity.
Oxidative stress has been postulated as an important contributing factor in diabetes mellitus . Chronic hyperglycemia induces carbonyl stress which in turn can lead to increased oxidation of lipids . STZ-induced diabetes in rats resulted in increased thiobarbituric acid (TBARS) level  which is an indirect evidence of intensified free radical production. The increased concentration of lipid peroxides may propagate oxidative damage by increasing peroxy and hydroxyl radicals.
3.3. Effect of Atrazine on Blood Glucose Levels. Significant changes were observed in blood glucose levels in diabetic control and diabetic atrazine rats when compared to normal rats. However, no significant change in the blood glucose levels was observed between diabetic control and diabetic atrazine treated rats (Table 1).
3.4. Effect of Atrazine on the Activities of Antioxidant Enzymes (SOD, CAT, and GPx) and on the GSH Content in Liver and Kidney. The antioxidant enzymes including SOD, CAT, and GPx protect against oxidative stress by converting free radicals or reactive oxygen intermediates to nonradical products . SOD provides the first line of defense against oxygen derived free radicals which decreases oxidative stress by dismutation of [O.sup.2-] . It is clearly evident from Figure 2 that atrazine administration led to increased SOD activity in both liver and kidney of atrazine treated as well as atrazine treated diabetic rats compared to normal control and diabetic control rats, respectively. The increased SOD activity was not significant in both liver and kidney of atrazine treated rats compared to normal control rats. However, the increased SOD activity was found to be significant (P [less than or equal to] 0.05) in the kidney but not significant in the liver of atrazine treated diabetic rats compared to diabetic control rats.
The increase in superoxide dismutase activity after atrazine administration appears to be an adaptive response to increased generation of reactive oxygen species. It has been reported in the literature that exposure of animals to xenobiotics increases SOD activity in various tissues .
Catalase and glutathione peroxidase are the two antioxidant enzymes which remove hydrogen peroxide. Changes in the activities of CAT in liver and kidney are depicted in Figure 3. Atrazine administration also led to increased CAT activity in both liver and kidney of atrazine treated as well as atrazine treated diabetic rats compared to normal control and diabetic control rats, respectively. This increase was significant (P [less than or equal to] 0.05) only in the liver of atrazine treated diabetic rats compared to diabetic control rats. Changes in the activities of GPx in liver and kidney are depicted in Figure 4. Atrazine administration led to increased GPx activity but not significantly in both liver and kidney of atrazine treated and atrazine treated diabetic rats compared to normal control and diabetic control rats, respectively. The increase in the activities of SOD, CAT, and GPx in this study reflects compensatory mechanism to increased oxidative stress.
Reduced glutathione (GSH) is the major intracellular thiol that plays a critical role in the cellular defense against oxidative stress. Changes in the level of reduced glutathione content in liver and kidney are depicted in Figure 5. Atrazine administration resulted in a significant (P [less than or equal to] 0.05) decrease in glutathione content in both liver and kidney of atrazine treated diabetic rats compared to diabetic control rats. Also, decreased GSH content was observed in atrazine treated rats compared to normal control rats, but this decrease was not significant.
Glutathione (GSH) is the most abundant antioxidant in body fluids and tissues. It scavenges the free radicals and thus protects the tissues from oxidative stress. GSH also participates in the detoxification of hydrogen peroxide by various glutathione peroxidases. However, reduced levels of GSH in the liver and kidney were also observed in this study suggesting that administration of low dose of atrazine might contribute to increased oxidative stress and thereby increased tissue damage.
Decrease in GSH levels after administration of various pesticides was observed . A decrease in GSH content in the liver of rats after atrazine exposure indicated prooxidant conditions in the liver.
In conclusion, atrazine induced early hepatic oxidative stress triggered defense mechanisms, that is, increased SOD and CAT activities, to maintain the integrity of the liver.
3.5. Effect of Atrazine on Liver and Kidney Damage Biomarkers. Changes in the liver markers (AST, ALT, and ALP) and kidney markers (creatinine and urea) are represented in Table 2. Atrazine administration led to increased levels of liver markers (AST, ALT, and ALP) as well as kidney markers (creatinine and urea) in both atrazine treated and atrazine treated diabetic rats.
The significantly higher AST and ALT activities in animals exposed to atrazine (300 [micro]g [kg.sup.-1] body weight) when compared with control groups are due to the leakage of aminotransferase (AT) enzymes from injured liver cells. These results are similar to other studies . On the contrary, another study reported that rats treated with 400mg [kg.sup.-1] atrazine for 14 consecutive days resulted in nonsignificant elevation in serum ALT enzyme . ALT is thought to be more specific for hepatic injury because it is present mainly in the cytosol of the liver and in low concentrations elsewhere . The elevation of ALT in the current study was attributed specifically to the injury of liver cells caused by atrazine , whereas the AST is a mitochondrial enzyme found in the heart, liver, skeletal muscle, and kidney and is normally present in plasma . The elevated serum AST is apparently due to mitochondrial damage by reactive oxygen species (ROS) induced by atrazine .
Atrazine exposure resulted in a significant increase in serum creatinine and urea in atrazine treated and atrazine treated diabetic rats when compared to normal control rats and diabetic control rats, respectively. Nephrotoxicity of atrazine is a consequence of its elimination through the kidneys which leads to a decrease in creatinine clearance and proteinuria. These results are in agreement with the previous report by Liu et al. .
An increase in the activity of ALP in serum may reflect pathologic changes in the liver. The serum level of both ALP and ALT is used as a marker of the cell membrane integrity. The injurious effects of atrazine may result from its generation of ROS that causes oxidative stress of various organs. Increased oxidative stress and lipid peroxidation are implicated in the pathogenesis of herbicide-induced hepatic injury .
From the above results, it can be concluded that exposure to atrazine at low dose (300 [micro]g [kg.sup.-1]) for a short time period can induce oxidative stress and damage the liver and kidney of both normal and diabetic rats
Conflict of Interests
The authors declare that there is no conflict of interests regarding the publication of this paper.
This research was supported by UGC-SAP (Grant no. F3-30/2011).
 P. T. Giboney, "Mildly elevated liver transaminase levels in the asymptomatic patient," American Family Physician, vol. 71, no. 6, pp. 1105-1110, 2005.
 F. D Sajad, S. Rasoul, M. Hassan, and A. S Rajab, "Atrazine in sub acute exposure results in sperm DNA disintegrity and nuclear immaturity in rats," Veterinary Research Forum, vol. 3, no. 1, pp. 19-26, 2012.
 M. O. Islam, M. Hara, and J. Miyake, "Induction of Pglycoprotein, glutathione-S-transferase and cytochrome P450 in rat liver by atrazine," Environmental Toxicology and Pharmacology, vol. 12, no. 1, pp. 1-6, 2002.
 M. Singh, P. Kaur, R. Sandhir, and R. Kiran, "Protective effects of vitamin E against atrazine-induced genotoxicity in rats," Mutation Research--Genetic Toxicology and Environmental Mutagenesis, vol. 654, no. 2, pp. 145-149, 2008.
 M. Singh, R. Sandhir, and R. Kiran, "Effects on antioxidant status of liver following atrazine exposure and its attenuation by vitamin E," Experimental and Toxicologic Pathology, vol. 63, no. 3, pp. 269-276, 2011.
 R. K. Pathak and A. K. Dikshit, "Atrazine and its use," International Journal of Research in Chemistry Environment, vol. 2, no. 1, pp. 1-6, 2012.
 X. Zhang, M. Wang, S. Gao, R. Ren, J. Zheng, and Y. Zhang, "Atrazine-induced apoptosis of splenocytes in BALB/C mice," BMC Medicine, vol. 9, article 117, 2011.
 WHO Study Group, "Diabetes mellitus," Technical Report 727, WHO (World Health Organization), Geneva, Switzerland, 1985.
 L. J. Marnett, "Oxyradicals and DNA damage," Carcinogenesis, vol. 21, no. 3, pp. 361-370, 2000.
 E. R. Stadtman and R. L. Levine, "Protein oxidation," Annals of the New York Academy of Sciences, vol. 899, pp. 191-208, 2000.
 S. Yla-Herttuala, "Oxidized LDL and atherogenesis," Annals of the New York Academy of Sciences, vol. 874, pp. 134-137, 1999.
 A. Ramachandran, M. V. Jali, V. Mohan, C. Snehalatha, and M. Viswanathan, "High prevalence of diabetes in an urban population in south India," The British Medical Journal, vol. 297, no. 6648, pp. 587-590, 1988.
 Atrazine Chemical Summary U.S. EPA, "Toxicity and Exposure Assessment for Children's Health," 2007, http://www.epa.gov/teach/chem summ/Atrazine summary.pdf.
 S. Lim, S. Y. Ahn, I. C. Song et al., "Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance," PLoS ONE, vol. 4, no. 4, Article ID e5186, 2009.
 H. Olsen, E. Enan, and F. Matsumura, "Regulation of glucose transport in the NIH 3T3 L1 preadipocyte cell line by TCDD," Environmental Health Perspectives, vol. 102, no. 5, pp. 454-458, 1994.
 F. G. De Felice and S. T. Ferreira, "Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease," Diabetes, vol. 63, no. 7, pp. 2262-2272, 2014.
 M. K. Sangeetha, H. R. Balaji Raghavendran, V. Gayathri, and H. R. Vasanthi, "Tinospora cordifolia attenuates oxidative stress and distorted carbohydrate metabolism in experimentally induced type 2 diabetes in rats," Journal of Natural Medicines, vol. 65, no. 3-4, pp. 544-550, 2011.
 K. Srinivasan, B. Viswanad, L. Asrat, C. L. Kaul, and P. Ramarao, "Combination of high-fat diet-fed and low-dose streptozotocin-treated rat: a model for type 2 diabetes and pharmacological screening," Pharmacological Research, vol. 52,no. 4, pp. 313-320, 2005.
 S. Marklund and G. Marklund, "Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase," European Journal of Biochemistry, vol. 47, no. 3, pp. 469-474, 1974.
 A. Claiborne, "Catalase activity," in CRC Handbook of Methods for Oxygen Radical Research, R. A. Greenwald, Ed., pp. 283-284, CRC Press, Boca Raton, Fla, USA, 1985.
 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.
 H. Ohkawa, N. Ohishi, and K. Yagi, "Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction," Analytical Biochemistry, vol. 95, no. 2, pp. 351-358, 1979.
 G. L. Ellman, "Tissue sulfhydryl groups," Archives of Biochemistry and Biophysics, vol. 82, no. 1, pp. 70-77, 1959.
 G. L. Kennedy Jr., "Chronic toxicity, reproductive, and teratogenic studies with oxamyl," Fundamental and Applied Toxicology, vol. 7, no. 1, pp. 106-118, 1986.
 Y. Sharma, S. Bashir, M. Irshad, T. C. Nag, and T. D. Dogra, "Dimethoate-induced effects on antioxidant status of liver and brain of rats following subchronic exposure," Toxicology, vol. 215, no. 3, pp. 173-181, 2005.
 A. L. Dutta and C. R. Sahu, "Emblica officinalis Garten fruits extract ameliorates reproductive injury and oxidative testicular toxicity induced by chlorpyrifos in male rats," SpringerPlus, vol. 2, article 541, 2013.
 A.-T. H. Mossa, A. A. Refaie, A. Ramadan, and J. Bouajila, "Amelioration of prallethrin-induced oxidative stress and hepatotoxicity in rat by the administration of Origanum majorana essential oil," BioMed Research International, vol. 2013, Article ID 859085, 11 pages, 2013.
 B. D. Roloff, D. A. Belluck, and L. F. Meisner, "Cytogenetic studies of herbicide interactions in vitro and in vivo using atrazine and linuron," Archives of Environmental Contamination and Toxicology, vol. 22, no. 3, pp. 267-271, 1992.
 C. Cantemir, C. Cozmei, B. Scutaru, S. Nicoara, and E. Carasevici, "p53 Protein expression in peripheral lymphocytes from atrazine chronically intoxicated rats," Toxicology Letters, vol. 93, no. 2-3, pp. 87-94, 1997.
 H. Kandori, S. Suzuki, M. Asamoto et al., "Influence of atrazine administration and reduction of calorie intake on prostate carcinogenesis in probasin/SV40 T antigen transgenic rats," Cancer Science, vol. 96, no. 4, pp. 221-226, 2005.
 K. Fukamachi, B. Seok Han, C. Kyu Kim et al., "Possible enhancing effects of atrazine and nonylphenol on 7,12-dimethylbenz[a]anthracene-induced mammary tumor development in human c-Ha-ras proto-oncogene transgenic rats," Cancer Science, vol. 95, no. 5, pp. 404-410, 2004.
 T. Gojmerac, B. Kartal, M. Zuric, S. Curic, and M. Mitak, "Serum biochemical and histopathological changes related to the hepatic function in pigs following atrazine treatment," Journal of Applied Toxicology, vol. 15, no. 3, pp. 233-236, 1995.
 F. M. El-Demerdash, M. I. Yousef, F. S. Kedwany, and H. H. Baghdadi, "Role of [alpha]-tocopherol and [beta]-carotene in ameliorating the fenvalerate-induced changes in oxidative stress, hemato-biochemical parameters, and semen quality of male rats," Journal of Environmental Science and Health. Part B Pesticides, Food Contaminants, and Agricultural Wastes, vol. 39, no. 3, pp. 443-459, 2004.
 C. T. Leong, U. J. A. D'Souza, M. Iqbal, and Z. A. Mustapha, "Lipid peroxidation and decline in antioxidant status as one of the toxicity measures of diazinon in the testis," Redox Report, vol. 18, no. 4, pp. 155-164, 2013.
 T. Wafa, K. Nadia, N. Amel et al., "Oxidative stress, hematological and biochemical alterations in farmers exposed to pesticides," Journal of Environmental Science and Health--Part B Pesticides, Food Contaminants, and Agricultural Wastes, vol. 48, no. 12, pp. 1058-1069, 2013.
 C. Datta, J. Gupta, A. Sarkar, and D. Sengupta, "Effects of organophosphorus insecticide phosphomidon on antioxidant defence components of human erythrocyte and plasma.," Indian Journal of Experimental Biology, vol. 30, no. 1, pp. 65-67, 1992.
 J. W. Baynes, "Role of oxidative stress in development of complications in diabetes," Diabetes, vol. 40, no. 4, pp. 405-412, 1991.
 J. W. Baynes and S. R. Thorpe, "Role of oxidative stress in diabetic complications: a new perspective on an old paradigm," Diabetes, vol. 48, no. 1, pp. 1-9, 1999.
 P. L. Montilla, J. F. Vargas, I. F. Tunez, M. C. Munoz, M. E. Valdelvira, and E. S. Cabrera, "Oxidative stress in diabetic rats induced by streptozotocin: protective effects of melatonin," Journal of Pineal Research, vol. 25, no. 2, pp. 94-100, 1998.
 J. Fujii, Y. Iuchi, S. Matsuki, and T. Ishii, "Cooperative function of antioxidant and redox systems against oxidative stress in male reproductive tissues," Asian Journal of Andrology, vol. 5, no. 3, pp. 231-242, 2003.
 J. M. McCord and I. Fridovich, "Superoxide dismutase: an enzymic function for erythrocuprein (hemocuprein)," The Journal of Biological Chemistry, vol. 244, no. 22, pp. 6049-6055, 1969.
 S. G. Konstantinova and E. M. Russanov, "Studies on paraquat-induced oxidative stress in rat liver," Acta Physiologica et Pharmacologica Bulgarica, vol. 24, no. 4, pp. 107-111, 1999.
 R. Hussain, F. Mahmood, A. Khan, M. T. Javed, S. Rehan, and T. Mehdi, "Cellular and biochemical effects induced by atrazine on blood of male Japanese quail (Coturnix japonica)," Pesticide Biochemistry and Physiology, vol. 103, no. 1, pp. 38-42, 2012.
 F. D. Campos-Pereira, C. A. Oliveira, A. A. Pigoso et al., "Early cytotoxic and genotoxic effects of atrazine on Wistar rat liver: a morphological, immunohistochemical, biochemical, and molecular study," Ecotoxicology and Environmental Safety, vol. 78, pp. 170-177, 2012.
 P. A. Fowler, M. Bellingham, K. D. Sinclair et al., "Impact of endocrine-disrupting compounds (EDCs) on female reproductive health," Molecular and Cellular Endocrinology, vol. 355, no. 2, pp. 231-239, 2012.
 J. F. Zilva, P. R. Pannall, and P. D. Mayne, "Plasma enzymes in diagnosis," in Clinical Chemistry in Diagnosis and Treatment, E. Arnold, Ed., pp. 310-315, A division of Holdder and Stoughton, London, UK, 1988.
 X.-M. Liu, J.-Z. Shao, L.-X. Xiang, and X.-Y. Chen, "Cytotoxic effects and apoptosis induction of atrazine in a grass carp (Ctenopharyngodon idellus) cell line," Environmental Toxicology, vol. 21, no. 1, pp. 80-89, 2006.
 R. S. Mohammad, A. L. Attabi, andA. L. Diwan, "Protective role of clomiphene citrate from the biochemical effects of atrazine exposure in adult male rats," Basrah Journal of Veterinary Research, vol. 11, no. 2, pp. 82-92, 2012.
Department of Biochemistry and Molecular Biology, School of Life Sciences, Pondicherry University, Puducherry 605014, India
Correspondence should be addressed to Latha Periyasamy; email@example.com
Received 20 May 2014; Revised 27 August 2014; Accepted 1 September 2014; Published 29 September 2014
Academic Editor: Peter J. O'Brien
Copyright [c] 2014 Dinesh Babu Jestadi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
TABLE 1: Effect of atrazine on the body weight and weights of the organs (liver and kidney). Weight (in grams) NC NA Initial body weight 163.33 [+ or -] 5.77 170.66 [+ or -] 5.13 Final body weight 242.33 [+ or -] 4.93 272.66 [+ or -] 14.18 Liver weight 7.81 [+ or -] 0.54 10.28 [+ or -] 0.68 Kidney weight 1.61 [+ or -] 0.16 1.79 [+ or -] 0.46 Blood glucose (*) 89.73 [+ or -] 1.05 90.89 [+ or -] 3.04 Weight (in grams) DC DA Initial body weight 140.00 [+ or -] 8.75 152.25 [+ or -] 5.90 Final body weight 193.25 [+ or -] 11.44 217.75 [+ or -] 6.75 Liver weight 8.29 [+ or -] 0.69 9.07 [+ or -] 0.78 Kidney weight 1.93 [+ or -] 0.28 1.79 [+ or -] 0.13 Blood glucose (*) 255.33 [+ or -] 9.60 268.67 [+ or -] 2.89 The data are represented as mean [+ or -] SD (n = 4) and evaluated by one-way analysis of variance (ANOVA) confirmed by Tukey's test. NC normal control rats, NA atrazine treated rats, DC diabetic control rats, and DA atrazine treated diabetic rats. (*) Blood glucose level values are in mg/dL. Significant difference (P <0.05) is observed only in blood glucose levels of normal control rats and normal atrazine treated rats compared with diabetic control rats and diabetic atrazine treated rats. TABLE 2: Effect of atrazine on the liver and kidney marker enzymes. Source Parameters NC NA AST 24.90 [+ or -] 2.26 35.75 + 2.47 (*) Liver markers ALT (IU/L) 14.85 [+ or -] 1.20 20.56 [+ or -] 2.34 (*) ALP 38.38 [+ or -] 2.78 50.68 [+ or -] 3.6 (*) Kidney markers Creatinine 0.4 [+ or -] 0.07 1.05 [+ or -] 0.21 (*) (mg/dL) Urea 33.05 [+ or -] 1.58 42.21 [+ or -] 1.70 (*) Source DC DA 49.73 + 3.60 60.64 + 3.42 (**) Liver markers (IU/L) 33.02 [+ or -] 2.29 45.33 [+ or -] 2.53 (**) 61.60 [+ or -] 4.6 71.41 [+ or -] 3.32 (**) Kidney markers 1.95 [+ or -] 0.07 2.12 [+ or -] 0.17 (**) (mg/dL) 56.21 [+ or -] 1.40 59.45 [+ or -] 1.86 (**) The data are represented as mean [+ or -] SD (n = 4) and evaluated by one-way analysis of variance (ANOVA) confirmed by Tukey's test. NC normal control rats, NA atrazine treated rats, DC diabetic control rats, and DA atrazine treated diabetic rats. (*) P [less than or equal to] 0.05 (normal control rats versus normal atrazine treated rats). (**) P [less than or equal to] 0.01 (diabetic control rats versus atrazine treated diabetic rats).
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||Research Article|
|Author:||Jestadi, Dinesh Babu; Phaniendra, Alugoju; Babji, Undru; Srinu, Thupakula; Shanmuganathan, Bhavathar|
|Publication:||Journal of Toxicology|
|Date:||Jan 1, 2014|
|Previous Article:||Xylazine as a drug of abuse and its effects on the generation of reactive species and DNA damage on human umbilical vein endothelial cells.|
|Next Article:||Analysis and determination of trace metals (nickel, cadmium, chromium, and lead) in tissues of Pampus argenteus and Platycephalus indicus in the Hara...|