Mehmet Erman ERDEMLİ, Zümrüt DOĞAN, Yilmaz ÇİĞREMİŞ, Müslüm AKGÖZ, Eyüp ALTINÖZ, Murat GEÇER, Yusuf TÜRKÖZ

Amelioration of subchronic acrylamide toxicity in large intestine of rats byorganic dried apricot intake

Acrylamide (AA) has neurotoxic, mutagenic, and genotoxic effects in humans and experimental animals. Fruit consumption is important for human health, because fruits are the source of many nutrients such as vitamins, minerals, carotenoids, dietary fiber, and phytonutrients. Many agricultural products provide natural melatonin in the diet. At the onset of the study, rats were weighted and randomly divided into four groups each containing 10 rats as follows: group 1: control (fed with normal diet and normal drinking water); group 2: apricot (fed with a daily diet with 5% apricot and normal drinking water); group 3: AA (administered daily acrylamide at 500 μg/kg b.w. Via drinking water and fed a normal diet); group 4: apricot-AA (administered daily acrylamide at 500 μg/kg b.w. Via drinking water and fed with a diet with 5% apricot). The diet schedule was continued for 12 weeks. At the end of the study, samples of large intestine were collected for biochemical analyses. The highest lipid peroxidation (as malondialdehyde, MDA) levels were observed in the AA groups, but MDA levels decreased significantly (P < 0.05) with apricot intake. Glutathione peroxidase activity in the apricot-AA group was higher than in the other three groups (P < 0.05). Glutathione S-transferase (GST) enzyme activity increased significantly in the AA group as compared with the other groups (P < 0.05). However, GST activity was significantly (P < 0.05) decreased by the apricot-supplemented diet. GST-Pi mRNA levels in the AA group increased significantly (P < 0.05) as compared with the other groups. In conclusion, the results of the current study demonstrated that AA caused large intestine damage and showed the efficiency of apricot in preventing this damage by inhibiting lipid peroxidation and improving antioxidant enzyme activities.

Anahtar Kelimeler:

Apricot, acrylamide, rat, large intestine, GST-Pi, antioxidant enzymes

Amelioration of subchronic acrylamide toxicity in large intestine of rats byorganic dried apricot intake

Keywords:

Apricot, acrylamide, rat, large intestine, GST-Pi, antioxidant enzymes,

PDF

___

Akın EB, Karabulut I, Topcu A (2008). Some compositional properties of main Malatya apricot (Prunus armeniaca L.) varieties. Food Chem 107: 939–948.
Altinoz E, Turkoz Y (2014). The protective role of n-acetylcysteine against acrylamide-induced genotoxicity and oxidative stress in rats. Gene Ther Mol Biol 16: 35–43.
Barber DS, Hunt JR, Ehrich MF, Lehning EJ, LoPachin RM (2001). Metabolism, toxicokinetics, and hemoglobin adduct formation in rats following subacute and subchronic acrylamide dosing. Neurotoxicology 22: 341–353.
Bowyer J, Latendresse J, Delongchamp R, Muskhelishvili L, Warbritton A, Thomas M, Tareke E, McDaniel L, Doerge D (2008). The effects of subchronic acrylamide exposure on gene expression, neurochemistry, hormones, and histopathology in the hypothalamus–pituitary–thyroid axis of male Fischer 344 rats. Toxicol Appl Pharmacol 230: 208–215.
Calleman CJ, Bergmark E, Costa LG (1990). Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Chem Res Toxicol 3: 406–412.
Dearfield KL, Douglas GR, Ehling UH, Moore MM, Sega GA, Brusick DJ (1995). Acrylamide: a review of its genotoxicity and an assessment of heritable genetic risk. Mutat Res 330: 71–99.
El-Demerdash FM, Yousef MI, Kedwany FS, Baghdadi HH (2004). Cadmium-induced changes in lipid peroxidation, blood hematology, biochemical parameters, and semen quality of male rats: protective role of vitamin E and β-carotene. Food Chem Toxicol 42: 1563–1571.
Fatemi F, Allameh A, Dadkhah A, Forouzandeh M, Kazemnejad S, Sharifi R (2006) Changes in hepatic cytosolic glutathione S-transferase activity and expression of its class-P during prenatal and postnatal period in rats treated with aflatoxin B1. Arch Toxicol 80: 572–579.
Favor J, Shelby MD (2005). Transmitted mutational events induced in mouse germ cells following acrylamide or glycidamide exposure. Mutat Res Genet Toxicol Environ Mutagen 580: 21–30.
Habig WH, Pabst MJ, Jakoby WB (1974). Glutathione S-transferases the first enzymatic step in mercapturic acid formation. J Biol Chem 249: 7130–7139.
Halliwell B (2014). Cell culture, oxidative stress, and antioxidants: avoiding pitfalls. Biomed J 37: 99–105.
Hayes JD, Pulford DJ (1995). The glutathione s-transferase supergene family: regulation of GST and the contribution of the isoenzymes to cancer chemoprotection and drug resistance Part II. Crit Rev Biochem Mol Biol 30: 521–600.
IARC (1995). Dry Cleaning, Some Chlorinated Solvents, and Other Industrial Chemicals. Lyon, France: International Agency for Research on Cancer.
Johnson KA, Gorzinski SJ, Bodner KM, Campbell RA, Wolf CH, Friedman MA, Mast RW (1986). Chronic toxicity and oncogenicity study on acrylamide incorporated in the drinking water of Fischer 344 rats. Toxicol Appl Pharmacol 85: 154–168.
Lindsay R (2002). Generalized potential origins of acrylamide in foods. In: Workshop on FRI Acrylamide Project, Chicago, IL, USA.
Livak KJ, Schmittgen TD (2001). Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔCT method. Methods 25: 402–408.
LoPachin RM, Balaban CD, Ross JF (2003). Acrylamide axonopathy revisited. Toxicol Appl Pharmacol 188: 135–153.
Lowry OH, Rosebrough NJ, Farr AL, Randall RJ (1951). Protein measurement with the Folin phenol reagent. J Biol Chem 193: 265–275.
Mansuri ML, Parihar P, Solanki I, Parihar MS (2014). Flavonoids in modulation of cell survival signalling pathways. Genes Nutr 3: 400.
Mottram DS, Wedzicha BL, Dodson AT (2002). Food chemistry: acrylamide is formed in the Maillard reaction. Nature 419: 448–449.
Nazıroğlu M (2007). New molecular mechanisms on the activation of TRPM2 channels by oxidative stress and ADP-ribose. Neurochem Res 11: 1990–2001.
Nazıroğlu M, Ciğ B, Ozgül C (2013). Neuroprotection induced by N-acetylcysteine against cytosolic glutathione depletion- induced Ca2+ influx in dorsal root ganglion neurons of mice: role of TRPV1 channels. Neuroscience 242: 151–160.
Nazıroğlu M, Tokat S, Demirci S (2012). Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling molecular pathways in breast cancer. J Recept Signal Transduct Res 6: 290–297.
Odland L, Romert L, Clemedson C, Walum E (1994). Glutathione content, glutathione transferase activity, and lipid peroxidation in acrylamide-treated neuroblastoma N1E 115 cells. Toxicol In Vitro 8: 263–267.
Ohkawa H, Ohishi N, Yagi K (1979). Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 95: 351–358.
Paglia DE, Valentine WN (1967). Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med 70: 158–169.
Piacentini L, Karliner JS (1999). Altered gene expression during hypoxia and reoxygenation of the heart. Pharmacol Ther 83: 21–37.
Pietta PG (2000). Flavonoids as antioxidants. J Nat Prod 63: 1035– 1042.
Ramos S, Alía M, Bravo L, Goya L (2005). Comparative effects of food-derived polyphenols on the viability and apoptosis of a human hepatoma cell line (HepG2). J Agric Food Chem 53: 1271–1280.
Tareke E, Rydberg P, Karlsson P, Eriksson S, Törnqvist M (2002). Analysis of acrylamide, a carcinogen formed in heated foodstuffs. J Agric Food Chem 50: 4998–5006.
Terrier P, Townsend AJ, Coindre J, Triche T, Cowan K (1990). An immunohistochemical study of pi class glutathione S-transferase expression in normal human tissue. Am J Pathol 137: 845–853.
Tietze F (1969). Enzymic method for quantitative determination of nanogram amounts of total and oxidized glutathione: applications to mammalian blood and other tissues. Anal Biochem 27: 502–522.
Vardi N, Parlakpinar H, Ozturk F, Ates B, Gul M, Cetin A, Erdogan A, Otlu A (2008). Potent protective effect of apricot and β-carotene on methotrexate-induced intestinal oxidative damage in rats. Food Chem Toxicol 46: 3015–3022.
Wang XT, Liu PY, Tang JB (2006). PDGF gene therapy enhances expression of VEGF and bFGF genes and activates the NF-κB gene in signal pathways in ischemic flaps. Plast Reconstr Surg 117: 129–137.
Yousef M, El-Demerdash F (2006). Acrylamide-induced oxidative stress and biochemical perturbations in rats. Toxicology 219: 133–141.
Zödl B, Schmid D, Wassler G, Gundacker C, Leibetseder V, Thalhammer T, Ekmekcioglu C (2007). Intestinal transport and metabolism of acrylamide. Toxicology 232: 99–108.