Civa Klorid ve Kurşun Nitrat'ın Erkek Ratlarda Kardiyotoksik Etkisi

Year 2016, Volume: 13 Issue: 2, 136 - 143, 29.08.2016

Suna Kalender

Abstract

Amaç: Kurşun nitrat ve civa klorid insan ve hayvan dokularında çeşitli değişikliklere yol açan çevresel ve
endüstriyel kirleticilerdir. Bu çalışmada, kurşun nitrat ve civa klorid'in erkek sıçanlardaki kardiyotoksik
etkisi araştırılmıştır.
Materyal ve metod: Kurşun nitrat (LN, 45 mg/kg vücut ağırlığı) ve civa klorid (MC, 0.02 mg/kg vücut
ağırlığı) ve bunların kombinasyonları 4 hafta boyunca oral yoldan hayvanlara uygulanmıştır. Bu çalışmada 4
deney grubu bulunmaktadır: kontrol, kurşun nitrat, civa klorid, kurşun nitrat ve civa klorid. Deney bitiminde
kalp dokularındaki malondialdehit seviyesi (MDA), antioksidan enzim aktiviteleri (süperoksit dismutaz
(SOD), katalaz (CAT), glutatyon peroksidaz (GPx), gluıtatyon-S- transferaz (GST) değerlendirme
yapılmıştır. Bulgular: Kontrol grubu ile karşılaştırıldığında, kurşun nitrat, civa klorid ve kurşun nitrat+civa klorid
uygulaması SOD, CAT, GPx ve GST aktivitelerinde artışa yol açmıştır. Aynı zamanda MDA seviyesi de
artmıştır. Işık mikroskobu incelemelerinde uygulama gruplarında kalp dokularında ciddi histopatolojik
değişimler gözlenmiştir.
Sonuç: Kurşun nitrat ve civa kloridin birlikte uygulanmasının tek başlarına uygulanmalarına göre daha
toksik etkili olduğu tespit edilmiştir.

Keywords

Kurşun, Civa, Oksidatif Stres, Patoloji, Kalp

Effects of Mercury Chloride And Lead Nitrate Induced Cardiotoxicity in Male Rats

Abstract

Background: Lead nitrate and mercury chloride are widespread environmental and industrial pollutant,
which induces severe alterations in the body tissues of both humans and animals. In the present study, the
effects of lead and mercury induced cardiotoxicity was studied in Wistar rats.
Methods: Lead nitrate (LN, 45 mg/kg bw/day) and mercury chloride (MC, 0.02 mg/kg bw/day) and their
combination were administered orally for four weeks. Four groups of rats were used in the study: control, LN,
MC and LN plus MC groups. Malondialdehyde (MDA) level, antioxidant enzyme activities [superoxide
dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST)] and
histopathological changes in heart tissue were evaluated.
Results: Results showed that LN and MC exposure and also their combination resulted in an increase in the
SOD, CAT, GPx, GST activities and also MDA levels, with respect to the control group. Light microscopic
investigations revealed that mercury chloride and lead nitrate and also co-treatment of them induced
histopathological changes in heart tissue.
Conclusion: As a result, combination of LN plus MC was more harmful than use them alone.

Keywords

Lead, Mercury, Oxidative Stress, Pathology, Heart

References

• 1) Cobbina SJ, Chen Y, Zhou Z, Wu X, Feng W, Wang W, Li Q, Zhao T, Mao G, Wu X, Yang L. Interaction of four low dose toxic metals with essential metals in brain, liver and kidneys of mice on sub-chronic exposure. Environ Toxicol Pharmacol 2015; 39(1): 280–291.
• 2) Cobbina SJ, Chen Y, Zhou Z, Wu X, Zhao T, Zhang Z, Feng W, Wang W, Li Q, Wu X, Yang L. Toxicity assessment due to subchronic exposure to individual and mixtures of four toxic heavy metals. J Hazard Mater 2015; 294: 109–120.
• 3) Apaydın FG, Kalender S, Baş H, Demir F, Kalender Y. Lead Nitrate Induced Testicular Toxicity in Diabetic and Non-Diabetic Rats: Protective Role of Sodium Selenite. Braz Arch Biol Technol 2015; 58(1): 68-74.
• 4) Apaydın FG, Baş H, Kalender S, Kalender Y. Subacute effects of low dose lead nitrate and mercury chloride exposure on kidney of rats. Environ Toxicol Pharmacol 2016; 41: 219–224.
• 5) Kalender S, Apaydin FG, Baş H, Kalender Y. Protective effect of sodium selenite on lead nitrateinduced hepatotoxicity in diabetic and non-diabetic rats. Environ Toxicol Pharmacol 2015; 40(2): 568–574.
• 6) Vijayakumar M, Jagadeesan G, Bharathi E. Ameliorative potential of ferulic acid on cardiotoxicity induced by mercuric chloride. Biomed Prevent Nutr 2014; 4(2): 239–243.
• 7) Sener G, Sehirli AO, Ayanoglu-Dulger G. Melatonin protects against mercury (II)-induced oxidative tissue damage in rats. Pharmacol Toxicol 2003; 93(6): 290–296.
• 8) Agarwal R, Goel SK, Chandra R, Behari JR. Role of vitamin E in preventing acute mercury toxicity in rat. Environ Toxicol Pharmacol 2010; 29(1): 70–78.
• 9) Harisa GI, Alanazi FK, El-Bassat RA, Malik A, Abdallah GM. Protective effect of pravastatin against mercury induced vascular cells damage: Erythrocytes as surrogate markers. Environ Toxicol Pharmacol 2012; 34(2): 428–435.
• 10) Rosales PC, Fernández SS, Saavedra JS, Cruz-Vega DE, Gandolfi AJ. Morphologic and functional alterations induced by low doses of mercuric chloride in the kidney OK cell line: ultrastructural evidence for an apoptotic mechanism of damage. Toxicology 2005; 210 (2-3): 111–121.
• 11) Rudd JW, Furutani A, Turner MA, Mercury methylation by fish intestinal contents. Appl Environ Microbiol 1980; 40 (4): 777–782.
• 12) Chehimi L, Roy V, Jelieli M, Sakly M. Chronic exposure to mercuric chloride during gestation affects sensorio motor development and later behavior in rats. Behav Brain Res 2012; 234 (1): 43–50.
• 13) Chang LW, Hartmann HA. Electron microscopic histochemical study on the localization of mercury in the nervous system after mercury intoxication. Exp Neurol 1972; 35 (1): 122–137.
• 14) Roshan VD, Assali M, Moghaddam AH, Hosseinzadeh M, Myers J. Exercise training and antioxidants: Effects on rat heart tissue exposed to lead acetate. Intl J Toxicol 2011; 30 (2): 190-196.
• 15) Lakshmi BVS, Sudhakar M, Aparna M. Protective potential of black grapes against lead induced oxidative stress in rats. Environ Toxicol Pharmacol 2013; 35(3): 361–368.
• 16) Liu C, Ma J, Sun Y. Quercetin protects the rat kidney against oxidative stress mediated DNA damage and apoptosis induced by lead. Environ Toxicol Pharmacol 2010; 30(3): 264–271.
• 17) Sarkar S, Mukherjee S, Chattopadhyay A, Bhattacharya S. Low dose of arsenic trioxide triggers oxidative stress in zebrafish brain: Expression of antioxidant genes. Ecotoxicol Environ Saf 2014; 107: 1–8.
• 18) Demir F, Uzun FG, Durak D, Kalender Y. Subacute chlorpyrifos-induced oxidative stress in rat erythrocytes and the protective effects of catechin and quercetin. Pestic Biochem Physiol 2011; 99(1): 77-81.
• 19) Garcia-Nino WR, Pedraza-Chaverri J. Protective effect of curcumin against heavy metals-induced liver damage. Food Chem Toxicol 2014; 69: 182–201.
• 20) Yole M, Wickstrom M, Blakley B. Cell death and cytotoxic effects in YAC-1 lymphoma cells following exposure to various forms of mercury. Toxicology 2007; 231(1): 40–57.
• 21) Sharma V, Sharma A, Kansal L. The effect of oral administration of Allium sativum extracts on lead nitrate induced toxicity in male mice. Food Chem Toxicol 2010; 48(3): 928-936.
• 22) Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the folin reagent. J Biol Chem 1951; 9: 265-275.
• 23) Marklund S, Marklund G. Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase. Eur J Biochem 1974; 47: 469-474.
• 24) Aebi H. Catalase in vitro. Methods Enzymol 1984; 105: 121-126.
• 25) Habig WH, Pabst MJ, Jakoby WB. Glutathione-Stransferases: the first enzymatic step in mercapturic acid formation. J Biol Chem 1974; 249: 7130-7139.
• 26) Paglia DE, Valentine WN. Studies on the quantitative and qualitative characterization of glutathione peroxidase. J Lab Clin Med 1987; 70: 158-165.
• 27) Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 1979; 95(2): 351-358.
• 28) Furieri LB, Galan M, Avendan˜ o MS, Garcia-Redondo AB, Aguado A, Martinez S, Cachofeiro V, Bartolome MV, Alonso MJ, Vassallo DV, Salaices M. Endothelial dysfunction of rat coronary arteries after exposure to low concentrations of mercury is dependent on reactive oxygen species. Br J Pharmacol 2011; 162 (8): 1819–1831.
• 29) Salonen JT, Seppanen K, Nyyssonen K. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men. Circulation 1995; 91: 645–655.
• 30) Baş H, Kalender S, Apaydın FG. Adverse effects of lead treatment: Relationship of histopathological changes and protective role of sodium selenite on non-diabetic and diabetic rat hearts. GU J Sci 2014; 27: (2):855-859.
• 31) Prince PSM, Rajakumar S, Dhanasekar K. Protective effects of vanillic acid on electrocardiogram, lipid peroxidation, antioxidants, proinflammatory markers and histopathology in isoproterenol induced cardiotoxic rats. Eur J Pharmacol. 2011; 668(1-2): 233-240.
• 32) Durak D, Kalender S, Uzun FG, Demir F, Kalender Y. Mercury chloride-induced oxidative stress and the protective effect of vitamins C and E in human erythrocytes in vitro. Afr J Biotechnol 2010; 9 (4): 488–495.
• 33) Uzun FG, Kalender Y. Chlorpyrifos induced hepatotoxicity in rats and the protective role of quercetin and catechin. Food Chem Toxicol 2013; 55: 549-556.
• 34) El-Demerdash, F.M., Nasr, H.M., Antioxidant effect of selenium on lipid peroxidation, hyperlipidemia and biochemical parameters in rats exposed to diazinon. J Trace Elem Med Bio 2014; 28(1): 89–93.
• 35) Messarah M, Klibet F, Boumendjel A, Abdennour C, Bouzerna N, Boulakoud MS, El Feki A. Hepatoprotective role and antioxidant capacity of selenium on arsenicinduced liver injury in rats. Exp Toxicol Pathol 2012; 64(3): 167–174.
• 36) Jihen EH, Imed M, Fatima H, Abdelhamid K. Protective effects of selenium (Se) and zinc (Zn) on cadmium (Cd) toxicity in the liver of the rat: effects on the oxidative stress. Ecotoxicol Environ Saf 2009; 72(5): 1559–1564.
• 37) Mansour SA, Mossa AH. Oxidative damage, biochemical and histopathological alterations in rats exposed to chlorpyrifos and the antioxidant role of zinc. Pestic Biochem Physiol 2010; 96(1): 14–23.
• 38) Haleagrahara N, Jackie T, Chakravarthi S, Rao M, Pasupathi T. Protective effects of Etlingera elatior extract on lead acetate-induced changes in oxidative biomarkers in bone marrow of rats. Food Chem Toxicol 2010; 48(10): 2688–2694.