RESEARCH PAPER
Effect of treatment with N-acetylcysteine on non-enzymatic antioxidant reserves and lipid peroxidation in workers exposed to lead
| 1 | Department of Biochemistry, School of Medicine with the Division of Dentistry, Medical University of Silesia, Katowice, Poland |
| 2 | Laboratory of Genetic Toxicology, Institute of Occupational Medicine and Environmental Health, Sosnowiec, Poland |
| 3 | Department of Molecular Biology and Translational Research, Institute of Rural Health, Lublin, Poland |
| 4 | Department of Public Health, University of Information Technology and Management, Rzeszów, Poland |
CORRESPONDING AUTHOR
Sławomir Kasperczyk
Department of Biochemistry, School of Medicine with the Division of Dentistry, Medical University of Silesia, Katowice, Poland
Department of Biochemistry, School of Medicine with the Division of Dentistry, Medical University of Silesia, Katowice, Poland
Ann Agric Environ Med. 2014;21(2):272–277
KEYWORDS
ABSTRACT
There are no published studies examining the effects of N-acetylcysteine (NAC) administration on the non-enzymatic defence systems in humans exposed to lead. In view of this, it was decided to measure the levels of uric acid (UA), albumin, bilirubin and alpha-tocopherol before and after treatment with NAC. An estimation was also made of the degree of oxidative stress by measuring the ferric reducing ability of plasma (FRAP), the levels of conjugated dienes (CD) and lipid hydroperoxides
(LHP). Male employees who worked with lead were randomized into two groups. The first group included workers who were not administered any drugs (n=49), while the second group (n=122) consisted of workers who were treated with NAC at three different doses (200 mg, 400 mg and 800 mg) for 12 weeks. The administration of NAC (400 mg, 800 mg) resulted in significant decreases in the LHP levels. Similarly, a strong tendency toward lower levels of CD was observed in the same groups. The UA levels were significantly lower only in the group receiving the 200 mg dose of NAC. However, the alpha-tocopherol levels were significantly elevated after treatment with NAC (400 mg, 800 mg). NAC administration did not significantly affect the levels of bilirubin and albumin, but a tendency toward higher values was observed for FRAP. NAC reduced the extent of lipid peroxidation in a dose-dependent manner. Elevated concentrations of alpha-tocopherol may have enhanced the beneficial effects of NAC. Treatment with NAC may contribute to the restoration of non-enzymatic antioxidant reserves when administered to lead-exposed workers.
REFERENCES (38)
1.
Brunet J, Boily MJ, Cordeau S, Des Rosiers C. Effects of N-acetylcysteine in the rat heart reperfused after low-flow ischemia: evidence for a direct scavenging of hydroxyl radicals and a nitric oxide-dependent increase in coronary flow. Free Radic Biol Med. 1995; 19(5): 627–638.
2.
Marthaler MT, Keresztes PA. Evidence-based practice for the use of N-acetylcysteine. Dimens Crit Care Nurs. 2004; 23(6): 270–273.
3.
Van Schooten FJ, Besaratinia A, De Flora S, D’Agostini F, Izzotti A, Camoirano A, Balm AJ, Dallinga JW, Bast A, Haenen GR, Van’t Veer L, Baas P, Sakai H, Van Zandwijk N. Effects of oral administration of N-acetyl-L-cysteine: a multi-biomarker study in smokers. Cancer Epidemiol Biomarkers Prev. 2002; 11(2): 167–175.
4.
Millea PJ. N-acetylcysteine: multiple clinical applications. Am Fam Physician. 2009; 80(3): 265–269.
5.
Olewińska E, Kasperczyk A, Kapka L, Kozłowska A, Pawlas N, Dobrakowski M, Birkner E, Kasperczyk S. Level of DNA damage in lead-exposed workers. Ann Agric Environ Med. 2010; 17(2): 231–236.
6.
Kasperczyk S, Przywara-Chowaniec B, Kasperczyk A, Rykaczewska-Czerwińska M, Wodniecki J, Birkner E, Dziwisz M, Krauze-Wielicka M. Function of heart muscle in people chronically exposed to lead. Ann Agric Environ Med. 2005; 12(2): 207–210.
7.
Khan DA, Qayyum S, Saleem S, Khan FA. Lead-induced oxidative stress adversely affects health of the occupational workers. Toxicol Ind Health. 2008; 24(9):611–8.
8.
Gurer H, Ercal N. Can antioxidants be beneficial in the treatment of lead poisoning? Free Radic Biol Med. 2000; 29(10): 927–945.
9.
Kasperczyk S, Birkner E, Kasperczyk A, Zalejska-Fiolka J. Activity of superoxide dismutase and catalase in people protractedly exposed to lead compounds. Ann Agric Environ Med. 2004; 11(2): 291–296.
10.
Moore K, Roberts LJ 2nd. Measurement of lipid peroxidation. Free Radic Res. 1998; 28(6): 659–671.
11.
Tandon SK, Singh S, Prasad S, Srivastava S, Siddiqui MK. Reversal of lead-induced oxidative stress by chelating agent, antioxidant, or their combination in the rat. Environ Res. 2002; 90(1): 61–66.
12.
Corongiu FP, Banni S, Dessi MA. Conjugated dienes detected in tissue lipid extracts by second derivative spectrophotometry. Free Radic Biol Med. 1989; 7(2):183–186.
13.
Södergren E, Nourooz-Zadeh J, Berglund L, Vessby B. Re-evaluation of the ferrous oxidation in xylenol orange assay for the measurement of plasma lipid hydroperoxides. J Biochem Biophys Methods. 1998; 37(3):137–146.
14.
Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power”: the FRAP assay. Anal Biochem. 1996; 239(1): 70–76.
15.
Shearer MJ. HPLC of Small Molecules-a Practical Approach. In: Lim CK (eds.). IRL Press, Oxford; 1986.
16.
Haleagrahara N, Jackie T, Chakravarthi S, Rao M, Kulur A. Protective effect of Etlingera elatior (torch ginger) extract on lead acetate--induced hepatotoxicity in rats. J Toxicol Sci. 2010; 35(5): 663–671.
17.
Jackie T, Haleagrahara N, Chakravarthi S. Antioxidant effects of Etlingera elatior flower extract against lead acetate – induced perturbations in free radical scavenging enzymes and lipid peroxidation in rats. BMC Res Notes 2011; 4: 67.
18.
Adonaylo VN, Oteiza PI. Lead intoxication: antioxidant defenses and oxidative damage in rat brain. Toxicology. 1999; 135(2–3): 77–85.
19.
Hsu PC, Guo YL. Antioxidant nutrients and lead toxicity. Toxicology. 2002; 180(1): 33–44.
20.
Rendón-Ramirez A, Cerbón-Solórzano J, Maldonado-Vega M, Quintanar-Escorza MA, Calderón-Salinas JV. Vitamin-E reduces the oxidative damage on delta-aminolevulinic dehydratase induced by lead intoxication in rat erythrocytes. Toxicol In Vitro. 2007; 21(6): 1121–1126.
21.
Patra RC, Swarup D, Dwivedi SK. Antioxidant effects of alpha tocopherol, ascorbic acid and L-methionine on lead induced oxidative stress to the liver, kidney and brain in rats. Toxicology. 2001; 162(2):81–8.
22.
Ergurhan-Ilhan I, Cadir B, Koyuncu-Arslan M, Arslan C, Gultepe FM, Ozkan G. Level of oxidative stress and damage in erythrocytes in apprentices indirectly exposed to lead. Pediatr Int. 2008; 50(1): 45–50.
23.
Prokopowicz A, Sobczak A, Szula M, Anczyk E, Kurek J, Olszowy Z, Radek M, Pawlas N, Ochota P, Szoltysek-Boldys I. Effect of occupational lead exposure on α- and γ-tocopherol concentration in plasma. Occup Environ Med. 2013; (in press).
24.
Caylak E, Aytekin M, Halifeoglu I. Antioxidant effects of methionine, alpha-lipoic acid, N-acetylcysteine and homocysteine on lead-induced oxidative stress to erythrocytes in rats. Exp Toxicol Pathol. 2008; 60(4–5): 289–294.
25.
Fuhua P, Xuhui D, Zhiyang Z, Ying J, Yu Y, Feng T, Jia L, Lijia G, Xueqiang H. Antioxidant status of bilirubin and uric Acid in patients with myasthenia gravis. Neuroimmunomodulation. 2012; 19(1): 43–49.
26.
Noriega GO, Tomaro ML, del Batlle AM. Bilirubin is highly effective in preventing in vivo delta-aminolevulinic acid-induced oxidative cell damage. Biochim Biophys Acta. 2003; 1638(2): 173–178.
27.
Abdel-Moneim AE, Dkhil MA, Al-Quraishy S. The redox status in rats treated with flaxseed oil and lead-induced hepatotoxicity. Biol Trace Elem Res. 2011; 143(1): 457–467.
28.
Flora G, Gupta D, Tiwari A. Toxicity of lead: A review with recent updates. Interdiscip Toxicol. 2012; 5(2): 47–58.
29.
Bener A, Obineche E, Gillett M, Pasha MA, Bishawi B. Association between blood levels of lead, blood pressure and risk of diabetes and heart disease in workers. Int Arch Occup Environ Health. 2001; 74(5): 375–378.
30.
Hernández-Serrato MI, Fortoul TI, Rojas-Martínez R, Mendoza-Alvarado LR, Canales-Treviño L, Bochichio-Riccardelli T, Avila-Costa MR, Olaiz-Fernández G. Lead blood concentrations and renal function evaluation: study in an exposed Mexican population. Environ Res. 2006; 100(2): 227–231.
31.
Ehrlich R, Robins T, Jordaan E, Miller S, Mbuli S, Selby P, Wynchank S, Cantrell A, De Broe M, D’Haese P, Todd A, Landrigan P. Lead absorption and renal dysfunction in a South African battery factory. Occup Environ Med. 1998; 55(7): 453–460.
32.
Berrahal AA, Lasram M, El Elj N, Kerkeni A, Gharbi N, El-Fazâa S. Effect of age-dependent exposure to lead on hepatotoxicity and nephrotoxicity in male rats. Environ Toxicol. 2011; 26(1): 68–78.
33.
Tayman C, Tonbul A, Kosus A, Hirfanoglu IM, Uysal S, Haltas H, Tatli MM, Andiran F. N-acetylcysteine may prevent severe intestinal damage in necrotizing enterocolitis. J Pediatr Surg. 2012; 47(3): 540–450.
34.
Peng F, Yang Y, Liu J, Jiang Y, Zhu C, Deng X, Hu X, Chen X, Zhong X. Low antioxidant status of serum uric acid, bilirubin and albumin in patients with neuromyelitis optica. Eur J Neurol. 2012; 19(2): 277–283.
35.
Turell L, Carballal S, Botti H, Radi R, Alvarez B. Oxidation of the albumin thiol to sulfenic acid and its implications in the intravascular compartment. Braz J Med Biol Res. 2009; 42(4): 305–311.
36.
Koo P, Nagai MK, Farber E. Multiple sites of control of glutathione S-transferase P1–1 in rat liver. J Biol Chem. 1994; 269(20): 14601–4606.
37.
Mikhail TH, El-Sawaf HA, Ibrahim KM, Awadallah R, El-Dessoukey EA. Evaluation of the effect of lead exposure on the liver in Egyptian lead tank welders. Z Ernahrungswiss. 1980; 19(1): 50–56.
38.
Al-Neamy FR, Almehdi AM, Alwash R, Pasha MA, Ibrahim A, Bener A. Occupational lead exposure and amino acid profiles and liver function tests in industrial workers. Int J Environ Health Res. 2001; 11(2): 181–188.
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