Influence of Noise Pollution on Oxidative Stress Parameters and Acetylcholinesterase in Gas Electric Stations

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Journal of Babylon University/Pure and Applied Sciences/ No.(1)/ Vol.(22): 2012

College of Science/Babylon University Scientific Conference

Influence of Noise Pollution on Oxidative Stress Parameters and Acetylcholinesterase in Gas Electric Stations

Abdulsaheb S Jubran Lamia A M Al-Mashhedy

Chemistry Department, Babylon University, Babel, Iraq


Background: exposure to noise cause a harmful effects on human health which increase production of free radicals causing to oxidative stress in workers.

Objective: to investigate the effect of noise pollution on oxidative stress parameters and acetylcholinesterase.

Patients And Methods: this study executed on 91 workers aged (40.055 ± 11.56) years old selected randomly from tow gas electric stations divided into three groups depend on the years of working for worker in the station compared with 70 person as healthy control group aged (38.366 ± 10.73) years old. serum Malondialdhyde (MDA), Glutathione peroxidase (GPx), Glutathione reductase (GR) and Acetylcholinesterase (AChE) were investigated.

Result: MDA, GPx and GR levels were significantly (P≤0.05) higher in worker than that in the controls and lower level of AChE was significantly (P≤0.05) in workers than that of the controls.

Conclusion: elevation of MDA, GPx and GR levels also decreasing of AChE activity may because of high production of free radicals caused by exposure to noise pollution.

Keywords: Oxidative stress, Noise pollution, Acetylcholiesterase, Lipid peroxidation, free radicals.


Noise is an audible auditory energy, disturbing, uncomforting has great harmful effects on health that perturbs the human environment physiological and psychological life of the people, the noise is generated from human activities, especially in the developing countries, W.H.O (World Health Organization) has issued the optimum noise level as 45 dB by day and 35 by night. Any sound level above 80 dB is risky (W.H.O., 1999). Noise cause many health problems as hearing loss (Catlin FI, et al., 1986), hypertension (Brinton TJ, et al., 1996), blood pressure increasing (Kryter KD, et al., 1985), coronary heart disease (Ta-yuan C, et al., 2007) and other harmful effects.

The damage effect of noise due to increasing generation of free radicals which effect on human health (Reha D et al., 2009), free radicals can cause oxidative damage varied cellular components, including membranes, proteins and DNA, if they are not counteracted by antioxidant defenses. The increase production of free radicals leads to increase producing lipid peroxidation end products such as Malondialdehyde (MDA) which consider an indicator of lipid peroxidation processes (Derekoy FS, et al., 2001).

The glutathione peroxidase (GPx) and glutathione reductase (GR) enzymes acting as free radicals scavengers limit the influence of oxidants molecules in tissues and oxidative injury (Jafar M, et al,. 2012), these enzymes act together to provide defense against reactive oxygen species mediated injury by remove free radical species. GPx act on convert H2O2 to H2O by using GSH converted it to GSSG using NADPH as cofactor (Sogut S, et al., 2003), and another enzyme GR reduced the oxidized glutathione to complete the cycle as Figure (1).

Nقوس متوسط أيمن 15قوس متوسط أيسر 16قوس متوسط أيمن 17قوس متوسط أيسر 18ADP+ GSH H2O2



Figure (1) Interrelationship of glutathione pathways. GSH, Reduced glutathione; GSSG, Oxidized glutathione.

Acetylcholinesterase (AChE) is an enzyme that terminates Acetylcholine (ACh) mediated neurotransmission; it is a key enzyme for cholinergic transmission and plays a pivotal role in the nervous system of both the vertebrates and the invertebrates (Massoulie J, et al., 1999). The increasing of free radical formation causing hydrolyses the Acetylcholine to acetate and choline (Junior HVN, et al., 2009), and the brain susceptible to reactive oxygen species mediated oxidative damage owing to its high lipid content (Cui K, et al., 2004), neurotoxicity also results from oxidative stress induced by acetylcholinesterase inhibition in the brain (Amajad I and Anna O, 2012).

Methods and Materials

This study involved of 91 workers aged (40.055 ± 11.56) years old, selected randomly from two different electric gas stations in Babel city and Al-Najaf Al-Ashraf city, while the control samples were collected from 70 apparently healthy persons aged (38.366 ± 10.73) years old.

The blood samples took place in the period extending from February to April 2012, serum obtained by allowing blood samples to clot then centrifuged at 2000 xg for 10 minute, the bloods sample of workers was divided into three groups according to the period time of work in the station, the period time of the first group was between 2-8 years and the number of workers in this group was included forty workers between 2-8 years of working, the second group have period time of work between 9-19 years and contain twenty seven workers, the third and last group involved twenty four workers with period time (19<) years.

Lipid peroxidation was estimated in serum based on the formation of thiobarbituric acid reactive substances (TBARS) as described in (Burtis and Ashwood, 1999).

Glutathione peroxidase (GPx) was assayed by the method (Rotruck JT, et al., 1973), GPx catalyzed the reduction of t-BuOOH as a substrate by using GSH as the reduced substrate.

Glutathione reductase (GR) was assayed by the method (Eyer P and Podhradsky D, 1986) monitoring the oxidation of NADPH in presence of glutathione (GSSG).

Acetylcholinesterase (AchE) activity was determined in serum by the method (Ellman GL, et al., 1961) using acetylthiocholine as substrate, the method is the measurement of the rate of production thiocholine, acetylthiocholine is hydrolyzed to produce the yellow anion 5-thio-2-nitro-benzoic acid (II), and the color production is read at 412 nm.

Statistical analysis was performed by Microsoft excel office 2010. The data as expressed as mean ± SD and statistical significance was set at (P ≤0.05). The T-Test was performed to compare data and regression analysis was calculated for correlation between parameters.


The present study investigated the effects of noise pollution on workers in gas electric stations compared with controls. Age, GPx, GR, MDA, AChE levels and controls were given in Table 1 that employed to three groups of workers according to the years of working in the stations.

Table 1: levels of MDA, GPx, GR and AChE of worker groups compared with control.

The group


MDA (µmole/L)

GPx (U/mL)

GR (U/mL)

AChE (U/L)



1.646 ± 0.5

2.298 ± 0.6

7.049 ± 0.58

41.921 ± 9.1



2.401 ± 0.7

3.185 ± 0.7

8.82 ± 1.05

32.059 ± 4.6



2.808 ± 0.6

3.621 ± 0.65

9.576 ± 1.4

31.54 ± 8.99



0.6 ± 0.3

1.284 ± 0.3

5.034 ± 0.7

63.244 ± 4.69

The significant rise in MDA levels, GPx, GR activities (P≥ 0.05), (P≥ 0.05), (P≥ 0.05) respectively for workers groups compared with control group, and the increasing of MDA levels, GPx, GR activities dependent on the increasing of working years, while the activity of AChE was significantly decreased (P≥ 0.05) for workers than control group as show in Table 1.


Noise pollution is an important stress factor related to it’s the effects of human health in industrialization plants like gas electric stations. More people have been exposed to noise causing many health problems; the major harmful effect of noise is elevating production of free radicals. Free radicals are produce from cellular aerobic metabolism, these unbalance molecules can damage cellular lipids, proteins and nucleic acids in DNA if the equilibrium of consistent antioxidants is interrupted (Van Campen LE, et al., 2002).

The study shows there was significant rise in MDA levels for workers than the level of control. This result is indication for oxidative stress in workers serum and it may be due to exposed to noise pollution which leading to increasing produce of free radicals such as super oxide radicals, hydroxyl radicals, hydrogen peroxide radicals. Lipid peroxidation is a process of free radicals species break down lipid molecules. MDA is a pointer of lipid peroxidation processes (Nielsen F, et al., 1997) that leading to cells damage (Henderson D, et al., 2006) by break-down of lipid molecules in cells such as the lipid membrane in presence of free radicals (Yamasoba T, et al., 1998).

GPx and GR are cellular antioxidants act on protect cell from the harmful effects of free radicals (Halliwell B, 1997). There is an opposite relation between lipid peroxidation and antioxidants systems (Indira A H et al., 2008) and may also using the lipid hydroperoxides as a substrate, the increasing of GPx activity may due to the elevated of lipid peroxidation (Sogut et al., 2003) and consumption of GSH as a substrate for the main reaction of GPx (Reha D et al., 2009). Increased the elevation of ROS caused by noise leads to increasing activity of GPx. Thus, there was the major oxidant in oxidative stress (Hisham W and Mohammed A. 2011).

Also the reason of increased GR activity for workers may be due to decreased concentration of reduced glutathione GSH effected by H2O2 and other free radicals which produced from oxidative stress that caused by noise, and the increasing of GR activity is maintains adequate levels of GSH and GSSG cycle (ZhenquanJia et al., 2009). In our study increasing of GPx and GR activities are to oxidative stress for workers at environment of noise (Ozgoner M F et al., 1999).

AChE was found in all the parts of cholinergic system in brain, which included acetylcholine. The exposure to noise leads to harmful behavioral and physiological roles by moderating central cholinergic system in the brain (K. Sembulingam et al., 2003). The activity of AChE is inhibit by increase production of free radicals (T. Carbonell and R. Rama, 2000) where, The free radicals modified the protein possibly, tyrosine residues were oxidized by free radicals at the surface of the enzyme caused reduction in enzyme activity (Totsune H et al., 1999) and this is the one of reasons that reduced AChE activity. The increasing elevate of free radicals produce disappointed the oxidant and antioxidant equilibrium in the brain leads to oxidative stress (T. Carbonell and R. Rama, 2000), and the exposure to stress cause many changes in adrenergic system in brain (K. Sembulingam et al., 2003). The inhibition of AChE can adequate suggests neurotoxicity in workers brain and central nervous system (Zhou JF et al., 2002) and may cause bad effects on cholinergic neurotransmission (Carlos G et al., 2010). Our study showed inhibition of AChE workers than controls. This inhibition increased with increasing the duration time of work in the station because the production of free radicals is increasing with increased noise pollution exposure.


Work supported by gas electric stations in (Babel, Iraq) and (Al-Najaf Al-Ashraf, Iraq) cities. And we thank Mr. Mahmmoud H Hadwan for his grateful help.


  1. Amajad I, Anna O. "Monocrotophos induced oxidative damage associates with severe acetylcholinesterase inhibition in rat brain". Neurotoxicology 2012; 3:156-161.

  2. Brinton TJ, Kailasam MT, Wu RA, Cerveenka JH, Chio SS, Parmer RJ, et al. "Arterial compliance by cuff sphygmomanometer: application to hypertension and only changes in subjects at genetic risk". Hypertension 1996; 28: 599-603.

  3. Burtis CA, Ashood ER. Tietz textbook of clinical chemistry; 3rd ed. W.B. Saunders Company, Tokyo 1999; 1034-54.

  4. Carlos G, Laura G, Toana S, Meilssa F, Anabela A, Lucia G. "Comparative study about the effects of pollution on glass and yellow eels (Anguilla anguilla) from theestuaries of minho. Lima and Douro Rivers (NW Portugal)". Ecotoxicology and Environmental safety 2010; 73: 524-33.

  5. Catlin FI. "Noise-induced hearing loss". Am J Otol. 1986; 7: 141-49.

  6. Cui K, Luo X, Xu K, Van Murthy MR. "Role of oxidative stress and nutraceutical antioxidants". Prog Neuropsychopharmacol Biol Psychiatry 2004; 28: 771-99.

  7. Derekoy FS, Dundar Y, Aslan R, Canjal A. "Influence of noise exposure an antioxidant system and TEOAFs in rabbits". Eur. Arch. Otokhinolaryngol 2001; 258: 518-22.

  8. Ellman GL, Courtney KD, Andres V, Featherstone RM. "A new and rapid colorimetric determination of acetylcholinesterase activity". Biochem Pharmacol 1961; 7: 88-95.

  9. Eyer P, Podhradsky D. Anal Biochem 1986; 153: 157-66.

  10. Halliwell B. "Antioxidant and human diseases: a general introduction". Nutr Rev 1997; 55: S44-52.

  11. Henderson, Bielefel EC, Harris KC, Hu BH. "The role of oxidative stress in noise-induced hearing loss". Ear Hear 2006; 27: 1-19.

  12. Hisham W, Mohammed A. "The effect of oxidative stress on human red cells glutathione peroxidase, glutathione reductase levels and prevalence of anemia among diabetics". North Am J Med Sci 2011; 3: 344-47.

  13. Indira AH, Ansuryaka, OB Rath. "Oxidative stress and antioxidant status in acute organophosphorous pesticides poisoning coses of north Karnataka (India)". Journal of Environmental Health Research 2008; 11: 1-39.

  14. Jafar M, Ladan H, Mohsen S. "Maternal oxidative stress and enzymatic antioxidant status in premature rapture of membranes". African Journal of Biochemistry Research 2012; 6(2): 27-32.

  15. Junior HVN, De Fonteles MM, Mende de Freitas R. "Acute Seizure activity promotes lipid peroxidation, increased nitrite levels and adaptive pathways against oxidative stress the Frontal cortex and striatum oxide". Med Cell longer 2009; 2: 130-7.

  16. Kryter KD. "The effect of noise on man". Academic press 1985.

  17. K. Sembulingam, P. Sembulingam, A. Namasivayam. "Effect of acute noise stress on acetylcholinesterase activity in discrete areas of rat brain". Indian Journal of Medical Sciences 2003; 57(11): 487-92.

  18. Massoulie J, Anselmet A, Bon S, Krejei E, Legay C, Morel N, et al. in "The polymorphism of acetylcholinesterase post-translational processing, quaternary associations and localization". Chemico-Biological Interactions 119-120(1999); 29-42.

  19. Ozgoner MF, Delisas N, Tahan V, Koyv A, Koylu H. "Effects of industrial noise on the blood levels of superoxide dismutase, glutathione peroxidase and malondialdehyde". Eastern Journal of Medicine 1999; 4: 13-15.

  20. Rotruek JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra WG. "Selenium: Biochemical Role as a component of glutathione peroxidase". SCIENCE 1973; 179 (4073): 588-90.

  21. Reha D, Hakan M, Hasan Y, Kagam U, Abdullah A, Muzaffer A, et al. "Noise induced oxidative stress in Rat". Eur. J Gen Med 2009; 6 (1): 20-24.

  22. Sogut S, Zoroglu SS, Ozyurt H. "Changes in nitric oxide levels and antioxidant enzyme activities may have a role in the pathophysiological mechanisms involved in autism". Clin. Chim. Acta 2003; 331: 111-7.

  23. Ta-Yuan C, Ta-Chen S, Shou-Yu L, Ruei-Man J, Chang-Chuan C. "Effect of occupational noise exposure on 24-hour Ambulatory vascular properties in male workers". Environ Health Perspect 2007; 115: 1660-4.

  24. T. Carbonell, R.Rama."Iron, oxidative stress and early neurological deterioration in ischemic stroke".Current Medicinal Chemistry 2000;33(2):857-74.

  25. Totsune H, Ohno C, Kambayashi Y, Nakano M, Ushijima Y, Tero-Kubota et al. "Characteristics of chemiluminescence observed in the horseradish peroxidase–hydrogen peroxide–tyrosine system". Archives of Biochemistry and Biophysics 1999; 369 (2),233-42.

  26. Van Campen LE, Murphy WJ, Franks JR, Mathias PI, Toraason MA. "Oxidative DNA damage is associated with intense noise exposure in the rat". Hear Res 2002; 164: 29-38.

  27. W.H.O. Guidelines for community noise London United Kingdom 1999.

  28. Yamasoba T, Harris C, Shoji F, Lee RJ, Nuttal AL, Miller JM. "Influence of intense sound exposure on glutathione synthesis in the cochlea". Brain Res 1998; 804: 72-8.

  29. Zhenquan J, Hong Z, Yunbo L, Hara P, Misra. "Cruciferous Nutraceutical 3H-1,2-dithiole 3-thione protects Human primary Astrocytes Against Neurocytotoxicity Elicited by MPTP MPP+, 6-OHOA, HNE and Aerolein". Neurochem Res 2009; 34: 1924-34.

  30. Zhou JF, Xu GB, Feing WJ. "Relationship between a cute organophosphorus pesticide poisoning and oxidative damages induced by free radicals". Biomed Environ Sci. 2002; 15: 177-86.

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