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Study the effect of gases rising from electric generators on sera lead, advanced oxidation protein products, acid, alkaline DNaes and ecto-5-prime-nucleotidase activity in Iraqi workers employed on the operation of diesel generators.


Diesel generators which are used in the living quarters when electricity is cut off, is a significant source of emissions of polluted air. In electricity generation, an electric generator is a device that converts mechanical energy to electrical energy[1]. Carbon monoxide is the product formed by the incomplete combustion of materials containing carbon. The molecular formula is CO. Carbon monoxide is usually present in the workplace as a gas. It can, however, be liquefied and solidified. Carbon monoxide is produced in large amounts by several industrial processes carbon monoxideis produced by the incomplete combustion of materials containing carbon[2]. Lead poisoning (also known as plumbism) is a medical condition in humans and other vertebrates caused by increased levels of the heavy metal lead in the body. Lead affects on a variety of body processes and is poisonous to many organs and tissues as well as the heart, kidneys, bones, nervous systems , and intestines. It interferes with the improvement of the nervous system and is therefore predominantly toxic to children, producing potentially enduring learning and behavior disorders. Symptoms include abdominal pain, confusion, headache, anemia, irritability, and in severe cases seizures, coma, and death[3]. Deoxyribonucleases are a great group of enzymes categorized by considerable structural and functional variety. In eukaryotic cells they are complicated in a range of cellular jobs, including DNA repair, recombination and genome degradation. The degradation of nuclear DNA, a stamp of programmed cell death (PCD), is a development that happened both in animals and in plants(4).The two main types of DNase originate in humans are known as Alkaline DNase (DNase I) and Acid DNase (DNase II) [5]. The activity of alkaline DNase is the result of a group of enzymes which depolymerise DNA in alkaline situations, whereas that of acid DNase, a group of enzymes have optimal activity in acid pH[6]. Ecto-5-prime-nucleotidase (5-prime-ribonucleotide phosphohydrolase; EC an enzyme that in humans is encoded by the NT5E gene [7]. It is catalyzes the conversion at neutral pH of purine 5-prime mononucleotides to nucleosides, the preferred substrate being AMP. The enzyme consists of a dimer of 2 identical 70-kD subunits bound by a glycosylphosphatidyl inositol linkage to the peripheral face of the plasma membrane. The enzyme is used as a indicator of lymphocyte differentiation. Accordingly, a deficiency of Ecto-5-prime-nucleotidase happens in a variation of immunodeficiency diseases. Other forms of 5prime nucleotidase be present in the cytoplasm and lysosomes and can be illustrious from ecto-NT5 by their substrate affinities, requirement for divalent magnesium ion, activation by ATP, and inhibition by inorganic phosphate[8]. The AOPPs are one of the biochemical parameters indicative of oxidation stress. The AOPPs are proteins, predominantly albumin and its cumulative damaged by oxidative stress [9]. The AOPPs are the dityrosine-containing and crosslinking protein products formed during oxidative stress through reaction of plasma protein with chlorinated oxidants[10]. The aim of the present study is to determine the effect of gases rising from electric generators on Iraqi workers employed on the operation of diesel generators especially increased lead poisoning symptoms such as headaches, muscle weakness irritability, fatigue, difficulty sleeping, difficulty learning or concentrating, aggressive behaviour, stomach pain, constipation, vomiting, nausea, weight loss, anemia, unusual paleness, kidney function disorder , and loss of appetite on some biochemical parameters.


The sampling procedure was done in 50 Iraqi workers employed on the operation of diesel generators (35.47[+ or -]5.29years) comparing with 40 male healthy (34.80[+ or -]4.28) years. The medical history was taken, bodyweight and height were measured and body mass index (BMI) was calculated as kg/[m.sup.2]. The blood was allowed to clot for 10-15 min. at room temperature, centrifuged for [10] min. at (3000xg). Serum was removed to measure the biochemical parameters. Serum total protein was determined by Lowry et al. method [11] using bovine serum albumin (BSA) as a standard protein. Acid DNase activity was determined in serum by a method of Kunitz [12] with some modification, where [0.05] ml of serum added to a mixture consist of 0.75 ml of substrate and0.75 ml of Tris-HCL buffer. The rate of increase in the absorbency of the sample solution was recorded at 260 nm and 25[degrees]C after 1.5 min. Alkaline DNase activity was determined in serumby a method of Kunitz[13]. Serum Lead was measured by atomic absorption spectrometry. The serum AOPP was measured by Enzyme Linked Immunosorbent Assay (ELISA)(CuSaBIO BIOTECH COM.). All statistical analysis in the study was performed using SPSS version 22.0 for Windows (Statistical Package for Social Science, Inc., Chicago, IL, USA). Descriptive analysis was showed the mean and standard deviation of variables. The significance of differences between mean values was evaluated by Student t-test. The probability p<0.05 was considered statistically significant, while p>0.05 was referred to statistically insignificant. Correlation analysis was used to test the linear relationship between the factors. ANOVA test was used to confirmation the differences between variables of different groups.


The results were observed as follows of fifty Iraqi workers employed on the operation of diesel generators[group A], 30 normal men [group B]were serve as control group. Demographic distribution of groups of man according to definite characteristics were shown in table 1.

As the results in table 2 show there are highly significant increases (p>0.001) in the mean value of serum lead and AOPP in group A [Iraqi workers employed on the operation of diesel generators] when compared to group B [control group].

The results in table 3 and 4 showed a significant increase in both acid and alkaline DNase activity and specific activity in sera group A [Iraqi workers employed on the operation of diesel generators] when compared to group B [control group] (p<0.001).

There were a highly significant increase in mean levels of activities and specific activities of sera Ecto-5prime- nucleotidas of group A [Iraqi workers employed on the operation of diesel generators] when compared to group B [control group] (p<0.001) as shown in table 5.

There were a significant positive correlations between alkaline, acid DNase activity and Ecto-5-prime nucleotidase with serum lead in group A [Iraqi workers employed on the operation of diesel generators] as shown in table 6. As our knowledge no previous study referred to these correlation.


The current reference range for acceptable blood lead concentrations in healthy persons without excessive exposure to environmental causes of lead is less than 5 [micro]g/dl for children(14). It was less than 25 [micro]g/dl for adults[15]. The National Institute for Occupational Safety and Health (CDC/NIOSH) reference blood lead level in adults is 10 [micro]g/dl[16]. The U.S. national BLL geometric mean among adults was 1.2 [micro]g/dl in 2009- 2010[17].

Lead is a toxic metal whose extensive use has produced extensive environmental contamination and health glitches in many parts of the world. Human exposure to lead is estimated to account for 143 000 deaths every year and 0.6% of the global burden of disease [18]. Lead is a accumulative toxicant that affects various body systems, as well as the neurological, haematological, gastrointestinal, cardiovascular and renal systems. Chronic exposure commonly causes haematological effects, such as anaemia, or neurological disturbances, including headache, irritability, lethargy, convulsions, muscle weakness, ataxia, tremors and paralysis. Acute exposures may cause gastrointestinal disturbances (anorexia, nausea, vomiting, abdominal pain), hepatic and renal damage, hypertension and neurological effects (malaise, drowsiness, encephalopathy) that may lead to convulsions and death[17]. The clinical diagnosis of lead poisoning can be difficult when there is no clear history of exposure, because poisoned individuals can be asymptomatic, and signs and symptoms, when they are present, are relatively nonspecific. Laboratory investigations are the only reliable way to diagnose lead-exposed individuals and therefore play an essential role in the identification and management of lead poisoning and in the assessment of occupational and environmental lead exposure[19]. Alkaline DNase, in addition to acid DNase, has been concerned in apoptosis [20]. Alkaline DNase has been found in the nuclei of apoptotic thymocytes[21]. Alkaline DNase was shown to be constitutively expressed in bovine epithelial lens cells [22] or lens fibers [23], and might be reflected as an enzyme associated with nuclear degradation proceedings, mainly with the final phases of the DNA degradation. In addition, another study suggested that Alkaline DNase could behave as a transcription factor which selectively regulated cell surface Fas expression in human cells and pointed towards a central role of Alkaline DNase in the regulation of the apoptotic machinery [24,25]. The primary cause of lead's toxicity is its interference with a variety of enzymes because it binds to sulfhydryl groups found on numerous enzymes. [26] Part of lead's toxicity results from its ability to mimic other metals that take part in biological processes, which act as cofactors in many enzymatic reactions, displacing them at the enzymes on which they act[27]. Serum AOPP are mainly carried via albumin. Its concentration thoroughly correlates with the level of dityrosine, a hallmark of oxidized protein. Therefore, AOPP have been considered such as the markers of oxidant-mediated protein damage[10]. Lead is able to bind to and interact with numerous of the same enzymes as these metals but, due to its different chemistry, does not properly function as a cofactor, therefore interfering with the enzyme's capability to catalyze its normal reaction [28]. As the present result the association of lead with chromatin in cells recommends that harmful metal effects may in part be mediated changes in gene function.

In conclusion Exposure to lead may also decrease lifespan and have health effects in the long term for these workers. Death rates from a variety of causes may be found to be higher in Iraqi workers employed on the operation of diesel generators with elevated blood lead levels; these include cancer, stroke, and heart disease, and common death rates from all causes. In the present result lead is considered a probable carcinogen in these workers. Suggestion in the current study moreover suggests that age-related mental decline and psychiatric symptoms are correlated with lead contact. According our result the accumulative contact over a continued period possibly will have a more important effect on some features of health than current exposure Some health effects, such as different cancer diseases are a significant risks when lead exposure is prolonged (over about one year).


Article history:

Received 2 April 2014

Received in revised form 13 May 2014

Accepted 28 June 2014

Available online 23 July 2014


[1] Goudarzi, N.A., 2013. Review on the Development of the Wind Turbine Generators across the World. International Journal of Dynamics and Control., 1(2): 192-202.

[2] Weaver, L.K., 2009. Clinical practice. Carbon monoxide poisoning. The New England Journal of Medicine, 360(12): 1217-1225.

[3] Guidotti, T.L., 2007. Ragain L. Protecting children from toxic exposure: three strategies. Pediatric clinics of North America, 54(2): 227-35.

[4] Lesniewicz, K., E. Por^ba, M. Smolarkiewicz, N. Wolff, S. Stanislawski and P. Wojtaszek, 2012. Plant plasma membrane-bound staphylococcal-like DNases as a novel class of eukaryotic nucleases. BMC Plant Biol., 12: 195-198.

[5] Mahckova, K., D. Duricova, M. Bortlik, Z. Hruskova, B. Svobodova, N. Machkova, V. Komarek, T. Fuakova, I. Janatkova, T. Zima and M. Lukas, 2011. ImpairedDeoxyribonuclease I Activity in Patients with Inflammatory Bowel Diseases. Autoimmune Dis., pp: 1-5.

[6] Taper, H.S., 2008. Altered Deoxyribonuclease Activity in Cancer Cells and its Role in Non Toxic Adjuvant Cancer Therapy with Mixed Vitamins C and K3. Anticancer Res., 28: 2727-2732.

[7] Misumi, Y., S. Ogata, K. Ohkubo, S. Hirose, Y. Ikehara, 1990. Primary structure of human placental 5'nucleotidase and identification of the glycolipid anchor in the mature form. Eur. J. Biochem., 191(3): 563-9.

[8] Katrina, L. and B. Charles, 2010. 5-Nucleotidases and their new roles in NAD+ and phosphate metabolism. New J. Chem., 34: 845-853.

[9] Kalousova, M., T. Zima, V. Tesar, S. Dusilova-Sulkova and J. Skrha, 2005. Advanced glycoxidation end products in chronic diseases-clinical chemistry and genetic background. Mutat. Res., 579: 37-46.

[10] Zhou, Q., S. Wu, J. Jiang, J. Tian, J. Chen, X. Yu, P. Chen, C. Mei, F. Xiong, W. Shi, W. Zhou, X. Liu, S. Sun, D.I. Xie, J. Liu, X. Xu, M. Liang and F. Hou, 2012. Accumulation of circulating advanced oxidation protein products is an independent risk factor for ischaemic heart disease in maintenance haemodialysis patients. Nephrology, 17(7): 642-649.

[11] Lowry, O., N. Rosebrough, A. Farr, at al., 1951. Protein measurement with the Folin phenol regent. J BiolChem.,193: 265-275.

[12] Smith, D.G., W.H. Stein and S. Moors, 1974. In "Methods in Enzymatic Analysis". Ed. Bergmeyer H.U., second ed., Academic Press, Inc., U.S.A., pp: 442.

[13] Kunitz, M., 2015. Crystalline desoxyribonuclease: ii. digestion of thymus nucleic acid(desoxyribonucleic acid) the kinetics of the reaction. J Gen Physiol, 33(4): 363-377.

[14] "Advisory, 2012. Committee On Childhood Lead Poisoning Prevention (ACCLPP)". CDC. May 2012. Retrieved. Wu. Tietz (2006) Clinical Guide to Laboratory Tests, 4th ed., Saunders Elsevier, St. Louis, MO, pp: 658-659.

[15] CDC., 2013. NIOSH Adult Blood Lead Epidemiology & Surveillance (ABLES) program description. Cincinnati, OH: US Department of Health and Human Services, CDC, National Institute for Occupational Safety and Health.

[16] CDC., 2012. Fourth National Report on Human Exposure to Environmental Chemicals. Updated Tables, September 2012. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. Available at http ://www. ables.

[17] Global health risks: Mortality and burden of disease attributable to selected major risks. Geneva, World Health Organization, 2009 (, accessed 20 December 2010).

[18] Exposure to lead: A major public health concern. Geneva, World Health Organization, 2010 (, accessed 20 December 2010).

[19] Shiokawa D. and S. Tanuma, 2001. Characterization of human DNase I family endonucleases and activation of DNase y during apoptosis. Biochemistry, 40: 143-152.

[20] Peitsch M., B. Polzar, H. Stephan, T. Crompton, H. McDonald, H.G. Mannherz and J. Tschopp, 1993. Characterization of the endogenous deoxyribonuclease involved in nuclear DNA degradation during apoptosis (programmed cell deathEMBO J., 12: 371-377.

[21] Rauch, F., B. Polzar, H. Stephan, S. Zanotti, R. Paddenberg and H.G. Mannherz, 1997. Androgen Ablation Leads to an Upregulation and Intranuclear Accumulation of Deoxyribonuclease I in Rat Prostate Epithelial Cells Paralleling Their Apoptotic Elimination J. Cell Biol., 137: 909-923.

[22] De Maria, A. and C. Arruti, 2003. Bovine DNase I: gene organization, mRNA expression, and changes in the topological distribution of the protein during apoptosis in lens epithelial cells Biochem. Biophys. Res. Commun., 312: 634-641.

[23] De Maria A. and C. Arruti, 2004. DNase I and fragmented chromatin during nuclear degradation in adult bovine lens fibersMol. Vision, 10: 74-82.

[24] Oliveri, M., A. Daga, C. Lunardi, R. Navone, R. Millo And A. Puccetti, 2004.DNase I behaves as a transcription factor which modulates Fas expression in human cellsEur. J. Immunol., 34: 273-279.

[25] Pearson, H.A, and D.J. Schonfeld, 2003. Lead. In Rudolph, C.D..Rudolph'sPediatrics, 21st edition. McGraw-Hill Professional., pp: 369.

[26] Dart, R.C., K.M. Hurlbut, L.V. Boyer-Hassen Lead. RC. In Dart, 2004. Medical Toxicology, 3rd edition. Lippinco. Williams & Wilkins., pp: 1426.

[27] Kosnett, M.J., 2006. Lead, in Poisoning and Drug Overdose, 5th edition (ed. K.R. Olson), Lange/McGrawHill, New York, pp: 238.

(1) Atheer A Mehde, (2) Wesen A Mehdi, (2) Rasha H. Alwan, (3) Ali L. Salih

(1) Department of Acceptable Analysis, Health and Medical Technical College, Baghdad, Iraq.

(2) Department of chemistry, College of sciences for women, university of Baghdad, Iraq.

(3) Medical City, Teaching Labs, Baghdad, Iraq.

Corresponding Author: Dr. Atheer A Mehde, Department of Acceptable Analysis, Health and Medical Technical College, Baghdad, Iraq. E-mail:
Table 1: The mean and standard deviation of Age, weight,
height and BMI in group A and group B.

Characteristic                Group A[n=50]

Age[year] Mean [+ or -] SD    35.47 [+ or -] 5.29
Range                         25.00-42.00

Weight[Kg] Mean [+ or -] SD   85.51 [+ or -] 11.88
Range                         78.50-115.00

Hight [m] Mean [+ or -] SD    1. 78 [+ or -] 0.52
Range                         1.75-1.80

BMI [Kg/[m.sup.2]]            28.65 [+ or -] 2.05
  Mean [+ or -] SD
Range                         26.55-30.21

Characteristic                Group B[n=40]         p Value

Age[year] Mean [+ or -] SD    34.80 [+ or -] 4.28   >0.05
Range                         22.040-41.00

Weight[Kg] Mean [+ or -] SD   86.43 [+ or -] 7.77   >0.05
Range                         80.00-100.00

Hight [m] Mean [+ or -] SD    1.79 [+ or -] 0.47    >0.05
Range                         1.76-1.83

BMI [Kg/[m.sup.2]]            28.90 [+ or -] 1.95
  Mean [+ or -] SD
Range                         27.15-29.41           >0.05

As shown in table 1 there were no significant different between
two groups in age ,weight , hight and BMI.

Table 2: The level of S. lead in of group A and Group B

Characteristic         Group A[n=50]

S.Lead [[micro]g/dl]   15.75 [+ or -] 0.90
AOPP [ng/dl]           110.23 [+ or -] 24.56

Characteristic         Group B [n=40]           p Value

S.Lead [[micro]g/dl]   3.39 [+ or -] 0.05       <0.001
AOPP [ng/dl]           63.75 [+ or -] 18.12     <0.001

Table 3: Activities and specific activities of sera acid
DNase of group A and Group B.

                              Group A[n=50]
Characteristic                (mean value  [+ or -] SD)

Activities*[10.sup.3] [U/L]   100.33 [+ or -] 22.23
S. Protein[g/dl]              7.00 [+ or -] 1.09
Specific Activities [U/mg]    1.42 [+ or -] 0.49

                              Group B[n=40]
Characteristic                (mean value  [+ or -] SD)   p Value

Activities*[10.sup.3] [U/L]   38.22 [+ or -] 9.99         <0.001
S. Protein[g/dl]              7.85 [+ or -] 0.92          <0.05
Specific Activities [U/mg]    0.48 [+ or -] 0.37          <0.001

Table 4:Activities and specific activities of sera alkaline
DNase of group A and Group B.

                              Group A[n=50]
Characteristic                (mean value [+ or -]SD)

Activities*[10.sup.3] [U/L]   89.98 [+ or -] 21.99
S. Protein[g/dl]              7.00 [+ or -] 1.09
Specific Activities [U/mg]    1.28 [+ or -] 0.56

                              Group B[n=40]
Characteristic                (mean value [+ or -]SD)   p Value

Activities*[10.sup.3] [U/L]   32.88 [+ or -] 10.29      <0.001
S. Protein[g/dl]              7.85 [+ or -] 0.92        <0.05
Specific Activities [U/mg]    0.41 [+ or -] 0.34        <0.001

Table 5: Activities and specific activities of sera
ecto-5-prime-nucleotidasof group A and Group B.

                      Group A[n=50]
Characteristic        (mean value [+ or -]SD)

Activities [U/L]      86.28 [+ or -] 20.93
S. Protein[g/dl]      7.00 [+ or -] 1.09
Specific              1.23 [+ or -] 0.52
  Activities [U/mg]

                      Group B[n=40]
Characteristic        (mean value [+ or -]SD)   p Value

Activities [U / L]    12.23 [+ or -] 4.19       <0.001
S. Protein[g/dl]      7.85 [+ or -] 0.92        <0.05
Specific              0.15 [+ or -] 0.24        <0.001
  Activities [U/mg]

Table 6: Correlation between s.lead, AOPP with DNase and Ecto-5-prime
nucleotidase in group A [Iraqi workers employed on the operation of
diesel generators].

Characteristic   Acid DNase[U/L]

                 Pearson        Sig.
                 correlation    (2-tailed)

S.Lead           0.80           0.01
S.AOPP           0.76           0.01

Characteristic   Alkaline DNase[U/L]

                 Pearson        Sig.
                 correlation    (2-tailed)

S.Lead           0.87           0.01
S.AOPP           0.83           0.01

Characteristic   [U/L]

                 Pearson        Sig.
                 correlation    (2-tailed)

S.Lead           0.75           0.01
S.AOPP           0.75           0.01
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Author:Mehde, Atheer A.; Mehdi, Wesen A.; Alwan, Rasha H.; Salih, Ali L.
Publication:Advances in Environmental Biology
Article Type:Report
Date:Jul 1, 2014
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