الفهرس 
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Abstract
- Summary
Wood dust is a complex substance that can cause different health problems during manufacture. These health problems may be a result of inducing oxidative stress which is causally related to inflammations. It is known to be a human carcinogen, with a considerable risk of lung cancer. The increased cancer risk is likely induced through its genotoxic effects resulting from oxidative DNA damage.
The aim of the current study is to evaluate effects of wood dust on antioxidants status in terms of SOD, CAT and GPx enzymes. Levels of serum MIP-2 as oxidative stress marker in exposed workers. Also, its genotoxic effects designated as comet parameters and EPHX gene polymorphism in exon 3 and exon 4 in different duration of exposure from 5, 10, 15 to 20 years.
This study was performed on 50 workers exposed to wood dust from a factory for furniture manufacture in Cairo governorate. Also, 50 healthy individuals not occupationally exposed to wood dust were recruited as controls. The workers and controls subjects were matched for age, socioeconomic status, dietary habits. Both groups were divided into four subgroups according to ages and
workers subgroups were classified according to duration of exposure to wood dust to 5, 10, 15 and 20 years. First subgroup includes twelve of workers exposed to wood dust for 5 years, their age range were (20 – 25 years), second subgroup includes thirteen of workers exposed to wood dust for 10 years and their age range were (25 -30 years), third subgroup includes twelve of workers exposed to wood dust for 15 years, their age range were (35- 45 years) and fourth subgroup includes twelve of workers exposed to wood dust for 20 years, their age range were (40 – 55 years). Blood samples were collected from each subjects and divided into: 1-Heparin tube for assessment of DNA damage in a portion of whole blood as Comet assay.2- EDTA tube for determination of EPHX gene polymorphisms by polymerase chain reaction (PCR- RFLP). Plasma was separated from other portion of whole blood for catalase determination by a colorimetric method. Washing packed RBCs for determination of antioxidant SOD and GPx enzyme activities by kinetic methods and. Other dry tube was used to collect blood in order to separate serum for MIP-2 estimation by enzyme-linked immunosorbent assay (ELISA).
Biochemical assessment of altered antioxidant enzyme activities illustrated role of oxidative stress (OS)
that may lead to depletion in antioxidant status. SOD, glutathione peroxidase (GPx) and catalase (CAT) (as radical-scavenging enzymes)
The observed results are:
Biochemical results: 1-Antioxidants
Levels of (SOD, CAT) antioxidants enzymes demonstrated significant reduction (P < 0.003 and 0.003 respectively) among workers exposed to wood dust for different duration of exposure (5,10,15 and 20 years),where mean levels of (SOD, CAT) were (219.91± 64.546 U/mL, 376.92 ± 133.64 U/L ), (252.23 ± 50.89 U/mL, 380.73 ±
124.23 U/L), (204.07 ± 56.77 U/mL, 476.69 ± 122.29 U/L)
and (236.91± 39.29 U/mL, 412.50±121.07 U/L
respectively) when comparing with healthy groups, where mean levels of (SOD, CAT) were (256.75±62.24 U/mL, 623.67±123.43 U/L), (282.85 ± 44.84U/mL, 702.93 ±
70.32U/L), (279.15 ± 54.38U/mL, 626.08 ± 91.42U/L), (257.83± 42.85U/mL, 651.42 ±102.96U/L). While GPx
levels recorded non-significant reduction between different durations.
2-Macrophages inflammatory portion-2 (MIP-2)
Macrophage inflammatory protein -2 levels recorded significant elevation (P<0.001) along different duration of exposure (5, 10, 15 and 20 years) where mean levels of
MIP-2 were (183.82 ±11.05 ng/L, 223.92 ±24.86ng/L,
327.76± 55.43 ng/L and 638.25± 219.45 ng/L, respectively) among workers exposed to wood dust when compared with healthy control groups, where mean levels were (174.58
±19.17 ng/L, 190.31 ± 16.88 ng/L, 215.15 ± 24.17 ng/L,
451.33 ± 102.51 ng/L respectively).
Molecular results 1- Comet assay
Comet assay result in terms of tail length, % DNA (DNA migration) and tail moment showed significant rise (P<0.001, P<0.001, P<0.001) among exposed workers along different duration of exposure (5,10,15 and 20) where mean levels of tail length were (9.75 ± 1.06 μm, 11.50
±1.73 μm, 13.60 ±3.50 μm, 14.70 ± 5.95 μm, respectively),
% DNA were (2.63 ± 0.82, 3.17 ± 0.11, 3.68± 0.61, 4.12±
1.24 respectively) and tail moment were (0.38 ± 0.11 μm/cell, 0.45 ± 0.2 μm/cell, 0.59 ± 0.28 μm/cell, and 0.78
± 0.17 μm/cell respectively) in comparison with healthy control group, where mean levels of tail length were (3.73
± 0.61 μm 3.10 ± 1.59 μm 3.50 ± 2.15 μm and 4.80 ±
1.41μm respectively), % DNA were (0.17 ± 0.06, 0.18 ± 0.041, 0.15 ± 0.05 and 0.16 ± 0.07). Levels of tail moment
were (0.06 ± 0.02 μm/cell, 0.06 ± 0.01 μm/cell, 0.07 ± 0.02 μm/cell and 0.07 ± 0.03 μm/cell respectively).
2- Microsomal epoxide hydrolase gene polymorphisms EPHX (exon 3 and 4).
Genotypes frequency of EPXH1 polymorphism at exon 3 illustrated significant difference (P< 0.047) in exposed workers along different duration of exposure (5, 10, 15 and 20 years compared with healthy control groups. Wild type (Tyr-Tyr) genotype was (25.0%, 30.77%, 23.08% and 41.67 %,) in exposed workers and (58.34%,
53.84 %, 84.61% and 50.00%) in healthy control group.
Heterozygote type (Tyr-Hist) was (50.00%, 30.77%, 38.46% and 25.00%) in exposed workers and in healthy group it was (33.33%, 38.46%, 7.69% and 50.00%). In addition, homozygous mutant genotype (Hist-Hist) was (25.0%, 38.46%, 38.46% and 33.33%) in exposed workers
and (8.33%, 7.70%, 7.69% and 0.00%) in healthy group.
On the other hand, genotypes frequency of EPHX1 polymorphism at exon 4 reported significant difference (P=0.05) among exposed workers for different exposure
duration (5, 10, 15 and 20 years) in comparison with healthy control groups. Wild type (Hist-Hist) genotype was (25.0%, 30.77%, 53.86% and 8.33%) in exposed workers
and (66.67%, 53.84%, 84.62% and 50.0%) in healthy control group. Heterozygote (Hist-Arg) genotype was (50.0
%, 38.46%, 15.38% and 50.0%) in exposed workers and
(25.0%, 30.76%, 15.38% and 33.33%) in healthy control groups. Homozygous mutant (Arg-Arg) genotype was (25.0%, 30.77%, 30.76% and 41.67%) in exposed workers
and (8.33%, 15.4%, 0.0% and 16.67%) in healthy control groups.
The results revealed that exposure to wood dust along different duration from 5, 10, 15, and 20 years) had deserve effects in antioxidants efficiency (SOD and CAT), it also promoted immune response through releasing humoral mediators (as MIP-2) which mediates the acute inflammatory response.
Increasing years of occupational exposure to wood dust raised levels of genetic damage. In addition to alterations in genotype frequency of EPXH1 at exon 3 and exon 4 leading to variation in the defense capacity against genotoxic compounds among workers in the surrounding working environment.
Thus, it was recommended to increase health education periodically for these workers about the potential hazard of occupational exposure and the importance of using protective measures. Antioxidant-rich foods (such as fruits and vegetables) should be suggested for those exposed workers.