فهرست مطالب jahanbakhsh asadi

Esophageal cancer stem cells (ECSCs) have been identified as the subset of cells within esophageal squamous cell carcinoma that possess tumorigenic, invasive, and metastatic properties. One important aspect of cancer metastasis is the binding of sialyl-Lewis X (CD15s) with E- or P-selectin, which facilitates the adhesion and migration of cancer cells to distant sites. This study was conducted to investigate the impact of fucosylation processes on the metastatic behavior of ECSCs.

The esophageal cancer cell line (KYSE-30) was cultured and divided into control and 2F-peracetyl fucose (2F-PerAcFuc) treated groups. Spheres were harvested from these cultures. Cell invasion assay and qPCR were conducted to examine migration and marker expression in both groups. Cancer cell line-derived xenografts were established in nude mice to validate findings in vivo.

Our results initially indicated that the addition of 2F-PerAcFuc, an inhibitor of fucosylation, resulted in the down-regulation of the Fut3/CD15s pathway in both cancer stem-like cells and the xenograft model. Measurements of subcutaneous xenograft tumor volume revealed a significant decrease in tumor size among nude mice after treatment with 2F-PerAcFuc. Additionally, a reduction in Fut8/E-cadherin levels was observed in the xenograft model of nude mice. Furthermore, the administration of 2F-PerAcFuc lowered the levels of fucosylated glycoconjugates in nude mice.

Our data suggest that inhibition of fucosyltransferase 3 and 8 can reduce the metastatic capacity of cancer stem-like cells by down-regulating CD15s and E-cadherin in a mouse model of esophageal cancer.

Herbal components, particularly sesquiterpenes, are progressively recognized as a crucial resource for developing effective therapeutic agents for breast cancer. In this study, the effect of a sesquiterpene lactone known as 8-O-dihydroxy-11α,13-dihydroeudesma-4(15)-en-12,6α-olide (persianolide- A) was examined in breast cancer cell lines.

Experimental approach: 

MDA-MB-231 and MCF-7 cancer cells were grown in DMEM solution with 10% FBS. Then, an MTT assay was performed to evaluate cell viability. Apoptosis was detected by annexin-PI staining. A caspase 3/7 activity assay kit was used to assess the activity of caspase-3 and caspase-7. Protein expression of Bcl-2, Bax, and p-ERK1/2 was determined by western blotting.

This study showed that the IC50 values of the persianolide-A for MCF-7 and MDA-MB- 468 cells are 34.76 and 54.48 μM, respectively. In addition, persianolide-A showed a significant increase in apoptosis in both MDAMB-231 and MCF-7 breast cancer cell lines. Persianolide-A significantly increased the expression of the pro-apoptotic protein Bax and decreased the expression of the anti-apoptotic protein Bcl-2. Also, presinolide-A treatment led to a substantial increase in caspase activity with a ratio of 3/7 in both MCF- 7 and MDA-MB-231 cancer cells. In addition, the study showed that persianolide-A decreased the expression of p-ERK1/2 protein.

Conclusion and implications: 

The results of this study suggest that persianolide-A, sourced from Artemisia kopetdaghensis, induces cell apoptosis in breast cancer cell types. The molecular mechanisms could be implicated in the modulation of the ERK1/2 signaling pathway.

The health and proper functioning of the endoplasmic reticulum in the liver can lead to an increase in the quality of the metabolism of liver cells. Exercise can lead to liver health by regulating liver enzymes and factors related to apoptosis pathway. Therefore, the aim of the current research is to compare the performance of the endoplasmic reticulum chaperone protein of the liver of healthy model rats with the intervention of different training sessions and starvation.

In this experimental research, 30 Wistar male rats with a weight range of 330 ± 25 grams were selected and divided into six groups: 1) control, 2) starvation, 3) 3 days of training per week, 4) 5 days of training per week, 5) starvation + 3 training days per week, 6) starvation + 5 training days per week. Training consisted of one hour of continuous running on a treadmill for 4 weeks, and starvation was performed for 14 hours when the rats were awake. Data analysis was performed using one-way analysis of variance and post hoc LSD statistical tests in SPSS version 23 software. A significance level of P≤ 0.05 was considered.

Data analysis showed a significant change in the levels of liver enzymes alanine aminotransferase (ALT) and aspartate transaminase (AST) (P≤ 0.05). This change in CHOP gene expression was also significant (P≤ 0.05).

Aerobic training for 3 and 5 days with starvation can lead to liver health by reducing liver enzymes (AST and ALT) and cell death-related factor (CHOP) through the apoptosis pathway.

Endoplasmic reticulum plays an essential role in many cellular pathways. Exercise and fasting can lead to liver health by activating mechanisms such as reticulophagy. Therefore, the aim of the current research is to  investigate the effect of fasting and aerobic exercise on atherogenic indicators, body mass and ATF6 gene expression in the endoplasmic reticulum of healthy liver of Wistar rats.

In this experimental research, 30 18-week-old Wistar rats with a weight range of 330.40 ± 25.34 grams were selected and divided into six groups: 1) control, 2) starvation, 3) 3-day training, 44) 5-day training, 5) starvation + 3-day training, 6) starvation + 5-day training were divided. The rats in the training group performed exercise on a treadmill for one month, 3 and 5 sessions per week for one hour. Starvation was done continuously for 14 hours when the rats were awake and for one month. Data analysis was done using one-way ANOVA and post hoc LSD statistical tests in SPSS version 23 software. A significance level of P≥0.05 was considered.

Data analysis showed a significant decrease in BMI, LDL/HDL, CHOL/HDL, TAG/HDL and a significant increase in ATF6 gene expression (P≥0.05).

Aerobic training with starvation led to liver health by reducing atherogenic indicators. Also, increasing the expression of ATF6 gene in the liver through exercise and starvation can lead to the regulation of reticulophagia and liver health.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive cancer. The maincause of death in ESCC is related to relapse, metastasis, and resistance to cancer therapy. Recentstudies have shown that a minor subset of cancer cells, known as cancer stem cells (CSCs), areresponsible for tumor formation initiation and cancer progression. Understanding the genesassociated with CSCs and metastasis can help in targeted cancer therapy. The aim of this studywas to assess the expression of LAMB3 and TOP2A metastasis-associated genes in CSCs andadherent cells in the xenograft mouse model.

Esophageal CSCs were enriched by the sphere formation method. The expressionlevel of LAMB3 and TOP2A genes were evaluated in spheres and adherent cells in vitro byqRT-PCR. A xenograft mouse model was established to investigate the tumorigenesis andmetastasis potential by subcutaneous and tail vein injection of CSCs and adherent YM-1 cells.Consequently, LAMB3 and TOP2A expression at the mRNA level was assessed in tumors.Immunohistochemistry was also used to evaluate the LAMB3 expression at the protein levelin tumors.

CSCs-derived tumor was developed more quickly than the adherent cells-derivedtumor. LAMB3 at mRNA and protein level was significantly down-regulated in sphere-derivedtumor compared with adherent cells-derived tumor (P value <0.05). TOP2A expression wasalmost similar in both sphere cells and adherent cells and there was no significant difference.

we concluded that YM-1 spheres have CSCs characteristics in vitro with highcapability of tumorigenicity in vivo. Our results were also shown that the LAMB3 expressionwas decreased in YM-1 spheres suggesting LAMB3 association with sphere formation.

Activation of adenosine A2a receptor has been shown to induce the growth and metastasis of cancer cells. The role of this receptor in esophageal cancer has not yet been determined. The present study aimed to investigate effects of an adenosine A2a receptor antagonist (3, 7-dimethyl-1-propargylxanthine) on growth of esophageal cancer cells.

Real-time polymerase chain reaction was performed to evaluate mRNA expression of the A2a adenosine receptor in KYSE-30 and YM-1 esophageal cancer cell lines. Effects of the antagonist on viability of the cells were evaluated by MTT assay.

At low concentrations, the antagonist had no effect on cell viability. However, at concentrations ≥200 μM, the antagonist significantly reduced viability of both cell lines (p<0.05).

The results of this study indicate that the adenosine A2a receptor antagonist exerts inhibitory effects on KYSE30 and YM-1 cancer cells in a dose-dependent manner. Therefore, the use of this antagonist can be exploited as a therapeutic target for the treatment of esophageal cancer.

The angiogenesis process is a pivotal cellular process involved in both developmental and pathological circumstances. In this study we investigated effect of Urtica dioica agglutinin (UDA), as an unusual phyto-lectin from the chitin-binding protein family, on the angiogenesis of chicken embryos. The UDA was extracted from plant rhizomes and purified by affinity chromatography column. The activity of this lectin was assayed by hemagglutination test on the human RBCs. Anti-angiogenic effect of UDA on the extra-embryonic layer of the chick egg was studied in the different concentrations. Our results showed that the minimum concentration of UDA for agglutination were 48.00 and 15.00 µg mL-1 in macro- and microscopic studies, respectively. Because the number and length of the vessels were dramatically decreased at 100 µg kg-1 of UDA, the lectin had an inhibitory effect on angiogenesis of the embryonic vasculature of the chick. We concluded that UDA might target the vascularization events through binding to GlcNAc-conjugates. More investigations are needed to clarify the angiogenesis-related therapeutic roles of this interesting biomolecule.

Glioblastoma is a type of brain cancer with aggressive and invasive nature. Such features result from increased proliferation and migration and also poor apoptosis of glioma cells leading to resistance to current treatments such as chemotherapy and radiotherapy. In recent studies, micro RNAs have been introduced as a novel target for treating glioblastoma via regulation of apoptotic signaling pathway, remarkably PI3K/AKT, which affect cellular functions and blockage or progression of the tumor. In this review, we focus on PI3K/AKT signaling pathway and other related apoptotic processes contributing to glioblastoma and investigate the role of micro RNAs interfering in apoptosis, invasion and proliferation of glioma through such apoptotic processes pathways. Databases NCBI, PubMed, and Web of Science were searched for published English articles using keywords such as 'miRNA OR microRNA', 'Glioblastoma', 'apoptotic pathways', 'PI3K and AKT', 'Caspase signaling Pathway' and 'Notch pathway'. Most articles were published from 7 May 2015 to 16 June 2020. This study focused on PI3K/AKT signaling pathway affecting glioma cells in separated subparts. Also, other related apoptotic pathways as the Caspase cycle and Notch have been also investigated. Nearly 40 miRNAs were found as tumor suppressors or onco-miRNA, and their targets, which regulated subcomponents participating in proliferation, invasion, and apoptosis of the tumoral cells. Our review reveals that miRNAs affect key molecules in signaling apoptotic pathways, partly PI3K/AKT, making them potential therapeutic targets to overcome the tumor. However, their utility as a novel treatment for glioblastoma requires further examination and investigation.

Docetaxel is a chemotherapeutic agent commonly used for treatment of many cancers, including esophageal squamous cell carcinoma. Docetaxel induces G2/M phase cell cycle arrest and ultimately cell death. In this study, we aimed to assess the effects of docetaxel on YM1 cells considering exposure time and dose.

After calculating the doubling time of YM1 cells, the anti-proliferative effect of different concentrations of docetaxel () [A1]  after 24, 48 and 72 hours was assessed by the standard colorimetric assay. In addition, the effect of docetaxel on cell cycle was evaluated by flow cytometry.

The results showed that docetaxel toxicity was not significant until 24 hours at the tested concentrations (P>0.05). In addition, the effect of docetaxel on the cells was time-dependent at all tested concentrations. Overall, the duration of exposure to docetaxel had more significant role in docetaxel toxicity in YM1 cells compared to concentration.

Our findings suggest that the cytotoxicity of docetaxel on YM1 cells is time-dependent.

Citrus fruits and their constituents especially naringin (NR), a natural predominant flavanone, have a wide range of pharmacological activities without toxicity against cancer cells. The aim of this study was to investigate the anticancer effects of orange peel extract (OPE) and naringin (NR) on esophageal squamous cell carcinoma (ESCC) cells.   

Amount of phenol, flavonoid and antioxidants in OPE was determined using Folin-Ciocalteu procedure, aluminum chloride colorimetric and DPPH assays, respectively. Effects of NR and OPE on viability, wound healing assay and DNA fragmentation using DAPI were investigated. Data were analyzed by ImageJ software and GraphPad Prism 6.0 at significance of 0.05       

Total amount of phenols, flavonoids and 1,1-diphenyl-2-picrylhydrazyl was 2.83, 2.143 and 60.76 g/100g of OPE. Amount of NR in the dried OPE was estimated to be 5.260 (µg/gr) using high-performance liquid chromatography. Treatment of ESCC cells with OPE or NR decreased viability y of cancer cells in a dose-dependent manner. In addition, both OPE and NR were able to decrease cell migration and increase DNA fragmentation.    

The findings of our study suggest that OPE and NR have anticancer effects on ESCC cells but the anticancer effects of OPE was better than that of NR alone.

Modeling cancer in vivo is a very important tool to investigate cancer pathogenesis and molecular mechanisms involved in cancer progression. Laboratory mice are the most common animal used for rebuilding human cancer in vivo. Cancer stem cells (CSCs) are the main reason of failure in cancer therapy because of tumor relapse and metastasis. Isolation of cancer stem cells helps us to study their function and behavior. In the current study we separate cancer stem-like cells using sphere formation assay then investigate their tumorigenicity in xenograft tumor model.

YM1 cancer cells were cultured in serum-free media (SFM) in low adherent culture dishes for enrichment of cancer stem cells. The resulting spheres containing cancer stem-like cells were dissociated into single cells and were injected into the dorsal flank of B6 nude mice.

A few days after injection, subcutaneous tumors formed. The growth curves of the resulting tumors were plotted using their weekly recorded lengths. The tumors' volume and weight were measured. The size of resulting tumors was appropriate to the number of cells injected. Pathological analysis confirmed esophageal origin of the resulting tumors.

Using laboratory mice models is a practical modeling system that provides us investigation of human tumors pathogenesis in vivo.

Mycobacterium tuberculosis is the causative agent of pulmonary tuberculosis, a main public health problem that results in 1.5 million deaths annually. A number of epidemiological studies suggested that host genetic factors could play a main role in susceptibility to tuberculosis infection.
SP110 is an interferon-induced nuclear body protein with vital roles in apoptosis, cell cycling and immunity. SP110 gene has been suggested to be a suitable candidate for limiting TB infections. Thus, we investigated the possible association between SP110 gene polymorphisms and susceptibility to tuberculosis in the Golestan Province, Iran.

We investigated the frequency of rs1135791 polymorphism of the SP110 gene among 100 pulmonary tuberculosis patients and 100 healthy individuals who were referred to the health centers in the Golestan Province (Iran) between 2014 and 2015. Frequency of genotypes was evaluated using amplification refractory mutation system-polymerase chain reaction.

The frequency distribution of TT, TC and CC genotypes among the patients was 65%, 31% and 4%, respectively. In the control group, the frequency distribution of TT, TC and CC genotypes was 56%, 46% and 7%, respectively. There was no significant difference in the frequency of rs1135791 between the patients with pulmonary tuberculosis and the healthy controls (P=0.42).

Based on the results, the SP110 rs1135791 variant is not a genetic risk factor for development of pulmonary tuberculosis in Golestan Province, Iran.

New risk factors, such as plasma homocysteine level, have been rencetly recognized as independent risk factors for coronary artery disease (CAD). Mutations in some genes, affecting plasma homocysteine level, may be associated with CAD. Association studies in many populations have demonstrated a significant association between the development of CAD and 2 polymorphisms, rs1801131 and rs1805087.
In this case-control study (case group, 120 cases; control group, 130 controls), performed in Golestan province, Iran, rs1801131 single-nucleotide polymorphism (SNP) was genotyped in 5, 10-methylene tetrahydrofolate reductase (MTHFR), and rs1805087 SNP was genotyped in 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR). Tetraprimer amplification refractory mutation system-polymerase chain reaction (tetraprimer ARMS-PCR) method was applied to analyze these 2 sites.
In the rs1801131 site, genotype frequencies of AA, AC, and CC were 51%, 34%, and 15%, respectively in the case group, while the corresponding frequencies in the controls were 43%, 38%, and 19%, respectively. The results indicated that the difference in A and C allele distribution of rs1801131 was not significant among the controls and patients (OR, 1.34). Genotyping of rs1805087 demonstrated no variety at this position in the population.
We conclude that the presence of C allele does not increase the risk of CAD in the population of Golestan province. In addition, MTR rs1805087 SNP is not a suitable marker for population-based studies related to CAD. However, further studies are needed in larger populations to confirm these findings.

Current acute myeloid leukemia (AML) therapeutic strategies have irreversible side-effects. Berberine (BBR) is an isoquinoline alkaloid, which has been known as an aryl hydrocarbon receptor (AhR) ligand. AhR is a cytoplasmic receptor, which is involved in the regulation of cellular and immune responses. Here, we investigated the expression profile of genes involved in the cell cycle and different cytokines upon BBR-mediated AhR activation on AML THP-1 cell line.
THP-1 cells and normal monocytes were treated with different concentrations of BBR (10 μM, 25 μM, 50 μM, and 100 μM) for 24 and 48 hr. The cell viability was measured by MTT assay. Real-time RT-PCR was conducted to evaluate the expression of AhR, cytochrome P450 1A1 (CYP1A1), interleukin 1 beta (IL1β), p21, p27, cyclin-dependent kinase 2 (CDK2) and p53. Cellular expression of AhR was also assessed using immunofluorescence method. ELISA was used to determine the level of IL-10 and IL-12 cytokines.
BBR inhibits the proliferation of THP-1 cells in a dose- and time-dependent manner with minimal toxicity on normal monocytes. Phorbol 12-myristate 13-acetate (PMA) treatment increased the cellular expression of AhR. The AhR target genes (CYP1A1, IL1β) were overexpressed upon BBR treatment. BBR downregulated Cdk2 and upregulated p21, p27 and p53 genes in THP-1 cells. IL-10 was significantly increased upon BBR treatment, while IL-12 was not significantly changed in all combinations.
BBR could be introduced as an effective chemotherapeutic agent against AML by giving rise to the expression of CDK inhibitors and anti-inflammatory cytokines and downregulation of CDK2.

Colorectal cancer (CRC) is one of the most common causes of cancer-related mortality worldwide. Early diagnosis of this neoplasm is critical and may reduce patients’ mortality. MicroRNAs are small non-coding RNA molecules whose expression pattern can be altered in various diseases such as CRC.
In this study, we evaluated the expression levels of miR-142-3p, miR-26a-5p (their reduced expression in plasma samples of CRC patients was previously confirmed), miR-4478 and miR-1295-3p (their reduced expression in stool samples of CRC patients was previously confirmed) in tissue samples of CRC patients in comparison to healthy subjects.
To achieve this purpose, total RNA including small RNA was extracted from 53 CRC and 35 normal subjects’ Formalin-fixed, Paraffin-embedded (FFPE) tissue samples using the miRNeasy FFPE Mini Kit. The expression levels of these four selected miRNAs were measured using quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR).
We found that the expression levels of miR-4478 and miR-1295b-3p (two previously down-regulated fecal miRNAs) were significantly decreased in FFPE samples of CRC patients compared to healthy controls. On the other hand, no significant differences were seen in expression levels of miR-142-3p and miR-26a-5p (two previously down-regulated circulating miRNAs) in FFPE samples between these two groups.
Regarding current findings, it may be concluded that to diagnose CRC patients based on the miRNAs approach, stool samples are more likely preferable to plasma samples; nevertheless, additional studies with more samples are needed to confirm the results.

H istone deacetylase inhibitors (HDIs), as radiation sensitizing agents, are considered as a novel class of anti-cancer factors, which are studied in various tumor cell-lines. Valproic acid (VPA) is an HDI, which is effectively used in the treatment of epilepsy, migraines, and some particular types of depression. In this study, we evaluated the effects of VPA and ionizing radiation separately, as well as combined, with the alterations of histone H2AX phosphorylation (γH2AX) at Ser139, a marker of DNA damage and its repair, on MCF-7 breast cancer cell line.
Three groups of cells were selected, including 1) pretreated with VPA for 48 h followed by irradiation, 2) VPA only, and 3) irradiation only. The levels of γH2AX expression were evaluated using Western blot.
The results of our study showed that VPA signifi­cantly enhanced the expression of γH2AX, when applied 48 h prior to irradiation compared to the IR or VPA only treated cells. We also concluded that VPA pre-treatment delayed γH2AX dephosphorylation and dispersal for up to 12 h after irradiation, while γH2AX dephosphorylation disappeared in just 2 h when using irradiation alone and without VPA pre-treatment.
Our findings are consistent with the general consensus that VPA efficiently sensitizes cancer cells to the effects of ionizing radiation and prevents DNA double-strand break repair, which leads to enhanced breast cancer cell death.

Metformin is used a drug to lower blood sugar in patients with type II diabetes. Recent research showed that metformin effects on cancer cell growth. Studies show that metformin can induce apoptosis in certain cancer cell lines. In this study examined the effect of metformin on apoptosis in T47D breast cancer cell lines.
T47D breast cancer cell line selected and were purchased from the Pasteur Institute (Tehran - Iran). Cells at 24, 48 and 72 hours were treated by doses 5, 10, 50μM of metformin. The transcription levels of genes involved in apoptosis: Caspase 3 , 8, 9 and PARP-1 was evaluated by real time PCR.
The results of this study showed that at all three doses (5, 10, 50μM) of metformin and at three times (24, 48 and 72 h), the expression of Caspase 8 and Caspase 9 were increased. Also metformin at 48 and 72 hours in any given three doses increases the expression of PARP-1 but at 24 hours on the expression of PARP-1 is not effective.
The result indicates that in none of the three doses and times, metformin on expression of Caspase 3 is not effective. This study showed that metformin by increasing the transcription of genes Caspase 8 and Caspase 9 causes cell death through apoptosis.

Valproic acid (VPA), a drug used in the treatment of neurological disorders, has been shown to have cytotoxic effects on cancer cells through different mechanisms. Telomerase, a ribonucleoprotein reverse transcriptase, is responsible for elongation of the telomere and is activated in cancers. A relation between telomerase activity and resistance to apoptosis has been established. This study focused on probable effects of VPA on MCF-7 cancer cells. In particular, we investigated VPA effects on viability, apoptosis and telomerase activity. Cytotoxicity effects of VPA on MCF-7 cells were determined by neutral red uptake assay. Cells were treated with different concentrations of VPA (0-32 mM) and telomerase activity and Bax and Bcl-2 protein levels were determined using TRAP assay (PCR-ELISA) method and ELISA method, respectively. The cytotoxic effects of different concentration of VPA on MCF-7 cells were observed as a reduction in cell viability and telomerase activity and altered expression of Bcl-2 family protein levels. The results also showed that there is a significant correlation between reduction of telomerase activity and increase in Bax/Bcl-2 ratio (P=0.001). Our study demonstrated that cell viability of MCF-7 cells was decreased after treatment with VPA, probably through a reduction of telomerase activity and an increase in Bax/bcl-2 ratio. Therefore, it could be concluded that VPA is a potent anti-cancer agent for breast cancer cells through inhibition of telomerase activity and induction of apoptosis.

Colorectal cancer is one of the most commonly diagnosed cancers and cancer- related death worldwide. Identification of new specific biomarkers could be helpful to detection of this malignancy. Altered plasma microRNA expression has been identified in many cancers, including colorectal cancer. The main objective of this study was to identify the circulating microRNAs with the most expression changes in colorectal cancer patients compared with neoplasm free healthy individuals. MicroRNA expression profiling was performed on plasma samples of 37 colorectal cancer patients and 8 normal subjects using microRNA microarray. Quantitative real-time reverse transcription polymerase chain reaction was used to validate the two selected altered microR NAs. Plasma samples from 61 colorectal cancer patients and 24 normal subjects were used in our validation study. In profiling study we found a panel of six plasma microRNAs with significant downregulation. MicroRNA-142-3p and microRNA-26a-5p were selected and validated by polymerase chain reaction. Our results demonstrated that expression levels of plasma microRNA-142-3p and microRNA-26a-5p were significantly downregulated in patients with colorectal cancer when compared to control group. Our findings suggest that downregulation of plasma microRNA-142-3p and microRNA-26a-5p might serve as novel noninvasive biomarkers in the diagnosis of colorectal cancer, although more studies are needed to highlight the theoretical strengths.

DNA damage is among the main consequences of radiation. Of many different classes of DNA damage, double-strand breaks are the most deleterious. Development of a sensitive biodosimetry method, which utilizes a detection material with a similar construction to the body, seems essential for monitoring radiation workers. In this study, histone H2AX protein was examined as a potential biodosimeter in radiation workers. Moreover, the presence of this protein after in vitro irradiation of blood samples was assessed simultaneously. Blood samples from 46 radiation workers were analyzed in Golestan province, Iran. Meanwhile, two groups of blood samples (five blood samples in each group) were irradiated in vitro by doses of 1 to 0.2 Gy and 0.09 to 0.01 Gy from a 60Co source, respectively. gH2AX level in lymphocytes was measured, using Western blot technique. ANOVA and Tukey’s tests were performed, using SPSS version 16. The significance level was considered to be 0.05. The results of Western blotting for the identification of gH2AX protein in radiation workers were negative. However, gH2AX level in lymphocytes of two in vitro irradiated groups showed a significant correlation with the radiation dose (P<0.0001). The results showed that gH2AX was a good indicator for acute or local exposure to ionizing radiation, while in chronically exposed individuals, including radiation workers, this protein was useless at least in autoradiography detection method. Regarding the presence of gH2AX protein in blood samples, which were irradiated in vitro at low doses, it can be concluded that this protein has powerful repair mechanisms.