Abstract 4929

Benzene is a volatile aromatic hydrocarbon solvent which is widely used in many industries. The chronic exposure of humans to benzene in the workplace has been associated with blood disorders, as well as toxicity in lymphopoiesis, including aplastic anemia and leukemia. Our previous study showed that skewed distribution and clonal expansion of TCR Vα/ Vβ subfamily T cells and changed CD3ζ gene expression in benzene-exposed workers. Little is known about the expression feature of CD3γ, CD3δ and CD3ε genes, which are also involved TCR signal transduction. To further identify the feature of CD3 complex gene in benzene-exposed workers, real-time PCR with SYBR Green I technique was used for detecting CD3γ, CD3δ, CD3ε gene expression level in peripheral blood mononuclear cells from 16 benzene-exposed workers, 8 chronic mild benzene-poisoning workers, 9 chronic middling benzene-poisoning workers and 9 chronic severely benzene-poisoning workers, respectively. Control group consisted of 26 healthy individuals. β2-microglobulin gene was used as an endogenous reference. Relative changes in these gene expression level was used by the 2ΔCt×100% method. The CD3γ gene expression in benzene-exposed (2.99±3.10) and each benzene-poisoned group (2.13±2.16, 2.65±1.73 and 1.29±0.74, respectively) decreased significantly compared with that of in healthy individuals (5.97±4.86) (P< 0.05). The CD3δ gene expression in benzene-exposed group (8.38±9.6) increased significantly compared with those from healthy individuals (1.09±1.1) (P< 0.05), while in each benzene-poisoned group (2.57±2.51, 1.60±2.55 and 0.74±0.51, respectively), decreased significantly compared with those from benzene-exposed (P< 0.05). No significant difference was found in expression level of CD3ε between the healthy group, benzene-exposed, different benzene-poisoning groups (5.95±6.94, 6.60±6.31, 7.01±5.99, 4.33±4.69, 3.73±4.48, respectively) (P> 0.05). In conclusions, the abnormality expression of CD3γ and CD3δ gene is also a common feature in benzene-exposed and benzene-poisoned workers, which might participate in part of T cell immune dysfunction.

Disclosures:

Li:Natural Science Foundation of Guangdong province (No. 07301046): Research Funding; Medical Science Technology Program of Guangzhou (2009-ZDI-18): Research Funding; Natural Science Foundation of Guangdong province (No. 07301046): Research Funding; China Postdoctoral Science Foundation funded project (No. 20070410840): Research Funding; National Natural Science Foundation of China (No. 30972455): Research Funding. Fan:Undergraduate Science and Technology Innovation project of Guangdong (1055911020): Research Funding. Wang:Undergraduate Science and Technology Innovation project of Guangdong (1055911020): Research Funding. Chen:Undergraduate Science and Technology Innovation project of Guangdong (1055911020): Research Funding. Chen:Medical Science Technology Program of Guangzhou□(2009-ZDI-18): Research Funding. Li:Medical Science Technology Program of Guangzhou(2009-ZDI-18): Research Funding; The Fundamental Research Funds for the Central Universities□iNo. 2011610408□j: Research Funding; Natural Science Foundation of Guangdong province (No. 07301046): Research Funding; China Postdoctoral Science Foundation funded project (No. 20070410840): Research Funding; National Natural Science Foundation of China (No. 30972455): Research Funding.

Author notes

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Asterisk with author names denotes non-ASH members.

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