The Quest Research On The Expression Levels Of AhR,CYP1A1,GSTA1 And TGF-α Genes In Epidermis Which Suffered Chloracne

Objective: Dioxins, as one of the most toxic compounds, induces a variety oftoxicological responses in human and laboratory animals. The most prominent effectof an exposure to dioxin in humans is the development of chloracne. In the presentstudies the human who suffered chloracne were chosen as subjects and for theanalysis of cell proliferation and differentiated disturbed by dioxins, meanwhile thesemi-quantitative reverse transcription PCR-technique was used for the measurementof the levels for the AhR,CYP1A1,GSTA1,TGF-αmRNA. The aim of the researchis to provide further evidences and clues for the pathogenesis of chloracne caused bydioxins.Methods: In this study, the exposed group was defined as those workers withchloracne who are engaged in the productions of PCP (Na-PCP) and the controlgroup was defined as the unexposed comparison population. The semi-quantitativereverse transcription PCR-technique was used for the measurement of the relativetranscription levels for the AhR, CYP1A1, GSTA1 and TGF-αmRNA of epidermis.Results: Compared with the control group, the level of AhR, CYP1A1, GSTA1andTGF-αmRNA were up-regulation in exposure group. AhR, CYP1A1 and GSTA1mRNA level were significantly increased (P=0.000, 0.000, 0.000); while the TGF-αmRNA level of epidermis were increased without significant difference (P=0.110).The relative expression amount of AhR, CYP1A1 and GSTA1 mRNA of exposuregroup were significant different from the control group with the 3.5-fold, 2.4-fold and1.8-fold increase respectively. Further analysis of the relevant relationship betweenthe amount of AhR mRNA and CYP1A1 mRNA, showed that highly positiverelevance exists with the coefficient of 0.665 (P=0.018).Conclusion: Molecular study proved that the expressions of AhR, CYP1A1 andGSTA1 in epidermis were significantly up-regulated. And there are strong positivecorrelations between AhR and CYP1A1 expression. Therefore we suppose that dioxin disturb normal proliferation of human epidermis and lead to the form of chlroacnewere through AhR by mediating CYP1A1 and GSTA1.