 we have studied the effect of several environmental chemicals on the transient expression of a chloramphenicol acetyltransferase ( cat ) reporter gene linked to the promoter sequences in the long terminal repeat ( ltr ) of the human immunodeficiency virus type 1 ( hiv-1 ) . 
 aflatoxin b1 , 2,3,7,8-tetrachlorodibenzo - p - dioxin ( tcdd ; dioxin ) and benzo[a]pyrene cause a significant increases in cat expression in mouse hepatoma hepa-1 cells . 
 the induction of cat after tcdd treatment is abolished by administration of n - acetyl - l - cysteine or 2-mercaptoethanol and does not take place in a mutant cell line that lacks cyp1a1 enzymatic activity . 
 linker - scanning mutational analysis of transcription factor binding sites in the promoter revealed that both the nf kappa b and an adjacent aromatic hydrocarbon response element ( ahre ) are required for tcdd - dependent cat expression . 
 in addition , mutation of the nfat / ap-1 binding sites in the negative regulatory region of the promoter increases the magnitude of the tcdd effect . we conclude that induction of a functional cyp1a1 monooxygenase by tcdd stimulates a pathway that generates thiol - sensitive reactive oxygen intermediates which , in turn , are responsible for the tcdd - dependent activation of genes linked to the ltr . 
 these data might provide an explanation for findings that tcdd increases infectious hiv-1 titers in experimental systems and for epidemiologic reports suggesting that exposure to aromatic hydrocarbons , such as found in cigarette smoke , is associated with an acceleration in aids progression.imagesp366-afigure 2.figure 3.figure 4.figure 5 . 
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