Dichlorodiphenyltrichloroethane in soil, river sediment, and fish in the Amazon in Brazil.

Dichlorodiphenyltrichloroethane (DDT), its main metabolites, and other organochlorines were analyzed in soils (n=6), fluvial sediments (n=14), and fish (n=10) that were collected in several areas of the Amazon region in Brazil. The samples were analyzed by capillary column gas chromatography coupled to electron capture detection. DDT residues were present in most of the collected sediments in concentrations of approximately 10 to 100 micro/kg (ppb, dry weight). Some urban top soils were found to have more than 1 mg/kg (ppm). In fish, as much as 0.5 mg/kg of total DDT (wet weight) was found in the edible parts. The presence of p,p'-DDT in most of the samples reflects the use of this insecticide against vectors of malaria between 1946 and 1993, which has led to its ubiquitous presence in the environment of the Brazilian Amazon.

Induction of CYP1A1 and CYP1B1 in T-47D human breast cancer cells by benzo[a]pyrene is diminished by arsenite.

Polycyclic aromatic hydrocarbons (PAHs) and metals are often environmental cocontaminants, yet there have been relatively few studies of combined effects of PAHs and metals on cytochrome P450 (P450)-catalyzed metabolism. We examined the effects of NaAsO(2) in combination with benzo[a]pyrene (BAP) on CYP1A1 and CYP1B1 in T-47D human breast cancer cells by using estrogen metabolism as a probe of their activities. Exposure to BAP caused elevated rates of the 2- and 4-hydroxylation pathways of estrogen metabolism, indicating induction of both CYP1A1, an estradiol 2-hydroxylase, and CYP1B1, an estradiol 4-hydroxylase. BAP-induced metabolism peaked 9 to 16 h after exposure and returned to near-basal levels by 48 h. Concentration-response studies showed maximal induction of the 2- and 4-hydroxylation pathways at 3 microM BAP; higher levels caused reduced rates of metabolism due to inhibition of CYP1A1 and CYP1B1. NaAsO(2) caused pronounced decreases in the induction of CYP1A1 and CYP1B1 by 3 microM BAP because cotreatment with 10 microM NaAsO(2) inhibited the rates of the 2- and 4-hydroxylation pathways by 86 and 92%, respectively. Western immunoblots showed diminished levels of BAP-induced CYP1A1 by coexposure to NaAsO(2). The levels of the CYP1A1 and CYP1B1 mRNAs induced by BAP were not significantly affected by coexposure to NaAsO(2); however, heme oxygenase 1 mRNA levels were markedly induced by coexposure to BAP and NaAsO(2). These results indicate a post-transcriptional inhibitory effect of arsenite on the expression of CYP1A1 and CYP1B1 in T-47D cells, possibly resulting from reduced heme availability.