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The dermal route is important in occupational exposure to polycyclic aromatic compounds (PACs), but other organs may be affected. We reported that kerosene-cleaning following treatment with used engine oil increased DNA adducts in the lungs of mice viz. animals treated with used oil alone. To determine the mechanism we topically applied 3H-BAP(100 nmol in 25 μL acetone) and washed half the mice with 25 μL kerosene 1 h after carcinogen application. Groups of four mice were sacrificed from 1 to 72 h after treatment. Lung, liver, and skin were harvested. The fraction of the radiolabel remaining in the skin of animals treated with benzo[a]pyrene (BAP) and washed with kerosene was significantly less than those not washed, beginning at 24 h (p < .05). Fractional distribution to the lungs and livers of these animals became significantly elevated. Kerosene increased transdermal water loss. Kerosene treatment compromises dermal barrier function, enhances carcinogen absorption, and alters organ distribution. [ABSTRACT FROM AUTHOR]

7H-Dibenzo[c,g]carbazole (DBC) is a potent multi-site, multi-species carcinogen present in a variety of complex mixtures derived from the incomplete combustion of organic matter. Like many carcinogens, DBC requires metabolic activation to an electrophilic species to exert its mutagenic and carcinogenic effects. One-electron oxidation, leading to the formation of radical cation intermediates, has been proposed as a mechanism of metabolic activation for DBC in vitro resulting in unstable DNA adducts. The purpose of this research was to determine whether one-electron oxidation is a mechanism of activation and DNA binding for DBC in vivo. Specific depurinating DBC–DNA adducts formed by one-electron oxidation were analyzed in mouse liver at 4 h following a single i.p. dose of 40 mg/kg of 11 μCi [14C]DBC. In addition to five previously published adduct standards, two newly identified adduct standards were characterized by mass spectrometry and NMR, namely DBC-6-N7-Ade and DBC-6-N1-Ade; however, neither was observed in mouse liver. Only the DBC-5-N7-Gua adduct was observed in mouse liver extracts at a level of 6.5 ± 1.8 adducts/106 nucleotides. In addition, the formation of AP sites and stable DBC–DNA adducts was analyzed in mouse liver and lung at 4, 12 and 24 h following a single i.p. dose of 0.4, 4 or 40 mg/kg DBC (n = 3/group). There was a distinct time– and dose–response of stable DBC–DNA adducts detected by 32P-post-labeling. There was not a clear dose–response for formation of AP sites; however, a significant increase over control levels was observed at the 4 and 40 mg/kg dose groups at 4 and 12 h post dosing, respectively. Quantitative comparisons indicate that the depurinating DBC-5-N7-Gua adduct constitutes ~0.4% of total adducts measured whereas the stable adducts detected by 32P-post-labeling constitute 99.6% of total adducts measured following a 40 mg/kg dose and a 4 h time-point. The data indicate that one-electron oxidation does occur in mouse liver in vivo. However, one-electron oxidation is a minor mechanism of activation in that the percentage of total adducts formed through this route constitutes a minor percentage of the total adducts formed. [ABSTRACT FROM PUBLISHER]