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Elevation of 8-Hydroxydeoxyguanosine in DNA from Isolated Mouse Lung Cells Following In Vivo Treatment with Aflatoxin B1

Abstract Aflatoxin B 1 (AFB 1 ) is a mycotoxin produced by some strains of Aspergillus and is a recognized pulmonary and hepatic carcinogen. The most widely accepted mechanism of AFB 1 carcinogenicity involves bioactivation to AFB 1 -8,9- exo -epoxide and binding to DNA to form AFB 1 -N 7 -guanine. Another potential cause of DNA damage is AFB 1 -mediated stimulation of reactive oxygen species formation, leading to oxidation of DNA bases. The objective of this study was to determine the ability of AFB 1 to cause oxidative DNA damage in lung cell types of the A/J mouse. The formation of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in freshly isolated mouse lung alveolar macrophages, alveolar type II cells, and nonciliated bronchial epithelial (Clara) cells was assessed by high-performance liquid chromatography with electrochemical detection. An approximately 3-fold increase in 8-OHdG formation occurred in both alveolar macrophage and Clara cell preparations isolated from A/J mice 2 h following treatment with a single tumorigenic dose of 50 mg/kg AFB 1 ip ( n = 3, p < 0.05). Prior treatment with 300 kU/kg polyethylene glycol–conjugated catalase prevented the AFB 1 -induced increase in 8-OHdG levels in all mouse lung cell preparations ( n = 3, p < 0.05). These results support the possibility that oxidative DNA damage in mouse lung cells contributes to AFB 1 carcinogenicity. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Toxicological Sciences Oxford University Press

Elevation of 8-Hydroxydeoxyguanosine in DNA from Isolated Mouse Lung Cells Following In Vivo Treatment with Aflatoxin B1

Abstract

Abstract Aflatoxin B 1 (AFB 1 ) is a mycotoxin produced by some strains of Aspergillus and is a recognized pulmonary and hepatic carcinogen. The most widely accepted mechanism of AFB 1 carcinogenicity involves bioactivation to AFB 1 -8,9- exo -epoxide and binding to DNA to form AFB 1 -N 7 -guanine. Another potential cause of DNA damage is AFB 1 -mediated stimulation of reactive oxygen species formation, leading to oxidation of DNA bases. The objective of this study was to determine the ability of AFB 1 to cause oxidative DNA damage in lung cell types of the A/J mouse. The formation of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in freshly isolated mouse lung alveolar macrophages, alveolar type II cells, and nonciliated bronchial epithelial (Clara) cells was assessed by high-performance liquid chromatography with electrochemical detection. An approximately 3-fold increase in 8-OHdG formation occurred in both alveolar macrophage and Clara cell preparations isolated from A/J mice 2 h following treatment with a single tumorigenic dose of 50 mg/kg AFB 1 ip ( n = 3, p < 0.05). Prior treatment with 300 kU/kg polyethylene glycol–conjugated catalase prevented the AFB 1 -induced increase in 8-OHdG levels in all mouse lung cell preparations ( n = 3, p < 0.05). These results support the possibility that oxidative DNA damage in mouse lung cells contributes to AFB 1 carcinogenicity.
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