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Objective Benzo[a]pyrene (B[a]P), a ubiquitous environmental pollutant, is a potent procarcinogen and mutagen that can elicit tumors, leading to malignancy. Heat shock proteins (Hsp) have been shown to protect cells against damages caused by various stresses including exposure to numerous chemicals. Whether Hsps, or more specifically Hsp70, are involved in repair of B[a]P-induced DNA damage is currently unknown. Methods We assessed the potential role of the inducible form of Hsp70 in B[a]P-induced DNA damage of human embryonic lung (HEL) cells using immunoblot and the comet assay (i.e., the single cell gel electrophoresis assay). Results Exposure to B[a]P induced a dose-dependent decrease in the level of Hsp70, but a dose-dependent +-increase in DNA damage both in untreated (control) HEL cells and in cells preconditioned by a heat treatment. Heat preconditioning prior to B[a]P exposure potentiated the effect of B[a]P at a low dose (10 μmol/L), but appeared to be protective at higher doses. There was a
Objective Benzo [a] pyrene (B [a] P), a ubiquitous environmental pollutant, is a potent procarcinogen and mutagen that can elicit tumors, leading to malignancy. Heat shock proteins (Hsp) have been shown to protect cells by damages caused by Whether Hsps, or more specifically Hsp70, are involved in repair of B [a] P-induced DNA damage is currently unknown. Methods We assessed the potential role of the inducible form of Hsp70 in B [a] ] P-induced DNA damage of human embryonic lung (HEL) cells using immunoblot and the comet assay (ie, the single cell gel electrophoresis assay). Results Exposure to B [a] P induced a dose- dependent decrease in the level of Hsp70 , but a dose-dependent + -increase in DNA damage both in untreated (control) HEL cells and in cells preconditioned by a heat treatment. Heat preconditioning prior to B [a] P exposure potentiated the effect of B [a] P at a low dose (10 μmol / L), but appeared to be protective at higher d There was a