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  • APOLIPOPROTEIN-E  (1)
  • 1
    Keywords: PROTECTION ; BLOOD ; Germany ; IN-VIVO ; LUNG ; VIVO ; EXPOSURE ; RISK ; ENZYMES ; MICE ; DNA ; SERA ; RISK-FACTORS ; animals ; BIOMARKERS ; P-32-postlabelling ; RATS ; TARGET ; PROGRESSION ; DIFFERENCE ; PLASMA ; STRESS ; risk factors ; DAMAGE ; RISK FACTOR ; NUCLEOTIDES ; DNA-DAMAGE ; ADDUCTS ; APOLIPOPROTEIN-E ; ATHEROSCLEROSIS ; LIPOPROTEIN ; LOW-DENSITY-LIPOPROTEIN ; WALL ; ETHENO-DNA ADDUCTS ; LIPID-PEROXIDATION ; OXIDATIVE STRESS ; atherosclerosis,benzo(a)pyrene,etheno-DNA adducts,lipid peroxidation ; LIPOPROTEINS ; OXIDATION ; PARAOXONASE
    Abstract: The genotoxic compound benzo[a]pyrene (B[a]P) enhances atherosclerotic plaque progression, possibly by inducing oxidative stress and subsequent lipid peroxidation (LPO). Since LPO plays a key role in atherosclerosis, stable LPO derived DNA modifications such as 1,N-6-ethenodeoxyadenosine (epsilondA) and 3,N-4-ethenodeoxy-cytidine (epsilondC) may be useful biomarkers for in vivo oxidative stress. In this study, benzo[a]pyrene-diol-epoxide (BPDE)-DNA, epsilondA and epsilondC were determined by P-32-postlabelling in apolipoprotein E knockout (ApoE-KO) mice treated with 5 mg/kg B[a]P by gavage. After 4 days, BPDE-DNA adduct levels were higher in aorta (10.8 +/- 1.4 adducts/10(8) nucleotides) than in lung (3.3 +/- 0.7, P 〈 0.05), which is a known target organ for B[a]P. Levels of εdA were higher in aorta of B[a]P-exposed animals than in unexposed controls (8.1 ± 4.4 vs 3.4 ± 2.1 adducts per 10(8) parent nucleotides, P 〈 0.05). On the other hand, epsilondC levels were not affected by B[a]P exposure. Serum low density lipoprotein (LDL) levels were lower in B[a]P-exposed mice than in controls (9.3 +/- 3.7 and 13.3 +/- 4.0 mmol/l, respectively), whereas high density lipoprotein (HDL) levels were higher (1.4 +/- 1.6 and 0.4 +/- 0.3 mmol/l, respectively). Consequently, a three-fold difference in the LDL/HDL ratio was observed (P = 0.001). epsilondA levels were positively related with plasma HDL concentrations (R = 0.68, P = 0.02), suggesting that the HDL mediated protection of the vessel wall against reactive lipid peroxides was reduced in B[a]P-exposed apoE-KO mice. Our observations show that direct as well as lipid peroxidation induced DNA damage is formed by B[a]P in aorta of apoE-KO mice, which may be involved in atherosclerotic plaque progression. This study further indicates that etheno-DNA adducts are useful biomarkers for in vivo oxidative stress in atherosclerosis
    Type of Publication: Journal article published
    PubMed ID: 14753754
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