活性氧过度产生的OXYS大鼠肝脏和大脑中乙撑脱氧核糖核酸加合物随年龄增长而增加。
Age-dependent increase of etheno-DNA-adducts in liver and brain of ROS overproducing OXYS rats.
作者信息
Nair Jagadeesan, Sinitsina Olga, Vasunina Elena A, Nevinsky Georgy A, Laval Jacques, Bartsch Helmut
机构信息
Division of Toxicology and Cancer Risk Factors, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
出版信息
Biochem Biophys Res Commun. 2005 Oct 21;336(2):478-82. doi: 10.1016/j.bbrc.2005.08.114.
Reactive oxygen species (ROS) and lipid peroxidation (LPO) play a role in aging and degenerative diseases. To correlate oxidative stress and LPO-derived DNA damage, we determined etheno-DNA-adducts in liver and brain from ROS overproducing OXYS rats in comparison with age-matched Wistar rats. Liver DNA samples from 3- and 15-month-old OXYS and Wistar rats were analyzed for 1,N6-ethenodeoxyadenosine (epsilondA) and 3,N4-ethenodeoxycytidine (epsilondC) by immunoaffinity/32P-postlabelling. While epsilondA and epsilondC levels were not different in young rats, adduct levels were significantly higher in old OXYS rats when compared to old Wistar or young OXYS rats. Frozen rat brain sections were analyzed for epsilondA by immunostaining of nuclei. Brains from old OXYS rats accumulated epsilondA more frequently than age-matched Wistar rats. Our results demonstrate increased LPO-induced DNA damage in organs of OXYS rats which correlates with their known shorter life-span and elevated frequency of chronic degenerative diseases.
活性氧（ROS）和脂质过氧化（LPO）在衰老和退行性疾病中起作用。为了关联氧化应激和LPO衍生的DNA损伤，我们测定了与年龄匹配的Wistar大鼠相比，过量产生ROS的OXYS大鼠肝脏和大脑中的乙烯基-DNA加合物。通过免疫亲和/ 32P后标记分析3个月和15个月大的OXYS和Wistar大鼠的肝脏DNA样品中的1，N6-乙烯基脱氧腺苷（εdA）和3，N4-乙烯基脱氧胞苷（εdC）。虽然幼鼠中εdA和εdC水平没有差异，但与老年Wistar或幼龄OXYS大鼠相比，老年OXYS大鼠的加合物水平显著更高。通过细胞核免疫染色分析冷冻大鼠脑切片中的εdA。老年OXYS大鼠的大脑比年龄匹配的Wistar大鼠更频繁地积累εdA。我们的结果表明，OXYS大鼠器官中LPO诱导的DNA损伤增加，这与其已知的较短寿命和慢性退行性疾病的高频率相关。
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