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目的 为了研究菲口罗啉对 2种氧化剂和抗癌药多柔比星诱发细胞DNA损伤的影响 ,并初步探讨其损伤机制。方法 用不同浓度菲口罗啉预处理CHL细胞 30min ,再分别加入 3种不同染毒受试物 ,共同培养一定时间 (0 .3mmol·L- 1重铬酸钾 :10 5min ;0 .5μmol·L- 1多柔比星 :75min ;0 .4mmol·L- 1过氧化氢(H2 O2 ) :2 5min)后 ,用碱性单细胞凝胶电泳方法 (AS CGE)测定DNA链断裂情况 ,并同时以菲口罗啉与二甲亚砜 (DMSO ,0 .33mol·L- 1)比较对H2 O2 致DNA损伤中·OH的产生和清除。结果 3种染毒受试物均可明显引起CHL细胞DNA链断裂 ;而当 3μmol·L- 1菲口罗啉预处理后 ,可使重铬酸钾、H2 O2 所致DNA迁移长度和细胞拖尾率明显降低 ,并超过DMSO降低H2 O2 的损伤作用 ,当菲口罗林浓度升至 12 μmol·L- 1时 ,可完全消除这两种因素所致的DNA链断裂损伤 ;10 μmol·L- 1菲口罗啉可抑制多柔比星所致DNA损伤 ,但浓度直至 60 μmol·L- 1仍不能完全消除多柔比星的损伤作用。结论 菲口罗啉对 2种氧化剂和多柔比星所致DNA损伤均有不同程度的防护作用 ,同时提示重铬酸钾和H2 O2 所致的DNA损伤主要与需过渡金属离子参与的·OH产生有关 ,而多柔比星所致损伤仅部分与此有关
Objective To investigate the effect of felodipine on DNA damage induced by two oxidants and doxorubicin, an anticancer drug, and to investigate its mechanism. Methods CHL cells were pretreated with felodipine at different concentrations for 30 min. Three different exposure doses were added to the culture medium for a certain period of time (0.3 mmol·L -1 potassium dichromate: 105 min; 0.5 μmol·L -1) L-1 doxorubicin: 75 min; 0 .4 mmol·L-1 hydrogen peroxide (H2 O2): 25 min), DNA strand breaks were determined by alkaline single cell gel electrophoresis (AS CGE) At the same time, forskolin and dimethyl sulfoxide (DMSO, 0.33mol · L-1) compared H2O2-induced DNA damage in · OH production and clearance. Results All the three exposure groups could obviously cause DNA strand breaks in CHL cells. When pretreated with 3 μmol·L-1 fipronil, DNA migration length and cell drag caused by potassium dichromate and H2 O2 The tail rate was significantly reduced and the damage effect of H 2 O 2 over DMSO was reduced. When fiferelin concentration was increased to 12 μmol·L -1, DNA damage caused by these two factors could be completely eliminated; 10 μmol·L - 1 phenanthroline can inhibit DNA damage induced by doxorubicin, but the concentration of 60 μmol·L -1 still can not completely eliminate the damaging effect of doxorubicin. Conclusions Feloprofen can protect cells from DNA damage induced by two oxidants and doxorubicin to a lesser extent, suggesting that DNA damage induced by potassium dichromate and H2O2 is mainly related to · OH Related, and doxorubicin-induced injury is only partially related to this