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疱疹病毒产生作为不同来源紫外线照射人皮肤细胞修复标志物的研究

Herpes virus production as a marker of repair in ultraviolet irradiated human skin cells of different origin.

作者信息

Coppey J, Moreno G, Nocentini S

出版信息

Bull Cancer. 1978;65(3):335-40.

PMID:214190
Abstract

When confluent human skin cultures are ultraviolet (UV)-irradiated before infection with Herpes Simplex type 1 virus (HSV), their capacity to support virus growth is impaired. When the time interval between UV-exposure and infection is increased up to 36 hours, different recoveries of HSV production capacity are observed according to the origin of the host cells. 1) Two normal donors: the cells present a dose dependent recovery which is maximal for a dose ( : formula: (see text) at which a plateau level of unscheduled DNA synthesis (UDS) is reached. 2) A mother of two Xeroderma Pigmentosum (XP) children: in this line which exhibits a normal level of UDS, the extent of recovery is significantly decreased after exposures : formula: (see text) 3) An XP child: these cells have a normal level of UDS (XP variant) whereas they present a low extent of recovery as compared with that of the normal subjects. 4) Five XP children: in these excision deficient lines (UDS less than 15%), HSV production capacity decreases with increasing time intervals after UV exposure for doses greater than or equal to 3 : formula: (see text). For doses less than 3 : formula: (see text), a small recovery with an overshoot of viral production is observed 24 h after UV exposure in the lines (three) which present the highest UDS (10--15%) and not in the two lines which present a very low UDS (1--2%).

摘要

当融合的人类皮肤培养物在感染单纯疱疹病毒1型(HSV)之前接受紫外线(UV)照射时,它们支持病毒生长的能力会受损。当紫外线照射和感染之间的时间间隔增加到36小时时,根据宿主细胞的来源观察到HSV生产能力的不同恢复情况。1)两名正常供体:细胞呈现剂量依赖性恢复,对于达到非预定DNA合成(UDS)平台水平的剂量(:公式:(见正文)),恢复达到最大值。2)一名患有色素性干皮病(XP)的两个孩子的母亲:在这条显示正常UDS水平的细胞系中,暴露后(:公式:(见正文))恢复程度显著降低。3)一名XP儿童:这些细胞具有正常的UDS水平(XP变体),但与正常受试者相比,它们的恢复程度较低。4)五名XP儿童:在这些切除缺陷型细胞系(UDS小于15%)中,对于大于或等于3:公式:(见正文)的剂量,紫外线照射后随着时间间隔的增加,HSV生产能力下降。对于小于3:公式:(见正文)的剂量,在具有最高UDS(10 - 15%)的三条细胞系中,紫外线照射后24小时观察到病毒产量有小幅度恢复并出现超调,而在两条UDS非常低(1 - 2%)的细胞系中未观察到这种情况。

相似文献

1
Herpes virus production as a marker of repair in ultraviolet irradiated human skin cells of different origin.疱疹病毒产生作为不同来源紫外线照射人皮肤细胞修复标志物的研究
Bull Cancer. 1978;65(3):335-40.
2
Herpes virus production as a marker of repair in ultra-violet irradiated human skin cells of different origin.疱疹病毒产生作为不同来源紫外线照射的人皮肤细胞修复标志物
Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Jul;36(1):1-10. doi: 10.1080/09553007914550761.
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Effects of microinjected photoreactivating enzyme on thymine dimer removal and DNA repair synthesis in normal human and xeroderma pigmentosum fibroblasts.显微注射光复活酶对正常人及着色性干皮病成纤维细胞中胸腺嘧啶二聚体去除和DNA修复合成的影响。
Cancer Res. 1990 Mar 15;50(6):1905-10.
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Cancer Res. 1989 Apr 15;49(8):1927-30.
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Xeroderma pigmentosum patients belonging to complementation group F and efficient liquid-holding recovery of ultraviolet damage.属于互补组F的着色性干皮病患者及紫外线损伤的高效液体保持恢复
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Enhanced transformation of xeroderma pigmentosum variant cells by ultraviolet light-irradiated simian virus 40.紫外线照射的猿猴病毒40对着色性干皮病变异细胞的转化增强作用
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7
Absence of induction of enhanced reactivation of herpes simplex virus in cells from xeroderma pigmentosum patients without skin cancer.在无皮肤癌的着色性干皮病患者的细胞中,单纯疱疹病毒增强再激活未被诱导。
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Roles of poly(ADP-ribose) synthesis in repair and replication in normal human, Cockayne syndrome, and xeroderma pigmentosum fibroblasts after UV irradiation.紫外线照射后,聚(ADP - 核糖)合成在正常人、科凯恩综合征患者和着色性干皮病成纤维细胞的修复与复制中的作用。
Princess Takamatsu Symp. 1983;13:209-18.
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Prolonged p53 protein accumulation in trichothiodystrophy fibroblasts dependent on unrepaired pyrimidine dimers on the transcribed strands of cellular genes.毛发硫营养不良成纤维细胞中p53蛋白的长期积累依赖于细胞基因转录链上未修复的嘧啶二聚体。
Mol Carcinog. 1997 Dec;20(4):340-7.