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紫外线诱导的细胞凋亡的形成与细胞周期有关。

Formation of UV-induced apoptosis relates to the cell cycle.

作者信息

Danno K, Horio T

出版信息

Br J Dermatol. 1982 Oct;107(4):423-8. doi: 10.1111/j.1365-2133.1982.tb00385.x.

DOI:10.1111/j.1365-2133.1982.tb00385.x
PMID:7126451
Abstract

The relationship of the rate of epidermal proliferation to ultraviolet (UV)-induced cell death, namely sunburn cell (SC) formation, was investigated in vivo using the guinea-pig model. The number of SCs was correlated with (1) cellophane tape stripping which stimulates the proliferation rate and (2) treatment with antimitotic and antimetabolic agents which suppress the proliferation rate. The tape stripping performed 14 h before UV irradiation significantly increased the number of SCs counted 24 h after UV irradiation from a mean of 17.4 to 62.6 per section, and the tritiated thymidine (TdR-3H)-labelling index (LI) increased from a mean of 8.1 to 27.4%. SC counts and LI were markedly decreased by the intradermal injection of colchicine, methotrexate, hydroxyurea or 5-fluorouracil given once immediately after the tape stripping. The autoradiographic study showed that 23.2% of SCs were labelled when TdR-3H was given intradermally 1 h before UV exposure, while no SCs were labelled when TdR-3H was given immediately after UV exposure. The labelled SC count (23.2%) which presumably represents S phase cells at the time of UV exposure, was higher than the LI (mean 8.1%). These results suggest that proliferating cells, possibly S phase cells, may be responsible for SC formation.

摘要

采用豚鼠模型在体内研究了表皮增殖速率与紫外线(UV)诱导的细胞死亡(即晒伤细胞(SC)形成)之间的关系。SC的数量与以下因素相关:(1)刺激增殖速率的透明胶带剥离;(2)使用抑制增殖速率的抗有丝分裂和抗代谢剂进行处理。在紫外线照射前14小时进行的胶带剥离显著增加了紫外线照射后24小时计数的SC数量,从每切片平均17.4个增加到62.6个,并且氚标记胸腺嘧啶核苷(TdR-3H)标记指数(LI)从平均8.1%增加到27.4%。在胶带剥离后立即皮内注射一次秋水仙碱、甲氨蝶呤、羟基脲或5-氟尿嘧啶,可使SC计数和LI显著降低。放射自显影研究表明,在紫外线照射前1小时皮内注射TdR-3H时,23.2%的SC被标记,而在紫外线照射后立即注射TdR-3H时,没有SC被标记。推测代表紫外线照射时处于S期细胞的标记SC计数(23.2%)高于LI(平均8.1%)。这些结果表明,增殖细胞,可能是S期细胞,可能是SC形成的原因。

相似文献

1
Formation of UV-induced apoptosis relates to the cell cycle.紫外线诱导的细胞凋亡的形成与细胞周期有关。
Br J Dermatol. 1982 Oct;107(4):423-8. doi: 10.1111/j.1365-2133.1982.tb00385.x.
2
Quantitative studies on sunburn cell formation in mouse epidermis.小鼠表皮晒伤细胞形成的定量研究。
Tohoku J Exp Med. 1983 Aug;140(4):395-405. doi: 10.1620/tjem.140.395.
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Cyclosporin-A suppresses p53-dependent repair DNA synthesis and apoptosis following ultraviolet-B irradiation.环孢菌素A抑制紫外线B照射后p53依赖的修复性DNA合成及细胞凋亡。
Photodermatol Photoimmunol Photomed. 2002 Aug;18(4):163-8. doi: 10.1034/j.1600-0781.2002.00765.x.
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Decreased DNA repair activity in sunburn cells. A possible pathogenetic factor of the epidermal sunburn reaction.晒伤细胞中DNA修复活性降低。表皮晒伤反应的一个可能致病因素。
Arch Dermatol Res. 1979 Aug;266(1):11-6. doi: 10.1007/BF00412857.
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Relationship of the cell cycle to sunburn cell formation.细胞周期与晒伤细胞形成的关系。
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Regenerative proliferation of mouse epidermal cells following adhesive tape stripping. Micro-flow fluorometry of isolated epidermal basal cells combined with 3H-TdR incorporation and a stathmokinetic method (colcemid).胶带剥离后小鼠表皮细胞的再生增殖。结合3H-TdR掺入和有丝分裂抑制法(秋水仙酰胺)对分离的表皮基底细胞进行微流荧光测定。
Cell Tissue Kinet. 1976 Nov;9(6):573-87.
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Effect of hypoxia on sunburn cell formation and inflammation induced by ultraviolet radiation.缺氧对紫外线诱导的晒伤细胞形成和炎症的影响。
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Infrared radiation suppresses ultraviolet B-induced sunburn-cell formation.红外线辐射可抑制紫外线B诱导的晒伤细胞形成。
Arch Dermatol Res. 1992;284(2):92-4. doi: 10.1007/BF00373376.
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Protective and therapeutic effects of fucoxanthin against sunburn caused by UV irradiation.岩藻黄质对紫外线照射引起的晒伤的保护和治疗作用。
J Pharmacol Sci. 2016 Sep;132(1):55-64. doi: 10.1016/j.jphs.2016.08.004. Epub 2016 Aug 12.
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Protection against UV-B by UV-A-induced tan.紫外线A诱导的晒黑对紫外线B的防护作用。
Arch Dermatol. 1982 Jul;118(7):483-6.

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