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首页> 外文期刊>The Journal of investigative dermatology. >Radiation-induced chromatid breaks and DNA repair in blood lymphocytes of patients with dysplastic nevi and/or cutaneous melanoma.
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Radiation-induced chromatid breaks and DNA repair in blood lymphocytes of patients with dysplastic nevi and/or cutaneous melanoma.

机译：发育不良痣和/或皮肤黑色素瘤患者血液淋巴细胞的辐射诱导染色单体断裂和DNA修复。

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摘要

Each chromatid contains a single continuous molecule of double-stranded DNA, so chromatid breaks represent unrepaired DNA double-strand breaks. Frequencies of chromatid breaks after G2 phase x-irradiation were determined in phytohemagglutinin-stimulated blood lymphocytes from normal subjects and from four categories of patients with dysplastic nevi with or without cutaneous melanoma or with melanoma alone. Some cells were treated with an inhibitor of DNA repair replication to determine enzymatic incision activity at damaged sites after exposure to x-rays, UVC, or fluorescent light. Whereas one of 16 normal controls had deficient DNA repair, all 17 patients from families with hereditary dysplastic nevi with or without melanoma (category I) had a deficiency in repair of radiation-induced DNA damage, manifested as an abnormally high frequency of chromatid breaks after x-irradiation or a reduced capacity to incise the damaged sites after UV exposure. Four of 11 patients with sporadic dysplastic nevi alone (category II) and eight of 12 with sporadic dysplastic nevi and melanoma (category III) showed deficient DNA repair after x-irradiation. One of two patients with sporadic melanoma and no dysplastic nevi (category IV) was also deficient in repair of x-ray-induced damage. Deficient DNA repair thus appears to be associated with hereditary dysplastic nevi with or without melanoma. It also characterizes some patients with sporadic dysplastic nevi or melanoma.
机译：每个染色单体包含一个连续的双链DNA分子，因此染色单体断裂代表未修复的DNA双链断裂。确定了正常受试者以及四类患有增生性痣的伴或不伴皮肤黑素瘤或仅伴有黑素瘤的植物血凝素刺激的血淋巴细胞中G2期x射线照射后染色单体断裂的频率。某些细胞用DNA修复复制抑制剂处理，以测定暴露于X射线，UVC或荧光后受损部位的酶切活性。 16个正常对照中有1个DNA修复不足，而遗传性增生性痣伴或不伴有黑色素瘤的家庭（I类）中的所有17例患者的放射线诱导的DNA损伤修复均不足，表现为术后出现的染色单体异常高频率X射线照射或紫外线照射后切开受损部位的能力降低。仅11例散发性增生痣的患者中有4例（II类），而12例散发性增生性痣和黑色素瘤（III类）中的8例在X射线照射后显示出DNA修复不足。两名散发性黑色素瘤，无增生性痣（IV类）的患者中，有一位也无法修复X射线引起的损伤。因此，DNA修复不足似乎与遗传性增生痣伴或不伴黑素瘤有关。它还表征了一些散发性增生性痣或黑色素瘤的患者。

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