{'fraction_non_alphanumeric': 0.027110766847405113, 'fraction_numerical': 0.015491866769945779, 'mean_word_length': 4.666666666666667, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Repair of radiation-induced chromatid aberrations: relationship to G2 arrest in CHO cells.

The literature suggests that the function of radiation-induced G2 arrest is to allow repair of potentially lethal damage before cell-entry into, and damage expression in, mitosis. The nature of the damage repaired is not known, but chromosome aberrations have been considered. To examine this possibility in G2 cells, the rate of repair of chromatid aberrations in CHO cells progressing to or arrested in G2 was compared with the rate of repair of the damage which gives rise to G2 arrest. To measure aberration repair rates, exponentially growing CHO cells arrested in G2 with 1.5, 2.5 or 3.5 Gy of X-rays were released into mitosis by treatment with 5 mM caffeine immediately or 1, 2 or 3 h after irradiation. Aberration frequencies in these cells were then related to the caffeine-free (repair) interval. To measure the rate of repair of arrest-causing damage a split-dose procedure was used. The half-times for aberration repair were approximately 1 h for achromatic gaps and 1.5 h for breaks, intrachanges and interchanges. The half-time for arrest damage repair varied with radiation dose. This result suggests that chromatid aberrations are not a primary cause of radiation-induced G2 arrest.