Sister Chromatid Exchange Analysis in Lymphocytes

Abstract

Sister chromatid exchanges (SCEs) are generally considered to arise from breakage and recombination of sister chromatid segments at homologous loci.(1) Although the fundamental nature of SCE is not well understood, interests in its frequency have been central both to historical and current studies. Early autoradiographic techniques used to detect this phenomenon were applied for a variety of investigations into its spontaneous and irradiationrelated incidences in somatic and germ cells.(2,3) Nearly a decade ago technically simpler bromodeoxyuridine (BrdUrd)-differential staining methodology was developed in a cultured human lymphocyte system and shown to provide much superior resolving power.(4) Chemical mutagens were clearly demonstrated to induce SCEs at significantly lower doses than those required to cause chromosome aberrations.(5,6) This observation coincided with timely autoradiographic determinations of mutagen action in SCE formation(7,8) and set a new course of emphasis — SCE induction stemming from exposure to environmental agents. The BrdUrd methodology has since been extended to a wide variety of in vitro and in vivo cellular systems, and hundreds of SCE induction trials have implicated numerous chemical, physical (i.e., UV irradiation), and biological (i.e., virus) agents in the production of this effect(9,10) A recent summary evaluation of accumulated results has concluded that most chemical carcinogens induce SCEs, the test being particularly sensitive to agents that cause DNA adducts.(1)