Homologous chromosome synapsis and crossing-over at meiosis are basic to mammalian gamete development: They achieve genetic recombination, regulate chromosome segregation, and are believed to function in repair and maturation. Synaptonemal complexes (SCs) are axial correlates of meiotic chromosome bivalents and develop in conjunction with homologous chromosome synapsis. It is shown here that various mutagens/anti-mitotic agents-cyclophosphamide (alkylating agent), colchicine (anti-tubulin alkaloid), amsacrine or m-AMSA (topoisomerase inhibitor), bleomycin (radiomimetic agent), and gamma radiation-induce diverse structural and synaptic errors in SCs of treated mice and hamsters. Conventional types of clastogenic effects as well as damage unique to meiotic prophase appear to be manifested in the SC. Distinctive patterns of damage are associated with specific mutagenic agents/mechanisms. Some SC aberrations are suggestive of a site specificity possibly related to crossing-over. (Copyright (c) 1990, Cold Spring Harbor Laboratory Press.)