In vitro analysis of clastogenic effects of adrenaline on human lymphocytes

and physiological effects of adrenaline and other catecholamines, little is known about possible genotoxic and mutagenic effects. There is an interesting experimental finding that dopamine induces DNA strand breaks in human skin fibroblasts and gene mutations in mouse lymphoma cells (M o l d e u s et al., 1983). However, dopamine did not exhibit genotoxic effects in the Salmonella/mammalian-microsome mutagenicity test, the sex-linked recessive lethal test in Drosophila melanogaster, the sister chromatid exchange (SCE) test in human lymphocytes , or the in vivo micronucleus assay in mouse and rat (M o l d e u s et al., 1983). Likewise, in cytogenetic analysis, adrenaline did not exhibit genotoxic effects on cultured human peripheral blood lymphocytes (D j e l i c , 1997). On the other hand, mutagenic effects of various catecholamines on mouse lymphoma cells resulted from the creation of superoxide anion (M c G r e g o r et al., 1988). In addition, catechol derivates, including adrenaline, induce DNA strand breakage by ferryl species, whereas the induction of 8-hydroxyguanine (8OHG) is due to a hydroxyl radical (·OH) (M i u r a et al., 2000). More recent studies revealed that noradrenaline induces primary DNA damage in the Comet assay on purified human lymphocytes (D j e l i c and A n d e r s o n , 2003) and sperm (D o b r z y n s k a et al., 2004), most likely due to formation of reactive oxygen species (ROS). This result is in agreement with findings that adrenaline and other catecholamines can be involved in redox cycling under the influence of superoxide anion (G e n o v a et al., 2006). Interestingly, superoxide anion may induce chromosome breakage and sister chromatid exchange (SCE) (M ’ b e m b a -M e k a et al., 2007).