Abstract
In previous studies we have described mechanisms of testicular atrophy whereby di-n-butyl phthalate (DBP) caused a sloughing of the germ cells, prior to the testicular atrophy ; this sloughing might be attributed to iron depletion in the blood and the testicular interstitial cells. To determine whether the iron depletion is mediated by iron-release from hemoglobin (Hb), the effects of DBP upon erythrocytes have been studied. In the in vivo studies, it was observed that DBP induced glutathione (GSH) depletion, a decrease in GSH reductase activity and Heinz body formation in the red blood cells, and iron release from Hb. In the in vitro studies, in which mono-n-butyl phthalate (MBP), a metabolite of DBP, was incubated with erythrocytes, Heinz bodies and iron release from Hb were observed. The present study proposes that a mechanism for the testicular atrophy induced by DBP might involve Heinz body formation, accompanied by iron release from Hb followed by depletion of iron in the blood and testes.
