Mechanism of testicular atrophy induced by Di-n-butyl phthalate in rats. VI. A possible origin of testicular iron depletion.
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.
Fukuoka
M
M
Division of Biological Chemistry, National Institute of Health Sciences, Tokyo, Japan.
Kobayashi
T
T
Hayakawa
T
T
D000818:Animals; D001284:Atrophy / Q000139:chemically induced / Q000473:pathology; D003993:Dibutyl Phthalate / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D005978:Glutathione / Q000097:blood; D006366:Heinz Bodies / Q000187:drug effects; D007501:Iron / Q000097:blood / Q000378:metabolism*; D008297:Male; D010795:Phthalic Acids / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013737:Testis / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology
D010795:Phthalic Acids; D003993:Dibutyl Phthalate; D007501:Iron; D005978:Glutathione; C028577:monobutyl phthalate