Mechanism of Testicular Atrophy Induced by Di-n-butyl Phthalate in Rats. VI. A Possible Origin of Testicular Iron Depletion

• Published in: Biological & pharmaceutical bulletin Vol. 17; no. 12; pp. 1609 - 1612
• Main Authors: FUKUOKA, Masamichi, KOBAYASHI, Tetsu, HAYAKAWA, Takao
• Format: Journal Article
• Language: English
• Published: Japan The Pharmaceutical Society of Japan 1994; Japan Science and Technology Agency
• Subjects: Animals; Atrophy - chemically induced; Atrophy - pathology; di-n-butyl phthalate; Dibutyl Phthalate - pharmacology; erythrocyte; Erythrocytes - drug effects; Erythrocytes - enzymology; Erythrocytes - metabolism; Glutathione - blood; Heinz Bodies - drug effects; Heinz body; hemoglobin; Iron - blood; Iron - metabolism; iron release; Male; Phthalic Acids - pharmacology; rat testicular atrophy; Rats; Rats, Wistar; Testis - drug effects; Testis - metabolism; Testis - pathology
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.17.1609

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.