{'fraction_non_alphanumeric': 0.030837004405286344, 'fraction_numerical': 0.0, 'mean_word_length': 4.855670103092783, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
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.