Alleman M A, Koster J F, Wilson J H, Edixhoven-Bosdijk A, Slee R G, Kroos M J, von Eijk H G
Biochem Pharmacol. 1985 Jan 15;34(2):161-6. doi: 10.1016/0006-2952(85)90118-2.
Hexachlorobenzene (HCB) induces a porphyria characterized by a diminished activity of the enzyme uroporphyrinogen decarboxylase (URO-D), presumably due to inactivation by reactive metabolites of HCB. We studied the effect of iron on HCB porphyria in female rats, to determine whether the iron dependent process of lipid peroxidation was involved in the pathogenesis of porphyria. We showed that malondialdehyde formation is increased in rat liver tissue of porphyric rats and that high molecular weight proteins due to cross-linking are formed. We also showed that the induction of porphyria by HCB is dependent on the presence of iron. Our findings suggest that lipid peroxidation is involved in the toxicity of HCB and that the aggravating effects of iron on HCB are mediated by lipid peroxidation.
六氯苯(HCB)可诱发一种卟啉症,其特征是尿卟啉原脱羧酶(URO-D)的活性降低,推测这是由于HCB的活性代谢产物使其失活所致。我们研究了铁对雌性大鼠HCB卟啉症的影响,以确定脂质过氧化的铁依赖性过程是否参与了卟啉症的发病机制。我们发现,患卟啉症大鼠的肝脏组织中丙二醛的生成增加,并且由于交联作用形成了高分子量蛋白质。我们还表明,HCB对卟啉症的诱导依赖于铁的存在。我们的研究结果表明,脂质过氧化参与了HCB的毒性作用,并且铁对HCB的加重作用是由脂质过氧化介导的。