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２，４，５－三氟苯胺（２，４，５－ＴＦＡ）与空气氧，ＮＡＤＰＨ及地塞米松（ＤＥＸ）预处理的大鼠肝微粒体共温育，可生成大量的一氧化碳（ＣＯ）．但是，未处理或β－萘黄酮预处理的大鼠肝微粒体却无上述能力。与ＤＥＸ相比，苯巴比妥（ＰＢ）诱导的鼠肝微粒体使２，４，５－ＴＦＡ生成ＣＯ的能力仅为前者的１／４．Ｐ４５０ⅢＡ是ＤＥＸ所诱导的最主要的Ｐ４５０亚族，亦能为ＰＢ所诱导，因而在Ｐ４５０ⅢＡ对２，４，５－ＴＦＡ降解为ＣＯ中或许起主要作用，为证实这一推论，我们研究了ＣＯ生成能力与Ｐ４５０不同亚族的特征催化活性间的相关性。在所选用的红霉素氮上去甲基化，三乙酰竹桃霉素（ＴＡＯ）代谢中间体（ＭＩ）络合物生成能力，对氨基苯甲酸叔丁酯ＭＩ络合物生成能力，戊氧基异吩唑氧上去烷基化，乙氧基异吩唑氧上去乙基化，以及氨基比林氮上去甲基化等活性指标中，仅表征Ｐ４５０ⅢＡ的活性指标──ＴＡＯ－ＭＩ络合物生成能力及红霉素氮上去甲基酶活性，与ＣＯ的生成能力明显相关。给ＤＥＸ诱导的大鼠以Ｐ４５０ⅢＡ的抑制剂ＴＡＯ处理，鼠肝微粒体的Ｐ４５０含量，ＴＡＯ－ＭＩ络合物生成能力，红霉素氮上去甲基化作用，及ＣＯ生成能力的丢失程度相近。上述结果表明，Ｐ４５０Ⅲ?
Co-incubation of 2,4,5-TFA with airborne oxygen, NADPH and dexamethasone (DEX) preconditioned rat liver microsomes produced large amounts of carbon monoxide (CO) . However, untreated or β-naphthoflavone preconditioned rat liver microsomes did not have the above ability. Compared with DEX, phenobarbital (PB) -induced rat liver microsomes produced 2,4,5-TFA only 1/4 of its CO production capacity. P450ⅢA is the major P450 subunit induced by DEX and is also induced by PB. Therefore, P450ⅢA may play a major role in the degradation of 2,4,5-TFA to CO. To confirm this hypothesis, we studied the CO Correlation between capacity and catalytic activity of different P450 subfamilies. Demethylation over the selected erythromycin nitrogen, ability to generate trimethylepirin (TAO) metabolic intermediate (MI) complex, tert-butyl-p-aminobenzoate MI complex formation capacity, The activity index of P450ⅢA, which is the activity index of P450ⅢA, is only de-alkylated by iso-deoxy alkyne oxygen, deethylated by ethoxy isoproxazole and demethylated by aminopyrine. The ability of formation and erythromycin nitrogen up-demethylase activity were significantly correlated with CO production ability. To DEX induced rats treated with P450IIIA inhibitor TAO, the P450 content of rat liver microsomes, TAO-MI complex formation capacity, erythromycin nitrogen up-demethylation, and loss of CO production ability were similar. The above results show that, P450Ⅲ?