Rhodes C, Soames T, Stonard M D, Simpson M G, Vernall A J, Elcombe C R
Toxicol Lett. 1984 Apr;21(1):103-9. doi: 10.1016/0378-4274(84)90230-3.
Previous studies have shown that ethylhexanol (2-EH) and its oxidation products, but not n-hexanol, produce hepatomegaly, peroxisomal proliferation and hypotriglyceridaemia. In the present studies we have confirmed that at 1 mmol/kg doses, neither the linear nor branched chain alcohols induce testicular atrophy, hepatomegaly, peroxisome proliferation or hypolipidaemia. In vivo, neither the free alcohols nor their metabolic products seem to be responsible for the activity of the parent plasticiser. The released monoesters are probably the more potent metabolic products responsible for the hepatomegaly, peroxisomal proliferation and hypolipidaemia. This contention is supported by the in vitro hepatocyte data which demonstrate the induction of peroxisomal oxidative enzymes by MEHP whereas the alcohols were without effects.
先前的研究表明，乙基己醇（2-EH）及其氧化产物可导致肝肿大、过氧化物酶体增殖和低甘油三酯血症，而正己醇则不会。在本研究中，我们已证实，给予1 mmol/kg剂量时，直链或支链醇均不会诱导睾丸萎缩、肝肿大、过氧化物酶体增殖或低脂血症。在体内，无论是游离醇还是其代谢产物似乎都与母体增塑剂的活性无关。释放出的单酯可能是导致肝肿大、过氧化物酶体增殖和低甘油三酯血症的更具活性的代谢产物。体外肝细胞数据支持了这一论点，该数据表明MEHP可诱导过氧化物酶体氧化酶，而醇类则无此作用。
