Milillo P, Burdino E, Danni O, Mina S, Ugazio G
Drug Chem Toxicol. 1982;5(2):125-41. doi: 10.3109/01480548209017774.
A PUFA-deficient diet causes deficiency symptoms and alters the fatty acid pattern in liver microsomal lipids. However, CCl4 lethality and sleeping time remain unchanged while the hepatic level of cytochrome P450 is only slightly lowered by the dietary regimen. In accordance, the amplitude of double bond shifting in microsomal lipids is far from being depressed in animals deprived of the peroxidative substrate. In fact, the experimental treatment does not impair intestinal absorption, liver uptake and metabolism of CCl4 given orally. Finally, both in vitro and in vivo peroxidative challenge of arachidonic acid content in hepatic microsomes causes comparable alterations of this parameter, whatever the initial fatty acid pattern following the dietary regimen. These findings provide evidence excluding an influence of the fatty acid composition of the diet on the severity of damages due to halogen-alkane exposure.
缺乏多不饱和脂肪酸的饮食会导致缺乏症状，并改变肝脏微粒体脂质中的脂肪酸模式。然而，四氯化碳致死率和睡眠时间保持不变，而饮食方案仅使细胞色素P450的肝脏水平略有降低。相应地，在缺乏过氧化底物的动物中，微粒体脂质中双键移动的幅度远未受到抑制。事实上，实验处理并不损害口服给予的四氯化碳的肠道吸收、肝脏摄取和代谢。最后，无论饮食方案后的初始脂肪酸模式如何，肝微粒体中花生四烯酸含量的体外和体内过氧化应激都会导致该参数发生类似的变化。这些发现提供了证据，排除了饮食中脂肪酸组成对卤代烷暴露所致损伤严重程度的影响。
