Effect of varying dietary fat levels on rat growth and oxidative DNA damage

Effect of varying dietary fat levels on rat growth and oxidative DNA damage
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DOI:
10.1207/s15327914nc392_9
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发表时间:
2001-01-01
影响因子:
2.9
通讯作者:
Hart, RW
Hart, RW
中科院分区:
医学4区
文献类型:
--
作者:
Djuric, Z;Lewis, SM;Hart, RW

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膳食脂肪先前已被证明与大鼠的氧化应激水平有某种复杂的关系。在这项研究中,我们检查了五种不同的饮食脂肪摄入量对大鼠氧化DNA损伤水平的影响。饲喂含有3%、5%、10%或15%玉米油的饲料的动物在20周后的体重相似。然而,脂肪含量为20%的动物的平均体重明显高于其他任何一组。5-羟甲基-2'-脱氧尿苷是DNA氧化损伤的标志之一,其水平与血液和乳腺中的膳食脂肪有不同的关系。在血液中,脂肪水平随着膳食脂肪水平的增加而增加,其中20%脂肪饮食的水平最高(比3%脂肪饮食的水平高65%)。在乳腺中,观察到平台型效应,使用10%脂肪获得最大水平的氧化DNA损伤(相对于3%脂肪饮食增加68%)。这可能是由于乳腺对高脂肪饮食的补偿机制的诱导,而不是短命的有核血细胞。因此,血液中的氧化DNA损伤水平似乎是饮食脂肪摄入量的一个标志。然而,在乳腺中,DNA损伤水平与先前观察到的饮食脂肪在低脂肪摄入水平下促进乳腺肿瘤发生的作用一致,而在高脂肪摄入水平下几乎没有或没有增加促进作用。
Dietary fat has previously been shown to have somewhat complicated relationships to levels of oxidative stress in rats. In this study, we examined the effects of five different dietary fat intakes on levels of oxidative DNA damage in rats. Animals fed diets containing 3%, 5%, 10%, or 15% corn oil had body weights that were similar after 20 weeks. Animals fed a 20% fat diet, however, had significantly higher mean body weight than any other group. Levels of 5-hydroxymethyl-2'-deoxyuridine, one marker of oxidative DNA damage, had different relationships to dietary fat in blood and mammary gland. In blood, levels increased with dietary fat levels, and the highest levels were observed with the 20% fat diet (65% higher levels than with the 3% fat diet). In mammary gland, a plateau-type effect was observed, with maximal levels of oxidative DNA damage being obtained using 10% fat (representing a 68% increase relative to the 3% fat diet). This could be a result of induction of compensatory mechanisms in response to a high fat diet in mammary gland but not in the short-lived nucleated blood cells. Oxidative DNA damage levels in blood thus appear to be a marker of dietary fat intake. In mammary gland, however, levels of DNA damage are consistent with previously observed promotional effects of dietary fat on mammary gland tumorigenesis at lower levels of fat intake with little or no incremental promoting effects at higher levels of fat intake.