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3-叔丁基-4-羟基茴香醚(BHA)诱导大鼠前胃早期病变

Induction of early lesions in the forestomach of rats by 3-tert-butyl-4-hydroxyanisole (BHA).

作者信息

Altmann H J, Wester P W, Matthiaschk G, Grunow W, van der Heijden C A

出版信息

Food Chem Toxicol. 1985 Aug;23(8):723-31. doi: 10.1016/0278-6915(85)90265-0.

DOI:10.1016/0278-6915(85)90265-0
PMID:4043878
Abstract

BHA was administered to Wistar rats at a dose level of 2% in a powdered diet for periods of 1, 2 and 4 wk. After 1 wk epithelial damage, mild hyperplasia and hyperkeratosis of the forestomach mucosa was observed. The hyperplasia and hyperkeratosis showed progression at wk 2 and 4 whereas other epithelial defects regressed. The lesions were most pronounced in the vicinity of the limiting ridge. A further 4 wk of feeding without BHA resulted in a complete regression of epithelial defects, although the hyperplastic changes were still apparent. Other rats were given 1 g BHA/kg body weight/day by gastric intubation in arachis oil for 1, 2, 4, 8, 16 or 32 days. Increased mitotic activity was observed after 1 day and mild hyperplasia after the second intubation, but inflammatory response and superficial defects were not prominent and the hyperplasia of the squamous epithelium did not appear to result from initial damage and subsequent hyper-regenerative activity. A gradual regression of the hyperplastic changes occurred after eight daily intubations. The lesions were found in the apex of the forestomach remote from the limiting ridge. It is concluded that BHA incorporated in powdered diet or given in arachis oil by oral intubation causes lesions in the rat forestomach similar to that reported for BHA given in a pelleted diet (Ito et al. J. natn. Cancer Inst. 1983, 70, 343; idem, Gann 1983, 74, 459). The hyperplastic changes in the mucosa occur rapidly and their localization is dependent on the mode of application. Following withdrawal of the BHA there was almost complete regression of the lesion, only a residual mild hyperplasia remaining after 4 wk.

摘要

将丁基羟基茴香醚(BHA)以2%的剂量添加到Wistar大鼠的粉状饲料中,分别喂养1周、2周和4周。1周后,观察到前胃黏膜出现上皮损伤、轻度增生和角化过度。增生和角化过度在第2周和第4周有所进展,而其他上皮缺陷则有所消退。病变在界限嵴附近最为明显。在不添加BHA的情况下再喂养4周,上皮缺陷完全消退,尽管增生性变化仍然明显。其他大鼠通过胃内插管给予1 g BHA/千克体重/天的花生油溶液,持续1天、2天、4天、8天、16天或32天。1天后观察到有丝分裂活性增加,第二次插管后出现轻度增生,但炎症反应和表面缺陷不明显,鳞状上皮增生似乎不是由初始损伤和随后的过度再生活动引起的。每日插管8次后,增生性变化逐渐消退。病变在前胃远离界限嵴的顶端发现。得出的结论是,添加到粉状饲料中的BHA或通过口服插管给予花生油溶液中的BHA会在大鼠前胃中引起病变,类似于在颗粒饲料中给予BHA所报道的病变(Ito等人,《国家癌症研究所杂志》,1983年,70卷,343页;同上,《癌症》,1983年,74卷,459页)。黏膜的增生性变化迅速发生,其定位取决于给药方式。停止给予BHA后,病变几乎完全消退,4周后仅残留轻度增生。

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Induction of early lesions in the forestomach of rats by 3-tert-butyl-4-hydroxyanisole (BHA).3-叔丁基-4-羟基茴香醚(BHA)诱导大鼠前胃早期病变
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