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四氯化碳或核黄素对单剂量黄曲霉毒素B1诱导肝癌发生的影响。

Influence of carbon tetrachloride or riboflavin on liver carcinogenesis with a single dose of aflatoxin b1.

作者信息

Scotto J M, Stralin H G, Lageron A, Lemonnier F J

出版信息

Br J Exp Pathol. 1975 Apr;56(2):133-8.

Abstract

Liver carcinogenesis with a single dose of aflatoxin B1 (7 mg/kg body weight) has been investigated in a group of female Wistar strain rats by repeated biopsies and necropsies. Another group received a subsequent intoxication with carbon tetrachloride by inhalation (approximately 200 doses) and another one was overloaded with riboflavin (25 parts/10(6) in drinking water). The frequency of hepatomata was almost equal in the aflatoxin and aflatoxin-carbon tetrachloride group. It was lowere in the riboflavin-aflatoxin group. In these 3 groups cirrhosis was never present in neoplastic livers. Megalocytosis was the first lesion observed. All tumoral livers had previous or concomitant megalocytosis. This modification was about as frequent, intense and widespread in aflatoxin-CCl4 and aflatoxin groups but appeared much earlier, as did the first hepatoma, in the aflatoxin-CCl4 group. It was less frequent, less intense and less widespread in the riboflavin-aflatoxin group than in the aflatoxin group. There was also a lower frequency of hepatomata in the riboflavin-aflatoxin group, but the difference was not significant due to the too small number of animals involved. The facts are not a proof of the existence of an obligatory link between megalocytosis and carcinogenesis since a slight megalocytosis was observed in the riboflavin group not affected by the neoplastic process. However, the simplest explanation of our results would be to consider that the potential tumour cells are located among the megalocytic cells, without admitting that every megalocyte is obligatorily a precancerous cell. CCl4 seems to act in shortening the time of appearance of megalocytosis. The protective effect of riboflavine should be regarded with more caution.

摘要

通过重复活检和尸检,对一组雌性Wistar品系大鼠进行了单剂量黄曲霉毒素B1(7毫克/千克体重)诱导肝癌发生的研究。另一组通过吸入方式随后接触四氯化碳(约200次剂量),还有一组给予核黄素过量(饮用水中25 ppm)。黄曲霉毒素组和黄曲霉毒素 - 四氯化碳组的肝癌发生率几乎相等。核黄素 - 黄曲霉毒素组的发生率较低。在这三组中,肿瘤性肝脏中从未出现肝硬化。巨细胞症是观察到的首个病变。所有肿瘤性肝脏均有先前或伴随的巨细胞症。这种改变在黄曲霉毒素 - 四氯化碳组和黄曲霉毒素组中出现的频率、强度和范围大致相同,但在黄曲霉毒素 - 四氯化碳组中出现得更早,与首个肝癌出现的时间一样早。在核黄素 - 黄曲霉毒素组中,其频率、强度和范围均低于黄曲霉毒素组。核黄素 - 黄曲霉毒素组的肝癌发生率也较低,但由于涉及的动物数量过少,差异不显著。这些事实并不能证明巨细胞症与致癌作用之间存在必然联系,因为在未受肿瘤形成过程影响的核黄素组中也观察到了轻微的巨细胞症。然而,对我们结果最简单的解释是认为潜在的肿瘤细胞位于巨细胞之中,而不是认为每个巨细胞必然是癌前细胞。四氯化碳似乎起到了缩短巨细胞症出现时间的作用。核黄素的保护作用应更谨慎看待。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e948/2072738/643b063f03c8/brjexppathol00398-0040-a.jpg

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