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黄曲霉毒素B1与苯并(a)芘的摄取、血管转运及细胞内化比较

Comparative uptake, vascular transport, and cellular internalization of aflatoxin-B1 and benzo(a)pyrene.

作者信息

Busbee D L, Norman J O, Ziprin R L

机构信息

Department of Anatomy, College of Veterinary Medicine, Texas A&M University, College Station 77843.

出版信息

Arch Toxicol. 1990;64(4):285-90. doi: 10.1007/BF01972988.

Abstract

Studies of the uptake of benzo(a)pyrene (BaP) and aflatoxin-B1 (AFB1) after gastric instillation showed that BaP was absorbed via the intestinal lymphatic drainage and transported to the vascular circulation sequestered within lipoproteins in thoracic duct lymph, while AFB1 was absorbed with water soluble compounds into the gastrointestinal venous drainage and was not transported in association with lipoproteins. BaP was taken up into plasma lipoproteins over a broad concentration range, while AFB1 was not sequestered within lipoproteins over the same concentration range. Low density lipoproteins (LDL) facilitated BaP uptake into fibroblasts and impeded BaP uptake into hepatocytes. High density lipoproteins (HDL) facilitated BaP uptake into hepatocytes and impeded BaP uptake into fibroblasts. The uptake of AFB1 into either fibroblasts or hepatocytes was not affected by lipoproteins.

摘要

胃内灌注苯并(a)芘(BaP)和黄曲霉毒素B1(AFB1)后的摄取研究表明,BaP通过肠道淋巴引流被吸收,并以脂蛋白形式隔离在胸导管淋巴中运输到血液循环,而AFB1则与水溶性化合物一起被吸收进入胃肠静脉引流,且不与脂蛋白结合运输。在很宽的浓度范围内,BaP被摄取到血浆脂蛋白中,而在相同浓度范围内,AFB1不被隔离在脂蛋白中。低密度脂蛋白(LDL)促进BaP摄取进入成纤维细胞,并阻碍BaP摄取进入肝细胞。高密度脂蛋白(HDL)促进BaP摄取进入肝细胞,并阻碍BaP摄取进入成纤维细胞。脂蛋白对AFB1摄取进入成纤维细胞或肝细胞均无影响。

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