饮食所致消化性溃疡的分子基础。
A molecular basis of peptic ulceration due to diet.
作者信息
Jayaraj A P, Rees K R, Tovey F I, White J S
出版信息
Br J Exp Pathol. 1986 Feb;67(1):149-55.
Abstract
Fresh rice oil protects against gastric ulceration in rats maintained on an impoverished diet, whereas stored oil is ulcerogenic. Rice oil contains ketoaldehydes which are ulcerogenic but their activity is prevented by the presence of antioxidants such as alpha-tocopherol, which is lost on storage. Protection may also be restored by the addition of cysteine. These results in rats in vivo can be duplicated in a rat liver microsomal system in vitro, in which malondialdehyde production is a measure of toxicity. It is proposed that the ulcerogenic activity of rice oil is the direct consequence of the stimulation of endogenous lipid peroxidation due to the lowering of the GSH content in the endoplasmic reticulum by the ketoaldehydes in stored rice oil. A similar mechanism is suggested for the ulcerogenic activity of an impoverished diet which directly lowers the tissue levels of GSH.
摘要
新鲜米油可保护以低营养饮食喂养的大鼠免受胃溃疡的侵害，而储存后的米油则具有致溃疡作用。米油中含有具有致溃疡作用的酮醛，但抗氧化剂如α-生育酚的存在可抑制其活性，而α-生育酚在储存过程中会流失。添加半胱氨酸也可恢复其保护作用。这些在大鼠体内的结果在体外大鼠肝微粒体系统中也能重现，在该系统中，丙二醛的产生是毒性的一种衡量指标。有人提出，米油的致溃疡活性是由于储存米油中的酮醛降低了内质网中谷胱甘肽（GSH）的含量，从而刺激内源性脂质过氧化的直接结果。对于低营养饮食的致溃疡活性也提出了类似的机制，即低营养饮食会直接降低组织中GSH的水平。
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