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A molecular basis of peptic ulceration due to diet.

机译:饮食引起的消化性溃疡的分子基础。

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摘要

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.
机译:新鲜的米油可防止饮食不良的大鼠发生胃溃疡,而储存的油具有致溃疡性。大米油中含有酮醛,可致溃疡,但由于存在抗氧化剂(如α-生育酚)而阻止了它们的活性,这些抗氧化剂在储存时会丢失。通过添加半胱氨酸也可以恢复保护。体内大鼠的这些结果可以在体外大鼠肝微粒体系统中复制,其中丙二醛的产生是毒性的量度。提出米油的致溃疡活性是由于储存的米油中的酮醛降低内质网中GSH含量而刺激内源性脂质过氧化的直接结果。对于贫困饮食的致溃疡活性,提出了类似的机制,这直接降低了GSH的组织水平。

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