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氧自由基增加与高糖饮食所致的胰腺损伤。

Increased oxygen radical and high-dietary-carbohydrate pancreatic damage.

作者信息

Novelli E L, Novelli Filho J L, Rodrigues N L, Ribas B O

机构信息

Departamento de Química, Universidade Estadual Paulista e UNESP, Botucatu, Sao Paulo, Brazil.

出版信息

Bol Estud Med Biol. 1994 Jan-Dec;42(1-4):21-5.

PMID:7786401
Abstract

These data suggest that an improved understanding of the relationship between high dietary carbohydrate and the rate of lipid peroxidation may give some insight into possible treatment modalities for pancreatic damages and may shed light on molecular mechanisms underlying certain pathological processes. High dietary carbohydrate lesions are age related and induced alterations on ceruloplasmin, phospholipids, total proteins, copper and zinc serum levels. Significantly increased serum and pancreatic amylase, and lipoperoxide determinations were observed in 20 month old rats. Cu-Zn superoxide dismutase was decreased in these animals. Daily injection of Cu-Zn superoxide dismutase conjugated with polyethylene glycol (SOD-PEG) prevented the serum and pancreatic changes, indicating that superoxide radical is an important intermediate to high dietary carbohydrate lesion.

摘要

这些数据表明,更好地理解高糖饮食与脂质过氧化速率之间的关系,可能有助于深入了解胰腺损伤的潜在治疗方式,并揭示某些病理过程的分子机制。高糖饮食损伤与年龄相关,并导致血浆铜蓝蛋白、磷脂、总蛋白、血清铜和锌水平发生改变。在20月龄大鼠中观察到血清和胰腺淀粉酶以及脂质过氧化物测定值显著增加。这些动物体内的铜锌超氧化物歧化酶减少。每日注射与聚乙二醇结合的铜锌超氧化物歧化酶(SOD-PEG)可防止血清和胰腺发生变化,这表明超氧自由基是高糖饮食损伤的重要中间介质。

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