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使用一种抑制氧化应激和亚硝化应激的泰诺组合能否预防I型糖尿病和早期失明?

Can diabetes I and early blindness be prevented using a tylenol combination which inhibits oxidative and nitrosative stress?

作者信息

Van Dyke Knox, Ghareeb Erica, Hoeldtke Robert, Van Dyke Mark, Van Dyke Chris, Van Thiel David

机构信息

Department of Biochemistry and Molecular Pharmacology, Robert C. Byrd Medical Center, West Virginia University Morgantown, WV 26506, USA.

出版信息

ISRN Toxicol. 2011 Oct 5;2011:461928. doi: 10.5402/2011/461928. Print 2011.

Abstract

Since oxidative/nitrosative stress cause diabetes, can we prevent this chemistry generating the disease? Streptozotocin causes diabetes by entering the pancreatic beta cell generating excessive nitric oxide which reacts with oxygen creating a toxin possibly peroxynitrite, dinitrogen trioxide, dinitrogen tetraoxide and so forth. The toxic compounds damage the DNA causing beta cell death. This prevents insulin synthesis, storage and release. By using antioxidant substances that destroy the nitric-oxide-based toxins (e.g., carboxy-PTIO (oxidizes nitric oxide), polyphenolic-quercetin and monophenolic acetaminophen (Tylenol)) which are oxidation and nitration targets can the diabetes I causing toxins in animals be destroyed? Will this tri-drug combination completely prevent the deleterious effects of diabetes namely poor blood glucose control and blindness from cataracts for the entire length of the experiment (one year). These disease reversal experiments were accomplished in rats where the streptozotocin-diabetic effects were completely thwarted. In vitro experiments were accomplished to provide the scientific basis for the experimental results in animals.

摘要

既然氧化/亚硝化应激会引发糖尿病,那么我们能否阻止这种化学反应引发疾病呢?链脲佐菌素通过进入胰腺β细胞引发糖尿病,它会产生过量的一氧化氮,一氧化氮与氧气反应生成一种毒素,可能是过氧亚硝酸盐、三氧化二氮、四氧化二氮等等。这些有毒化合物会损害DNA,导致β细胞死亡。这会阻止胰岛素的合成、储存和释放。通过使用抗氧化物质来破坏基于一氧化氮的毒素(例如,羧基-PTIO(氧化一氧化氮)、多酚类槲皮素和单酚类对乙酰氨基酚(泰诺)),这些物质是氧化和硝化的目标,那么能否在动物体内破坏引发1型糖尿病的毒素呢?这种三联药物组合能否在整个实验过程(一年)中完全预防糖尿病的有害影响,即血糖控制不佳和白内障导致的失明呢?这些疾病逆转实验是在大鼠身上完成的,链脲佐菌素导致的糖尿病效应在大鼠身上被完全抑制。进行了体外实验,为动物实验结果提供科学依据。

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