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Molecular cytotoxic mechanims of fru...

University of Toronto (Canada).

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Molecular cytotoxic mechanims of fructose and some metabolites in isolated rat hepatocytes.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Molecular cytotoxic mechanims of fructose and some metabolites in isolated rat hepatocytes./
作者:	Lee, Owen.
面頁冊數:	83 p.
附註:	Source: Masters Abstracts International, Volume: 47-04, page: 2170.
Contained By:	Masters Abstracts International47-04.
標題:	Health Sciences, Nutrition. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MR45179
ISBN:	9780494451793

Molecular cytotoxic mechanims of fructose and some metabolites in isolated rat hepatocytes.
Lee, Owen.

Molecular cytotoxic mechanims of fructose and some metabolites in isolated rat hepatocytes. - 83 p.

Source: Masters Abstracts International, Volume: 47-04, page: 2170.

Thesis (M.Sc.)--University of Toronto (Canada), 2008.

Dietary fructose consumption is associated with the development of obesity and hepatic steatosis. A two hit hypothesis has been proposed for the pathogenesis of non-alcoholic steatohepatitis (NASH), the first hit: hepatic steatosis, and second: oxidative stress. In addition, rats fed fructose developed insulin resistance and increased their serum methylglyoxal, a fructose metabolite. As previously reported, glyoxal induced hepatocyte cytotoxicity could be attributed to mitochondrial toxicity. However the toxic mechanism of fructose, a glyoxal precursor has not been investigated. Isolated hepatocytes incubated with different concentrations of fructose were assessed for toxicity and the molecular cytotoxic mechanisms involved were investigated. Fructose itself was toxic at 1.5M, whereas 12mM was toxic when hepatocytes were also exposed to a non-cytotoxic dose of H2O2. The molecular mechanism for fructose cytotoxicity involved oxidative stress as endogenous reactive oxygen species (ROS) and H2O2 formation preceded cytotoxicity. Toxicity was decreased by radical scavengers, ROS scavengers, and lipid antioxidants.

ISBN: 9780494451793Subjects--Topical Terms:

1017801
Health Sciences, Nutrition.

Molecular cytotoxic mechanims of fructose and some metabolites in isolated rat hepatocytes.
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520 $a Dietary fructose consumption is associated with the development of obesity and hepatic steatosis. A two hit hypothesis has been proposed for the pathogenesis of non-alcoholic steatohepatitis (NASH), the first hit: hepatic steatosis, and second: oxidative stress. In addition, rats fed fructose developed insulin resistance and increased their serum methylglyoxal, a fructose metabolite. As previously reported, glyoxal induced hepatocyte cytotoxicity could be attributed to mitochondrial toxicity. However the toxic mechanism of fructose, a glyoxal precursor has not been investigated. Isolated hepatocytes incubated with different concentrations of fructose were assessed for toxicity and the molecular cytotoxic mechanisms involved were investigated. Fructose itself was toxic at 1.5M, whereas 12mM was toxic when hepatocytes were also exposed to a non-cytotoxic dose of H2O2. The molecular mechanism for fructose cytotoxicity involved oxidative stress as endogenous reactive oxygen species (ROS) and H2O2 formation preceded cytotoxicity. Toxicity was decreased by radical scavengers, ROS scavengers, and lipid antioxidants.
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