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Metabolic basis of ethanol-induced hepatic and pancreatic injury in hepatic alcohol dehydrogenase deficient deer mice.
Although the present studies clearly indicate a metabolic basis of ethanol-induced hepatic and pancreatic injury, detailed dose- and time-dependent toxicity studies in this ADH(-) deer mouse model could reveal further a better understanding of mechanism(s) of alcohol-induced liver disease and pancreatitis-like injuries. Expand
Hepatic lipid profiling of deer mice fed ethanol using ¹H and ³¹P NMR spectroscopy: a dose-dependent subchronic study.
The data indicate that dose of ethanol and hepatic ADH deficiency are two key factors involved in initiation and progression of alcoholic fatty liver disease. Expand
¹H and ³¹P NMR lipidome of ethanol-induced fatty liver.
The results show that alcohol consumption alters metabolism of cholesterol, triglycerides, and phospholipids that could contribute to the development of fatty liver and indicate that fatty liver precedes oxidative stress and inflammation. Expand
Ethanol-induced cytotoxicity in rat pancreatic acinar AR42J cells: role of fatty acid ethyl esters.
The hypothesis that alcohol-induced cytotoxicity in AR42J cells is mediated by the non-oxidative metabolite(s) of ethanol, and caspase-3 mediated apoptosis could be one of the mechanisms involved in ethanol-induced pancreatic injury is supported. Expand
Pancreatic injury in hepatic alcohol dehydrogenase-deficient deer mice after subchronic exposure to ethanol.
It is suggested that ADH-deficiency and high alcohol levels in the body are the key factors in ethanol-induced pancreatic injury. Expand
Hepatic alcohol dehydrogenase deficiency induces pancreatic injury in chronic ethanol feeding model of deer mice.
The single most common cause of chronic pancreatitis (CP, a serious inflammatory disease) is chronic alcohol abuse, which impairs hepatic alcohol dehydrogenase (ADH, a major ethanol oxidizingExpand
A simple quantitative in vitro macrophage migration assay.
In vitro results showed higher macrophage chemotaxis response against the 'concentrated' cocktails as compared to routine 'diluted' cocktail, and responsiveness was seen better with sodium caseinate cocktail asCompared to oyster glycogen in vitro as well as in vivo. Expand
Thelazia skrjabini Erschow, 1928 from an Indian buffalo (Bubalus bubalis).