Background And Aims: Rats are resistant to acetaminophen (APAP) hepatotoxicity. In this study, we evaluated whether by augmentation of the hepatic oxidative stress, through the induction of hepatic iron overload (IO), it will be feasible to overcome the resistance of rats to the toxic effects of APAP.
Method: Rats with no or increased hepatic IO.
Exp Clin Endocrinol Diabetes
October 2016
Exp Clin Endocrinol Diabetes
October 2016
The metabolic syndrome may be associated with cognitive impairment and increased oxidative stress. To document the association between metabolic syndrome, cognitive impairment and oxidative stress activity in metabolically healthy obese and in metabolically unhealthy obese individuals. 60 obese individuals aged (49±10 years, 52% male) were enrolled.
View Article and Find Full Text PDFBiol Trace Elem Res
February 2015
An increase in hepatic iron concentration might exacerbate liver injury. However, it is unknown whether hepatic iron overload may exacerbate acute liver injury from various toxins. Therefore, we evaluated how manipulations to increase hepatic iron concentration affected the extent of acute liver injury from thioacetamide.
View Article and Find Full Text PDFCopper deficiency had been suggested to link between fructose-enriched diet (FED) and the development of non-alcoholic fatty liver disease (NAFLD). In this study, we characterized changes in hepatic copper concentrations and hepatic oxidative milieu, in rats with the metabolic syndrome and NAFLD as a result of FED with pharmacological manipulations to reduce blood pressure or plasma triglycerides. Changes in plasma and hepatic copper concentrations were correlated with changes observed in the immunohistochemical hepatic expression of copper-zinc-superoxide dismutase (CuZnSOD; SOD1), metallothionein (MT) and nitrotyrosine (NITT).
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