Search

Objective: Oxidative stress, defined as an imbalance between reactive oxygen species production and breakdown by endogenous antioxidants, is closely associated with diabetes mellitus. The diabetes is characterized by hyperglycemia together with biochemical alterations of glucose and lipid peroxidation. Oxidative stress has been implicated in the pathogenesis of type 2 diabetes and its complications., Methods: This study was conducted to investigate the variation in oxidative stress-related parameters in type 2 diabetes. Blood serum samples were collected from diabetes patients and nondiabetes healthy controls. Glucose concentrations, levels of glycated hemoglobin (A1C) and serum oxidative stress markers (glucose-6-phosphate dehydrogenase [G6PDH], malondialdehyde [MDA], glutathione [GSH], glutathione reductase [GR], glutathione peroxidase [GPx] and superoxide dismutase [SOD]) were estimated., Results: Fasting serum glucose concentration in type 2 diabetes patients of both sexes was increased significantly as compared with the healthy controls. Level of A1C was greater than standards. Significant elevation in MDA level and depletion in GSH content were observed in diabetes patients in comparison with controls. The diminution in G6PDH activity was accompanied in part by a decrease in the antioxidative enzymes activities (GPx and GR), and in part by an increase in SOD activity in all diabetes patients as compared with the control group. The regression analysis showed no correlation between diabetes duration and severity of oxidative stress; however, there was a significant association between A1C and severity of oxidative stress., Conclusions: The present study shows that there is an oxidative stress state in type 2 diabetes patients compared with healthy subjects. Our data suggest that chronic hyperglycemia causes a significant change in oxidative stress markers., (Copyright © 2015 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)

Association of paracetamol (PARA) and diclofenac (DiCF) is the aim of our study. 60 male rats "Albinos wistar" were treated by oral gavage (per os) during seven days. A control group was treated by mineral water (0+0) mg/kg and a second group was treated with only a toxic dose of 100 mg/kg of PARA (100+0). Remaining lots were treated with a combination of different toxic doses of PARA and a therapeutic dose of DiCF (15+3, 100+3, 200+3 and 400+3) mg/kg. Plasma concentration of amiotransferases (ASAT, ALAT), alkalines phosphatase (ALP), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione (GSH), glucose, cholesterol, creatinin, direct and total bilirubin, significantly varied in the treated rats regarding to the witness's rats. The toxicity of PARA revealed by a dose dependant blood increases of ASAT, ALAT, ALP, GPx, GR, glucose, creatinin, bilirubin, and by decreases of cholesterol concentration and tissue GSH in comparisons to controls. The depletion of GSH and the increase of the oxidative stress enzymes (GPx and GR) suggest a detoxification function of the glutathione system. The association (PARA + DiCF) revealed a protective effect, resulting in the increase of the concentrations of ASAT, ALAT, ALP, GPx, GR, bilirubin and the increase of GSH. Regarding to all these results, it has been suggested that DiCF has a protective action towards the toxic effects of PARA.

Copyright of Phytothérapie is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Phytothérapie is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The evaluation of the effect of ginger on the modulation of toxic effects induced by lead is the objective of our study. Forty male rats were randomly divided into four groups and treated daily for 3 consecutive months. Group I (0-0) was kept as control; group II (0-G) received an experimental diet with 2% of ginger; group III (Pb-0) received 2% lead acetate dissolved in drinking water with a normal diet; and group IV (Pb-G) received 2% lead acetate in drinking water and an experimental diet containing 2% ginger. Lead acetate exposure caused a significant increase of organosomatic indexes, hepatic, lipid, and urine profiles. In addition, lead acetate has a pro-oxidative effect expressed by a significant decrease in tissue GSH levels and the enzymatic activity of GPx and CAT. This pro-oxidative action was also marked by an increase in MDA level and GST activity in lead-treated group. Feeding ginger-supplemented diet to lead acetate-treated rats restored all the parameters studied as compared to control. These results suggest that ginger treatment exerts a protective effect on metabolic disorders by decreasing the oxidative stress. [ABSTRACT FROM AUTHOR]

Copyright of Phytothérapie is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Phytothérapie is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)