scholarly journals Effects of the pharmaceutical contaminants ibuprofen, diclofenac, and carbamazepine alone, and in combination, on oxidative stress parameters in early life stages of tench (Tinca tinca)

2017 ◽  
Vol 62 (No. 2) ◽  
pp. 90-97 ◽  
Author(s):  
V. Stancova ◽  
L. Plhalova ◽  
J. Blahova ◽  
D. Zivna ◽  
M. Bartoskova ◽  
...  

In the present study, the effects of sub-lethal sub-chronic doses of ibuprofen, diclofenac, and carbamazepine alone, and in combination (concentration range 0.02–60 µg/l), on the early life stages of tench (Tinca tinca) were investigated. The lower concentrations of pharmaceuticals tested (0.02, 0.2, 2 µg/l) represent the concentration values of these substances commonly present in surface waters or effluents from wastewater treatment plants. Multiple biomarkers of biotransformation, antioxidant defence systems, and lipid peroxidation were determined in fish after 35 days of exposure. The evaluated pharmaceuticals induced oxidative stress in fish both alone and in combination with each other. Generally, 60 µg/l of each single pharmaceutical influenced the activity of antioxidant enzymes significantly (P < 0.05), whereas the same concentration of these pharmaceuticals in combination (1 : 1 : 1) did not have any impact on the activity of these enzymes. However, changes in biotransformation and antioxidant enzymes were apparent if lower concentrations of these pharmaceuticals were administered in the mixture. Significant changes (P < 0.05) in the activities of glutathione reductase, glutathione peroxidase, and glutathione-S-transferase were observed even at environmental concentration ranges. A significant effect (P < 0.05) on lipid peroxidation levels was found only in the experimental group exposed to carbamazepine.

2018 ◽  
Vol 3 (4) ◽  
Author(s):  
Lital Argaev Frenkel ◽  
Hava Rozenfeld ◽  
Konstantin Rozenberg ◽  
Sanford R Sampson ◽  
Tovit Rosenzweig

ABSTRACT Background Oxidative stress contributes to the pathologic process leading to the development, progression, and complications of type 1 diabetes (T1D). Objective The aim of this study was to investigate the effect of the antioxidant N-acetyl-l-cysteine (NAC), supplemented during early life or adulthood on the development of T1D. Methods NAC was administered to nonobese diabetic (NOD) female mice during pregnancy and lactation, and the development of diabetes was followed in offspring. In an additional set of experiments, offspring of untreated mice were given NAC during adulthood, and the development of T1D was followed. Morbidity rate, insulitis and serum cytokines were measured in the 2 sets of experiments. In addition, markers of oxidative stress, glutathione, lipid peroxidation, total antioxidant capacity and activity of antioxidant enzymes, were followed. Results Morbidity rate was reduced in both treatment protocols. A decrease in interferon γ, tumor necrosis factor α, interleukin 1α, and other type 1 diabetes-associated proinflammatory cytokines was found in mice supplemented with NAC in adulthood or during early life compared with control NOD mice. The severity of insulitis was higher in control NOD mice than in treated groups. NAC administration significantly reduced oxidative stress, as determined by reduced lipid peroxidation and increased total antioxidant capacity in serum and pancreas of mice treated in early life or in adulthood and increased pancreatic glutathione when administrated in adulthood. The activity of antioxidant enzymes was not affected in mice given NAC in adulthood, whereas an increase in the activity of superoxide dismutase and catalase was demonstrated in the pancreas of their offspring. Conclusion NAC decreased morbidity of NOD mice by attenuating the immune response, presumably by eliminating oxidative stress, and might be beneficial in reducing morbidity rates of T1D in high-risk individuals.


PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e38282 ◽  
Author(s):  
Rui Rosa ◽  
Marta S. Pimentel ◽  
Joana Boavida-Portugal ◽  
Tatiana Teixeira ◽  
Katja Trübenbach ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document