Effect of nickel exposure on peripheral tissues: Role of oxidative stress in toxicity and possible protection by ascorbic acid

2007 ◽  
Vol 22 (2) ◽  
Author(s):  
K.K. Das ◽  
V. Büchner
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Islam M. El-Garawani ◽  
Elsayed A. Khallaf ◽  
Alaa A. Alne-na-ei ◽  
Rehab G. Elgendy ◽  
Gaber A. M. Mersal ◽  
...  

AbstractImidacloprid (Imid), a systemic neonicotinoid insecticide, is broadly used worldwide. It is reported to contaminate aquatic systems. This study was proposed to evaluate oxidative stress and genotoxicity of Imid on Nile tilapia (Oreochromis niloticus) and the protective effect of ascorbic acid (Asc). O. niloticus juveniles (30.4 ± 9.3 g, 11.9 ± 1.3 cm) were divided into six groups (n = 10/replicate). For 21 days, two groups were exposed to sub-lethal concentrations of Imid (8.75 ppm, 1/20 of 72 h-LC50 and 17.5 ppm, 1/10 of 72 h-LC50); other two groups were exposed to Asc (50 ppm) in combination with Imid (8.75 and 17.5 ppm); one group was exposed to Asc (50 ppm) in addition to a group of unexposed fish which served as controls. Oxidative stress was assessed in the liver where the level of enzymatic activities including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in addition to mRNA transcripts and, Lipid peroxidation (LPO) were evaluated. Moreover, mitotic index (MI) and comet assay were performed, in addition, the erythrocytic micronucleus (MN), and nuclear abnormalities (NA) were observed to assess genotoxicity in fish. Imid exposure induced significant (p ˂ 0.05) changes in the antioxidant profile of the juveniles' liver by increasing the activities and gene expression of SOD, CAT and GPX as well as elevating the levels of LPO. DNA strand breaks in gill cells, erythrocytes and hepatocytes along with erythrocytic MN and NA were also significantly elevated in Imid-exposed groups. MI showed a significant (p ˂ 0.05) decrease associated with Imid exposure. Asc administration induced a significant amelioration towards the Imid toxicity (8.75 and 17.5 ppm). A significant protective potency against the genotoxic effects of Imid was evidenced in Asc co-treated groups. Collectively, results highlight the importance of Asc as a protective agent against Imid-induced oxidative stress and genotoxicity in O. niloticus juveniles.


2016 ◽  
Vol 6 (1) ◽  
pp. 39 ◽  
Author(s):  
Muneer Ahmad Dar ◽  
Rajinder Raina ◽  
Arshad Hussain Mir ◽  
Pawan Kumar Verma ◽  
Nrip Kishore Pankaj ◽  
...  

2001 ◽  
Vol 132 (4) ◽  
pp. 941-949 ◽  
Author(s):  
Pier Andrea Serra ◽  
Giovanni Esposito ◽  
M Rosaria Delogu ◽  
Rossana Migheli ◽  
Gaia Rocchitta ◽  
...  

2011 ◽  
Vol 38 (3) ◽  
pp. 635-643 ◽  
Author(s):  
Ferbal Özkan ◽  
Suna Gül Gündüz ◽  
Mehmet Berköz ◽  
Arzu Özlüer Hunt ◽  
Serap Yalın

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Vanessa Palermo ◽  
Fulvio Mattivi ◽  
Romano Silvestri ◽  
Giuseppe La Regina ◽  
Claudio Falcone ◽  
...  

In recent years, epidemiological and biochemical studies have shown that eating apples is associated with reduction of occurrence of cancer, degenerative, and cardiovascular diseases. This association is often attributed to the presence of antioxidants such as ascorbic acid (vitamin C) and polyphenols. The substances that hinder the presence of free radicals are also able to protect cells from aging. In our laboratory we used yeast, a unicellular eukaryotic organism, to determinein vivoefficacy of entire apples and their components, such as flesh, skin and polyphenolic fraction, to influence aging and oxidative stress. Our results indicate that all the apple components increase lifespan, with the best result given by the whole fruit, indicating a cooperative role of all apple components.


2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Petr Ježek ◽  
Andrea Dlasková ◽  
Lydie Plecitá-Hlavatá

We reviewed mechanisms that determine reactive oxygen species (redox) homeostasis, redox information signaling and metabolic/regulatory function of autocrine insulin signaling in pancreaticβcells, and consequences of oxidative stress and dysregulation of redox/information signaling for their dysfunction. We emphasize the role of mitochondrion inβcell molecular physiology and pathology, including the antioxidant role of mitochondrial uncoupling protein UCP2. Since in pancreaticβcells pyruvate cannot be easily diverted towards lactate dehydrogenase for lactate formation, the respiration and oxidative phosphorylation intensity are governed by the availability of glucose, leading to a certain ATP/ADP ratio, whereas in other cell types, cell demand dictates respiration/metabolism rates. Moreover, we examine the possibility that type 2 diabetes mellitus might be considered as an inevitable result of progressive self-accelerating oxidative stress and concomitantly dysregulated information signaling in peripheral tissues as well as in pancreaticβcells. It is because the redox signaling is inherent to the insulin receptor signaling mechanism and its impairment leads to the oxidative and nitrosative stress. Also emerging concepts, admiting participation of redox signaling even in glucose sensing and insulin release in pancreaticβcells, fit in this view. For example, NADPH has been firmly established to be a modulator of glucose-stimulated insulin release.


2021 ◽  
Author(s):  
Islam M. El-Garawani ◽  
Elsayed A. Khallaf ◽  
Alaa A. Alne-na-ei ◽  
Rehab G. Elgendy ◽  
Gaber A.M. Mersal ◽  
...  

Abstract Imidacloprid (Imid), a systemic neonicotinoid insecticide, is broadly used worldwide. It is reported to contaminate aquatic systems. This study was proposed to evaluate oxidative stress and genotoxicity of Imid on Nile tilapia (Oreochromis niloticus) and the protective effect of ascorbic acid (Asc). O. niloticus juveniles (30.4 ± 9.3 g, 11.9 ± 1.3 cm) were divided into six groups (n=10/replicate). For 21 days, two groups were exposed to sub-lethal concentrations of Imid (8.75 ppm, 1/20 of 72h-LC50 & 17.5 ppm, 1/10 of 72h-LC50); other two groups were exposed to Asc (50 ppm) in combination with Imid (8.75 & 17.5 ppm); one group was exposed to Asc (50 ppm) in addition to a group of unexposed fish which served as controls. Oxidative stress was assessed in the liver where the level of enzymatic activities including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in addition to mRNA transcripts and, Lipid peroxidation (LPO) were evaluated. Moreover, mitotic index (MI) and comet assay were performed, in addition to the erythrocytic micronucleus (MN), and nuclear abnormalities (NA) were observed to assess genotoxicity in fish. Imid exposure induced significant (p˂ 0.05) changes in the antioxidant profile of the juveniles' liver by increasing the activities and gene expression of SOD, CAT and GPX as well as elevating the levels of LPO. DNA strand breaks in gill cells, erythrocytes and hepatocytes along with erythrocytic MN and NA were also significantly elevated in Imid-exposed groups. MI showed a significant (p˂ 0.05) decrease associated with Imid exposure. Asc administration induced a significant amelioration towards the Imid toxicity (8.75 & 17.5 ppm). A significant protective potency against the genotoxic effects of Imid was evidenced in Asc co-treated groups. Collectively, results highlight the importance of Asc as a protective agent against Imid-induced oxidative stress and genotoxicity in O. niloticus juveniles.


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