scholarly journals IN-VIVO EVALUATION OF HEXAVALENT CHROMIUM INDUCED DNA DAMAGE BY ALKALINE COMET ASSAY AND OXIDATIVE STRESS IN CATLA CATLA

2013 ◽  
Vol 9 (6) ◽  
pp. 470-482 ◽  
Author(s):  
Arunachalam
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Comet Assay ◽  
Hexavalent Chromium ◽  
Catla Catla ◽  
Alkaline Comet Assay ◽  
And Oxidative Stress

scholarly journals DNA Damaging Effects, Oxidative Stress Responses and Cholinesterase Activity in Blood and Brain of Wistar Rats Exposed to Δ9-Tetrahydrocannabinol

Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1560 ◽  
Author(s):  
Nevenka Kopjar ◽  
Nino Fuchs ◽  
Suzana Žunec ◽  
Anja Mikolić ◽  
Vedran Micek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Comet Assay ◽  
Stress Responses ◽  
Blood Cells ◽  
Genome Stability ◽  
White Blood Cells ◽  
Brain Cells ◽  
Alkaline Comet Assay

Currently we are faced with an ever-growing use of Δ9-tetrahydrocannabinol (THC) preparations, often used as supportive therapies for various malignancies and neurological disorders. As some of illegally distributed forms of such preparations, like cannabis oils and butane hash oil, might contain over 80% of THC, their consumers can become intoxicated or experience various detrimental effects. This fact motivated us for the assessments of THC toxicity in vivo on a Wistar rat model, at a daily oral dose of 7 mg/kg which is comparable to those found in illicit preparations. The main objective of the present study was to establish the magnitude and dynamics of DNA breakage associated with THC exposure in white blood and brain cells of treated rats using the alkaline comet assay. The extent of oxidative stress after acute 24 h exposure to THC was also determined as well as changes in activities of plasma and brain cholinesterases (ChE) in THC-treated and control rats. The DNA of brain cells was more prone to breakage after THC treatment compared to DNA in white blood cells. Even though DNA damage quantified by the alkaline comet assay is subject to repair, its elevated level detected in the brain cells of THC-treated rats was reason for concern. Since neurons do not proliferate, increased levels of DNA damage present threats to these cells in terms of both viability and genome stability, while inefficient DNA repair might lead to their progressive loss. The present study contributes to existing knowledge with evidence that acute exposure to a high THC dose led to low-level DNA damage in white blood cells and brain cells of rats and induced oxidative stress in brain, but did not disturb ChE activities.

Genotoxic and oxidative stress potential of nanosized and bulk zinc oxide particles in Drosophila melanogaster

2016 ◽  
Vol 32 (12) ◽  
pp. 1987-2001 ◽  
Author(s):  
Erico R Carmona ◽  
Claudio Inostroza-Blancheteau ◽  
Laura Rubio ◽  
Ricard Marcos
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Zinc Oxide ◽  
Drosophila Melanogaster ◽  
Comet Assay ◽  
Food Additives ◽  
Spot Test ◽  
Genotoxic Activity ◽  
And Oxidative Stress

Zinc oxide nanoparticles (ZnONP) are manufactured on a large scale and can be found in a variety of consumer products, such as sunscreens, lotions, paints and food additives. Few studies have been carried out on its genotoxic potential and related mechanisms in whole organisms. In the present study, the in vivo genotoxic activity of ZnONP and its bulk form was assayed using the wing-spot test and comet assay in Drosophila melanogaster. Additionally, a lipid peroxidation analysis using the thiobarbituric acid assay was also performed. Results obtained with the wing-spot test showed a lack of genotoxic activity of both ZnO forms. However, when both particle sizes were tested in the comet assay using larvae haemocytes, a significant increase in DNA damage was observed for ZnONP treatments but only at the higher dose applied. In addition, the lipid peroxidation assay showed significant malondialdehyde (MDA) induction for both ZnO forms, but the induction of MDA for ZnONP was higher for the ZnO bulk, suggesting that the observed DNA strand breaks could be induced by mediated oxidative stress. The overall data suggest that the potential genotoxicity of ZnONP in Drosophila can be considered weak according to the lack of mutagenic and recombinogenic effects and the induction of primary DNA damage only at high toxic doses of ZnONP. This study is the first assessing the genotoxic and oxidative stress potential of nano and bulk ZnO particles in Drosophila.

scholarly journals The Protective Effect of Naringenin-Oxime on Cisplatin-Induced Toxicity in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Ismail Koyuncu ◽  
Abdurrahim Kocyigit ◽  
Ataman Gonel ◽  
Erkan Arslan ◽  
Mustafa Durgun
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Comet Assay ◽  
Protective Effect ◽  
Stress Index ◽  
Mononuclear Leukocytes ◽  
Albino Rats ◽  
Peripheral Blood Mononuclear ◽  
Liver And Kidney ◽  
And Oxidative Stress

The aim of this study is to examine the protective effect of naringenin-oxime (NOX) on cisplatin-induced major organ toxicity and DNA damage in rats. Thirty-five male Wistar albino rats were equally split into five groups as follows: control (i.p., 0.1 ml of saline), Cis administration (i.p., 7 mg/kg b.w.), NOX treatment (i.p., 20 mg/kg b.w., daily for ten days), Cis + NOX20, and Cis + NOX40 combination (i.p., 20 and 40 mg/kg b.w., daily for ten days). Serum and peripheral blood mononuclear leukocytes (PBMC) were obtained from blood. Malondialdehyde, glutathione, total antioxidant and oxidant status, and catalase were measured in serum, liver, and kidney, and oxidative stress index was calculated. In parallel, paraoxonase and arylesterase activities were tested in liver and serum. We used 8-OHdOG as a marker for DNA damage in serum via ELISA and in PMBC via comet assay. Treatment with Cis elevated the levels of serum biochemical parameters, oxidative stress, and DNA damage. Pretreatments of NOX restored biochemical and oxidative stress parameters in serum, renal, and liver tissues (p<0.01) and reduced 8-OHdG level, a finding further supported by comet assay in PBMC. Observations of the present study support the fact that treatment with NOX prevents Cis-induced hepatotoxicity, nephrotoxicity, and genotoxicity by restoring antioxidant system.

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