TiO2 Nanoparticles Induced Oxidative Stress Mediated DNA Damage In The Liver Of Adult Male Wistar Rats

2018 ◽  
Vol 10 (2) ◽  
pp. 145-150
Author(s):  
Dasal Vasantharaja ◽  
◽  
Venugopal Ramalingam ◽  
Shanmugam Thangapandiyan ◽  
Nagarajan Sridhar ◽  
...  
2017 ◽  
Vol 93 ◽  
pp. 616-625 ◽  
Author(s):  
Imen Hammami ◽  
Ridha Ben Ali ◽  
Afef Nahdi ◽  
Olfa Kallech-Ziri ◽  
Marwa Boussada ◽  
...  

2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora

Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain – parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50 ppm sodium arsenite in drinking water) for 10 months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.


2012 ◽  
Vol 259 (1) ◽  
pp. 54-65 ◽  
Author(s):  
Quaiser Saquib ◽  
Sabry M. Attia ◽  
Maqsood A. Siddiqui ◽  
Mourad A.M. Aboul-Soud ◽  
Abdulaziz A. Al-Khedhairy ◽  
...  

Author(s):  
Babatunde Ogunlade ◽  
Sunday Adelakun ◽  
Kingsley Iteire

Background: The exposure of male individual to environmental toxicant is regarded as a channel that results in reduced sperm counts and infertility. Objective: This study investigated the ameliorative response of Sulforaphane (SFN) on Aluminum trichloride (AlCl3) induced testicular toxicity in adult male Wistar rats. Materials and Methods: A total of 32 adult male Wistar rats (180-200 gm between 8-10 wk) were divided into four groups (n = 8/each). Group A) received distilled water orally as placebo; Group B) received 100 mg/kgbw AlCl3 only orally; Group C) received 100 mg/kgbw AlCl3 and 100 mg/kgbw SFN orally; and Group D) received 100 mg/kgbw SFN only orally. After 28 days of experiment, animals underwent cervical dislocation, blood serum was obtained for analysis, and testes were harvested for biochemical assays, histology, hormonal profile, and sperm characterization. Results: The sperm parameters showed a significant difference within the AlCl3 only group compared with the control and SFN only groups (p = 0.02). However, AlCl3 and SFN co-treatment showed improvement in the motility, viability, and sperm count compared with the AlCl3 only group (p = 0.02). Furthermore, there was a significant decline in the levels of hormones profile and antioxidant status in AlCl3 only group compared to the control and SFN only (p = 0.02). The testicular histoarchitecture of the AlCl3 only group showed shrinkage of seminiferous tubules, spermatogenesis disruption, and empty lumen compared to the control and SFN only groups. Conclusion: The present study revealed the ameliorative response of SFN on AlCl3-induced testicular toxicity on serum hormone profiles, antioxidant status, lipid peroxidation, and histomorphometric analysis through oxidative stress. Key words: Sulforaphane, Aluminum trichloride, Oxidative stress, Testis, Histology.


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