Comparative study of the effect of verapamil and vitamin D on iron overload-induced oxidative stress and cardiac structural changes in adult male rats

2014 ◽  
Vol 21 (4) ◽  
pp. 293-300 ◽  
Author(s):  
Eman S.H. Abd Allah ◽  
Marwa A. Ahmed ◽  
Asmaa Fathi Abdel Mola

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Arwa A. El-Sheikh ◽  
Shimaa Hamed Ameen ◽  
Samaa Salah AbdEl-Fatah

Objective. The aim of our study is to compare the role of the new natural alternative (Quercetin) with the current iron-chelation therapy (Deferoxamine (DFO)) in the effect of iron overload on small intestinal tissues and to investigate the possible underlying molecular mechanisms of such toxicity. Methods. Forty-two adult male albino rats were divided into six groups: control groups, DFO, Quercetin, iron overload, iron overload+DFO, and iron overload+Quercetin groups. Animals received daily intraperitoneal injection of Deferoxamine (125 mg /kg), Quercetin (10 mg/kg), and ferric dextran (200 mg/kg) for 2 weeks. Results. Iron overloaded group showed significant increase in serum iron, total iron binding capacity (TIBC), transferrin saturation percentage (TS %) hepcidin (HEPC), serum ferritin, nontransferrin bound iron (NTBI), and small intestinal tissues iron levels. Iron overload significantly increased the serum oxidative stress indicator (MDA) and reduced serum total antioxidant capacity (TAC). On the other hand, iron overload increased IL6 and reduced IL10 in small intestinal tissues reflecting inflammatory condition and increased caspase 3 reactivity indicating apoptosis and increased iNOs expressing cell indicting oxidative stress especially in ileum. In addition, it induced small intestinal tissues pathological alterations. The treatment with Quercetin showed nonsignificant differences as compared to treatment with DFO that chelated the serum and tissue iron and improved the oxidative stress and reduced tissue IL6 and increased IL10 and decreased caspase 3 and iNOs expressing cells in small intestinal tissues. Moreover, it ameliorated the iron overload induced pathological alterations. Conclusion. Our study showed the potential role of Quercetin as iron chelator like DFO in case of iron overload induced small intestinal toxicity in adult rats because of its serum and tissue iron chelation, improvement of serum, and small intestinal oxidative stress, ameliorating iron induced intestinal inflammation, apoptosis, and histopathological alterations.



2012 ◽  
Vol 26 (12) ◽  
pp. 522-532 ◽  
Author(s):  
Suganya Sekaran ◽  
Selvakumar Kandaswamy ◽  
Krishnamoorthy Gunasekaran ◽  
Elumalai Perumal ◽  
Fariya Yasmine Afsar Basha ◽  
...  


2014 ◽  
Vol 74 (12) ◽  
pp. 1184-1193 ◽  
Author(s):  
Bertha Segura ◽  
Angel I. Melo ◽  
Alison S. Fleming ◽  
Maria Eugenia Mendoza-Garrido ◽  
Margarita González del Pliego ◽  
...  


Author(s):  
Abdel-Moniem A. Makhlouf ◽  
Atef M. Mahmoud ◽  
Rania G. Ibrahim ◽  
Yasmeen S. Abdel Aziz

Purpose: This study was aimed to evaluate the antioxidant and anti-inflammatory effects of vitamin D and Simvastatin (SIM) on a high-fat diet (HFD) induced-obese rats. Methods: 40 adult male rats were divided into four groups: control group, HFD, HFD + vitamin D, and HFD + SIM for 14 weeks. Vitamin D or SIM supplementation was done for the last 6 weeks. Vitamin D dosage was 500 IU/kg, while SIM dosage was 10 mg/kg. Interleukin-6 (IL-6) concentration and markers of oxidative stress including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and reduced glutathione(GSH) concentrations in serum were determined using ELISA kits and spectrophotometry methods, respectively. Results: Treatment with vitamin D or SIM could significantly reduce IL-6 and MDA and increases SOD, GPx activities, and GSH levels. Oxidative stress can result not only from increased ROS production but also from dysfunctional antioxidant defenses. Conclusion: From the experimental results, it was observed that SIM and vitamin D could attenuate oxidative stress and inflammation markers associated with obesity.



Author(s):  
Yasmeen El Sayed ◽  
Nagah Ali ◽  
Amal Elshazly ◽  
Rabab Salim ◽  
Bodour Baioumy ◽  
...  


Author(s):  
Faezeh Abbasi Balochkhaneh ◽  
Somayeh Farhang Dehghan ◽  
Abbas Haghparast ◽  
Mohammad Hossein Vaziri ◽  
Mehrdad Helmi Kohanehshari ◽  
...  


Pharmacology ◽  
2019 ◽  
Vol 103 (3-4) ◽  
pp. 202-211 ◽  
Author(s):  
Marwan Abdel-Latif Ibrahim ◽  
Alaa-Eldin Salah-Eldin

Aim: The present study aimed to elucidate the effects of tramadol on the testicular functions of adult male rats due to the chronic usage of tramadol and the effect of its withdrawal. Method: Adult male albino rats were classified into the following 3 groups: (I) a control administered with normal saline and (II) tramadol-treated rats (40 mg/kg b.w. orally) for 21 successive days; and (III) like the rats in the second group but kept for 4 weeks after the last tramadol dose to study the effect of tramadol withdrawal. At the end of the experimental period, blood was collected and specimens from testis were taken for histopathological, biochemical, and molecular studies. A reverse transcription-polymerized chain reaction after RNA extraction from specimens was detected for the anti-apoptotic and pro-apoptotic genes in testicular tissues. Also, malondialdehyde (MDA) was measured in tissues homogenate and antioxidant enzymes activities were evaluated. Results: The results of this study demonstrated histological changes in testicular tissues in groups II and III compared to the control group, accompanied with increased apoptotic index and proved by increased B-cell lymphoma-2 (Bcl-2) associated-X-protein and caspase-3 expression, whereas anti-apoptotic Bcl-2 markedly decreased. Moreover, in tramadol-abused and -withdrawal groups, the MDA level increased, while the antioxidant enzymes activity decreased and revealed oxidative stress, indicating that tramadol is harmful at the cellular level and can induce apoptotic changes in testicular tissues. The withdrawal effect showed signs of improvement, but it did not return to normal levels. Conclusions: It could be concluded that the administration of tramadol causes abnormalities on testicular tissues associated with oxidative stress, which confirmed the risk of increased oxidative stress on testicular tissues due to tramadol abuse.



Andrologia ◽  
2016 ◽  
Vol 49 (1) ◽  
pp. e12593 ◽  
Author(s):  
E. H. Aksu ◽  
F. M. Kandemir ◽  
M. Özkaraca ◽  
A. D. Ömür ◽  
S. Küçükler ◽  
...  


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