Hypothalamic superoxide dismutase, xanthine oxidase, nitric oxide, and malondialdehyde in rats fed with fish ω-3 fatty acids

Author(s):  
Ahmet Songur ◽  
Mustafa Sarsilmaz ◽  
Sadik Sogut ◽  
Birsen Ozyurt ◽  
Huseyin Ozyurt ◽  
...  
2005 ◽  
Vol 21 (1-2) ◽  
pp. 67-73 ◽  
Author(s):  
H Ramazan Yilmaz ◽  
Sadik Sogut ◽  
Birsen Ozyurt ◽  
Fikret Ozugurlu ◽  
Semsettin Sahin ◽  
...  

The aim of this experimental study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on cisplatin-induced hepatotoxicity through adenosine deaminase (AD), xanthine oxidase (XO), catalase (CAT), superoxide dismutase (SOD) activities and malondialdehyde (MDA) and nitric oxide (NO) levels in liver tissue of rats. Wistar albino rats were divided into three groups: control group (n-6), cisplatin group (n-9) and CAPE+cisplatin group (n-8). All the chemicals used were applied intraperitoneally. Spectrophotometric methods were used to determine the activities of the above-mentioned enzymes in the liver tissue. NO level and XO activity were found to be increased in the cisplatin group compared to the control group. NO level was found to be decreased in the cisplatin+CAPE group in comparison with the cisplatin group. There was no significant change in the activity of XO between the cisplatin and cisplatin+CAPE groups. The activity of SOD was lower in the cisplatin group than both the control and cisplatin+CAPE groups. There was no significant change in the activity of CAT between the control and cisplatin groups. CAT activity was increased in the cisplatin+CAPE group compared to the cisplatin group. The AD activity and MDA level remained unchanged in all groups. The results obtained suggested that CAPE significantly attenuated the hepatotoxicity as an indirect target of cisplatin in an animal model of cisplatin-induced nephrotoxicity.


Author(s):  
Sami Bahcebasi ◽  
Gulden Baskol ◽  
Mevult Baskol

<p class="abstract"><strong>Background:</strong> Hepatic encephalopathy is a serious neuropsychiatric complication of cirrhosis. Changes in the oxidative and anti-oxidative system and nitric oxide levels in brain tissue contribute to the development of symptoms related to HE and HE. Purpose of the study to reveal the alterations in oxidative, anti-oxidative system and nitric oxide levels in cirrhotic patients during and after hepatic encephalopathy periods.</p><p class="abstract"><strong>Methods:</strong> This was a randomized controlled double-blind study conducted in Erciyes University Hospital between 3 July 2010 and 30 March 2011. We investigated the oxidative and anti-oxidative stress parameters by quantification of total antioxidant capacity (TAC), total oxidant capacity (TOC), nitric oxide (NO), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), total thiol and xanthine oxidase (XO) levels in serum. We compared the group of patients with hepatic encephalopathy, post-hepatic encephalopathy (clinically recovered) and control groups (healthy control).  </p><p class="abstract"><strong>Results:</strong> Thirty hepatic encephalopathy patients were studied. Serum levels of nitric oxide and xanthine oxidase were statistically significantly high in the hepatic encephalopathy group according to control group (p&lt;0.031, and p&lt;0.001, respectively). Serum thiol levels were significantly low in hepatic encephalopathy patients than the controls (p&lt;0.001). Total oxidant capacity, total antioxidant capacity, glutathione peroxidase and superoxide dismutase levels were not significantly different in hepatic encephalopathy group than the controls. Serum thiol levels were low and serum NO levels were high in recovered clinically from hepatic encephalopathy group according to control group currently (p&lt;0.001, p&lt;0.001, respectively). Total antioxidant capacity, total oxidant capacity, glutathione peroxidase, superoxide dismutase and xanthine oxidase levels were similar in both groups (p&gt;0.05). Total antioxidant capacity and especially xanthine oxidase levels were significantly decreased in recovered clinically from hepatic encephalopathy group compared to hepatic encephalopathy group (p&lt;0.05, p&lt;0.001, respectively).</p><p class="abstract"><strong>Conclusions:</strong> Oxidative system, in   systemic circulation, is activated during hepatic encephalopathy and changes in XO level during and after hepatic encephalopathy is very different. This parameter may be a potential marker in differential diagnosis of hepatic encephalopathy from other coma causes. Further investigation is needed.</p>


1981 ◽  
Vol 45 (03) ◽  
pp. 290-293 ◽  
Author(s):  
Peter H Levine ◽  
Danielle G Sladdin ◽  
Norman I Krinsky

SummaryIn the course of studying the effects on platelets of the oxidant species superoxide (O- 2), Of was generated by the interaction of xanthine oxidase plus xanthine. Surprisingly, gel-filtered platelets, when exposed to xanthine oxidase in the absence of xanthine substrate, were found to generate superoxide (O- 2), as determined by the reduction of added cytochrome c and by the inhibition of this reduction in the presence of superoxide dismutase.In addition to generating Of, the xanthine oxidase-treated platelets display both aggregation and evidence of the release reaction. This xanthine oxidase induced aggreagtion is not inhibited by the addition of either superoxide dismutase or cytochrome c, suggesting that it is due to either a further metabolite of O- 2, or that O- 2 itself exerts no important direct effect on platelet function under these experimental conditions. The ability of Of to modulate platelet reactions in vivo or in vitro remains in doubt, and xanthine oxidase is an unsuitable source of O- 2 in platelet studies because of its own effects on platelets.


2020 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Mohamed Abdellatif ◽  
Alaa Ibrahim ◽  
Mohamed Arafa ◽  
Amal Abdelazeim

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