scholarly journals NADPH Oxidase Activity and Reactive Oxygen Species Production in Brain and Kidney of Adult Male Hypertensive Ren-2 Transgenic Rats

2015 ◽  
pp. 849-856 ◽  
Author(s):  
M. VOKURKOVÁ ◽  
H. RAUCHOVÁ ◽  
L. ŘEZÁČOVÁ ◽  
I. VANĚČKOVÁ ◽  
J. ZICHA

Hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) play an important role in brain control of blood pressure (BP). One of the important mechanisms involved in the pathogenesis of hypertension is the elevation of reactive oxygen species (ROS) production by nicotine adenine dinucleotide phosphate (NADPH) oxidase. The aim of our present study was to investigate NADPH oxidase-mediated superoxide (O2-) production and to search for the signs of lipid peroxidation in hypothalamus and medulla oblongata as well as in renal medulla and cortex of hypertensive male rats transgenic for the murine Ren-2 renin gene (Ren-2 TGR) and their age-matched normotensive controls ‒ Hannover Sprague Dawley rats (HanSD). We found no difference in the activity of NADPH oxidase measured as a lucigenin-mediated O2- production in the hypothalamus and medulla oblongata. However, we observed significantly elevated NADPH oxidase in both renal cortex and medulla of Ren-2 TGR compared with HanSD. Losartan (LOS) treatment (10 mg/kg body weight/day) for 2 months (Ren-2 TGR+LOS) did not change NADPH oxidase-dependent O2- production in the kidney. We detected significantly elevated indirect markers of lipid peroxidation measured as thiobarbituric acid-reactive substances (TBARS) in Ren-2 TGR, while they were significantly decreased in Ren-2 TGR+LOS. In conclusion, the present study shows increased NADPH oxidase activities in renal cortex and medulla with significantly increased TBARS in renal cortex. No significant changes of NADPH oxidase and markers of lipid peroxidation were detected in the studied brain regions.

Author(s):  
O. M. Larycheva

The experiments on male rats demonstrated that under the conditions of pleurisy induced by carrageenan and short melatonin deficit, a significant increase in the level of reactive oxygen species and products of lipid peroxidation in the lungs takes place.


Author(s):  
Felicia Nmeazi Okwakpam ◽  
S. Abarikwu ◽  
M. O. Monanu

Nonsteroidal anti-inflammatory drugs are associated with an increase in cardiovascular events despite its uses in the therapeutic agent for the management of long- and short-term pain. Over the last years, evidence has accumulated showing that oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Oxidative stress is no longer considered as a simple imbalance between the production and scavenging of reactive oxygen species (ROS), but as a dysfunction of enzymes involved in ROS production. This study investigated the effect of diclofenac on the activity of oxidative stress enzymes as well as formation of lipid peroxidation. Male rats weighing about 100-120 g were divided into four groups: group one (control, feed+water) group two, group three and group four treated with different mg/kg/day of drugs (50 mg/kg/day, 100 mg/kg/day and 150 mg/kg/day) feed and water respectively for 7 days. Analysis on the effect of diclofenac on the activities of stress enzymes such as nicotine adenosine dinucleotide phosphate hydrogenase oxidase (NADPHoxidase), xanthine oxidase(XOD), catalase(CAT), superoxide dismutase(SOD) and Glutathione Peroxidase as well as evaluation of lipid peroxidation by measuring malondialdehyde (MDA) in the heart homogenate were carried out and the result showed a significant increase in each parameter given rise to the production of reactive oxygen species (ROS) if not moderated by the antioxidant defense can lead to cardiac impairment as a result of oxidative stress damage or injury. The result obtained implies that diclofenac (NSAIDs) affects the redox status of vascular tissues (heart tissues).


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.


Planta ◽  
2014 ◽  
Vol 240 (5) ◽  
pp. 1023-1035 ◽  
Author(s):  
Jiangli Zhang ◽  
Changsheng Chen ◽  
Di Zhang ◽  
Houhua Li ◽  
Pengmin Li ◽  
...  

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