Effect of Zinc Deficiency and Supplementation on Lipid Peroxidation of Renal Tissue in Ovariectomized Rats

2004 ◽  
Vol 101 (3) ◽  
pp. 231-240 ◽  
Author(s):  
Abdulkerim Kasim Baltaci ◽  
Fusun Sunar ◽  
Rasim Mogulkoc ◽  
Esma Oztekin
Toxicology ◽  
2004 ◽  
Vol 203 (1-3) ◽  
pp. 77-82 ◽  
Author(s):  
Abdulkerim Kasim Baltaci ◽  
Fusun Sunar ◽  
Rasim Mogulkoc ◽  
Esma Oztekin

Renal Failure ◽  
1996 ◽  
Vol 18 (4) ◽  
pp. 537-543 ◽  
Author(s):  
C. Dioudis ◽  
D. Grekas ◽  
G. Papageorgiou ◽  
S. Iliadis ◽  
N. Botsoglou ◽  
...  

2008 ◽  
Vol 295 (2) ◽  
pp. R543-R549 ◽  
Author(s):  
Analía Lorena Tomat ◽  
Felipe Inserra ◽  
Luciana Veiras ◽  
María Constanza Vallone ◽  
Ana María Balaszczuk ◽  
...  

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.


2003 ◽  
Vol 96 (1-3) ◽  
pp. 227-236 ◽  
Author(s):  
Abdülkerim Kasim Baltaci ◽  
Kursat Ozyurek ◽  
Rasim Mogulkoc ◽  
Erdal Kurtoglu ◽  
Yasemin Ozkan ◽  
...  

2016 ◽  
Vol 94 (9) ◽  
pp. 961-972 ◽  
Author(s):  
Ionut Caravan ◽  
Alexandra Sevastre Berghian ◽  
Remus Moldovan ◽  
Nicoleta Decea ◽  
Remus Orasan ◽  
...  

Menopause is accompanied by enhanced oxidative stress and behavioral changes, effects attenuated by antioxidants. The aim of this study was to evaluate the effects of caffeine on behavior and oxidative stress in an experimental model of menopause. Female rats were divided into the following groups: sham-operated (CON), sham-operated and caffeine-treated (CAF), ovariectomized (OVX), ovariectomized and caffeine-treated (OVX+CAF). Caffeine (6 mg/kg) and vehicle were administered for 21 days (subchronic) and 42 days (chronic), using 2 experimental subsets. Behavioral tests and oxidative stress parameters in the blood, whole brain, and hippocampus were assessed. The subchronic administration of caffeine decreased the lipid peroxidation and improved the antioxidant defense in the blood and brain. The GSH/GGSG ratio in the brain was improved by chronic administration, with reduced activities of antioxidant enzymes and enhanced nitric oxide and malondialdehyde levels. In particular, the lipid peroxidation in the hippocampus decreased in both experiments. The rats became hyperactive after 21 days of treatment, but no effect was observed after chronic administration. In both experimental subsets, caffeine had anxiolytic effects as tested in elevated plus maze. The administration of low doses of caffeine, for a short period of time, may be a new therapeutic approach to modulating the oxidative stress and anxiety in menopause.


2006 ◽  
Vol 65 (1) ◽  
pp. 140-144 ◽  
Author(s):  
Serap Yalin ◽  
Ulku Comelekoglu ◽  
Selda Bagis ◽  
N. Ozlen Sahin ◽  
Oya Ogenler ◽  
...  

2017 ◽  
Vol 44 ◽  
pp. 71-79 ◽  
Author(s):  
Flávia R.M. da Silva ◽  
Tony F. Grassi ◽  
Joyce R. Zapaterini ◽  
Lucas T. Bidinotto ◽  
Luis F. Barbisan

2014 ◽  
Vol 111 (11) ◽  
pp. 1932-1944 ◽  
Author(s):  
Leucio D. Vieira-Filho ◽  
Edjair V. Cabral ◽  
Juliane S. Farias ◽  
Paulo A. Silva ◽  
Humberto Muzi-Filho ◽  
...  

In the present study, we investigated the development of hypertension in prenatally undernourished adult rats, including the mechanisms that culminate in dysfunctions of molecular signalling in the kidney. Dams were fed a low-protein multideficient diet throughout gestation with or without α-tocopherol during lactation. The time course of hypertension development followed in male offspring was correlated with alterations in proximal tubule Na+-ATPase activity, expression of angiotensin II (Ang II) receptors, and activity of protein kinases C and A. After the establishment of hypertension, Ang II levels, cyclo-oxygenase 2 (COX-2) and NADPH oxidase subunit expression, lipid peroxidation and macrophage infiltration were examined in renal tissue. Lipid peroxidation in undernourished rats, which was very intense at 60 d, decreased at 90 d and returned to control values by 150 d. During the prehypertensive phase, prenatally undernourished rats exhibited elevated renal Na+-ATPase activity, type 2 Ang II receptor down-regulation and altered protein kinase A:protein kinase C ratio. Stable late hypertension coexisted with highly elevated levels of Ang II-positive cells in the cortical tubulointerstitium, enhanced increase in the expression of p47phox (NADPH oxidase regulatory subunit), marked down-regulation of COX-2 expression, expanded plasma volume and decreased creatinine clearance. These alterations were reduced when the dams were given α-tocopherol during lactation. The offspring of well-nourished dams treated with α-tocopherol exhibited most of the alterations encountered in the offspring of undernourished dams not treated with α-tocopherol. Thus, alterations in proximal tubule Na+ transport, subcellular signalling pathways and reactive oxygen species handling in renal tissue underpin the development of hypertension.


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