Investigation of the relationship cellular and physiological degeneration in the mandible with AQP1 and AQP3 membrane proteins

2020 ◽  
Vol 45 (5) ◽  
pp. 621-629
Author(s):  
Mustafa Çiçek ◽  
Velid Unsal ◽  
Mehmet Kemal Tümer

AbstractObjectiveIn this study, we aimed to investigate the changes in the levels of oxidative stress and antioxidant enzymes on the mandibular bone caused by the expression of aquaporin-1 and aquaporin-3 proteins.Material and method14 Balb/C white mice were divided into two groups of seven, based on whether they are young or old. Mandibular tissue samples were taken for biochemical and histological analysis.ResultsFindings of our study has shown that, AQP-1 and AQP-3 immunoreactivity significantly decreased in mandibular bone tissues of aged mice in comparison to younger mice (p < 0.05). MDA and AOPP levels, which are the indicators of oxidative stress, increased in elderly mice and antioxidant defense system SOD enzyme activity was decreased (p < 0.05). The TNF-α cytokine level, which is the indicator for inflammations, was found to be higher in older mice than in young mice (p < 0.05).ConclusionAs a result, it was observed that cellular damage, disruption in water – electrolyte balance and increased inflammation that occur during the natural process of aging had caused serious and irreversible disturbances.

2019 ◽  
Author(s):  
Osama M. Ahmed ◽  
Tarek M. Ali ◽  
Mohamed A. Abdel Gaid ◽  
Ahmed A. Elberry

AbstractThis study aimed to assess the renopreventive effect of the angiotensin converting enzyme inhibitor (ACEI), enalapril, and/or vitamin D receptor (VDR) activator, paricalcitol, on streptozotocin (STZ) diabetes-induced nephropathy and to elucidate the mechanisms of action through investigation of the effects on renal oxidative stress, antioxidant defense system and expressions of TNF-α, P53, caspase-3, and Bcl-2. Diabetes mellitus was induced in fasting male Wistar rats by single intraperitoneal injection of STZ (45 mg /kg b.w.) dissolved in citrate buffer pH 4.5. Ten days after STZ injection, the diabetic rats were treated with enalapril (25 mg/l of drinking water) and/or paricalcitol (8 µg/kg b.w.per os) dissolved in 5% DMSO daily for 4 weeks. The obtained data revealed that the treatment of diabetic Wistar rats with enalapril and/or paricalcitol led to a significant decrease in the elevated serum urea, uric acid, creatinine and sodium, potassium levels; thereby reflecting improvement of the impaired kidney function. The deteriorated kidney lipid peroxidation, GSH content and GST and catalase activities in diabetic rats were significantly ameliorated as a result of treatment with enalapril and/or paricalcitol. The elevated fasting and post-prandial serum glucose levels and the lowered serum insulin and C-peptide levels were also improved. Moreover, the treatment of diabetic rats successfully prevented the diabetes-induced histopathological deleterious changes of kidney and islets of Langerhans of pancreas. In association, the immunohistochemically detected pro-inflammatory cytokine TNF-α and apoptotic mediators P53 and caspase-3 were remarkably decreased in kidney of diabetic rats as a result of treatment, while the expression of anti-apoptotic protein Bcl-2 was increased. Based on these findings, it can be concluded that enalapril and paricalcitol can prevent STZ diabetes-induced nephropathy though amelioration of the glycemic state and antioxidant defense system together with the suppression of oxidative stress, inflammation and apoptosis.


2021 ◽  
Vol 22 (22) ◽  
pp. 12504
Author(s):  
Laura Cannavò ◽  
Serafina Perrone ◽  
Valeria Viola ◽  
Lucia Marseglia ◽  
Gabriella Di Rosa ◽  
...  

Premature infants are exposed to increased generation of reactive oxygen species, and on the other hand, they have a deficient antioxidant defense system. Oxidative insult is a salient part of lung injury that begins as acute inflammatory injury in respiratory distress disease and then evolves into chronic and structural scarring leading to bronchopulmonary dysplasia. Oxidative stress is also involved in the pathogenesis of pulmonary hypertension in newborns through the modulation of the vascular tone and the response to pulmonary vasodilators, with consequent decrease in the density of the pulmonary vessels and thickening of the pulmonary arteriolar walls. Oxidative stress has been recognized as both a trigger and an endpoint for several events, including inflammation, hypoxia, hyperoxia, drugs, transfusions, and mechanical ventilation, with impairment of pulmonary function and prolonged lung damage. Redoxomics is the most fascinating new measure to address lung damage due to oxidative stress. The new challenge is to use omics data to discover a set of biomarkers useful in diagnosis, prognosis, and formulating optimal and individualized neonatal care. The aim of this review was to examine the most recent evidence on the relationship between oxidative stress and lung diseases in preterm newborns. What is currently known regarding oxidative stress-related lung injury pathogenesis and the available preventive and therapeutic strategies are also discussed.


2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.


2009 ◽  
Vol 39 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Jihong Qin ◽  
Qing Liu

In the subalpine zone of the Qinghai–Tibetan Plateau of China, Dragon spruce (Picea asperata Mast.) is commonly used for reforestation. The aim of the present work was to study the effects of seasonally frozen soil on the germination of P. asperata seeds and to investigate whether these effects were associated with resumption of the antioxidant defense system. The nonfrozen treatment resulted in near failure of germination (1%) and was associated with relatively high levels of hydrogen peroxide (H2O2) and low activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxide (APX). Germination of P. asperata seeds at 10 cm under the seasonally frozen soil was higher than that at 5 cm by 26%; this higher germination rate was associated with the recovery of SOD, CAT, and APX activities. The levels of malondialdehyde (MDA) in seeds from seasonally frozen treatments were higher than those in the nonfrozen treatment, implying greater lipid peroxidation and that frozen seeds might have suffered from oxidative stress. The results indicate that seasonally frozen soil facilitated the germination of P. asperata seeds and that germination was closely related to the resumption of antioxidant enzymes activity. Overall, these findings suggest that the disappearance of seasonally frozen ground caused by global warming might result in failure of regeneration of P. asperata.


2007 ◽  
Vol 23 (5-6-1) ◽  
pp. 181-191
Author(s):  
U. Kravchenko ◽  
G. Borjaev ◽  
M. Nevitov ◽  
A. Ostapchuk ◽  
E. Kistanova

The purpose of the present work was, under conditions of the model experiment on rats, to tap the information about the features of shortterm acclimatization of the antioxidant system in various organs to toxicity of cadmium at stages of an ontogenesis and about the preventive role of the antioxidant selenopyran in this process. The obtained results showed the ontogenetic differences in the adaptive reactivity of the enzymatic antioxidant defense system in the most important organs and tissues of rats under conditions of oxidative stress induced by cadmium. The ontogenetic differences of Se redistribution in a body under influence of cadmium administration were found. The discovered decrease of Se concentration in the liver of young animals and the increase of its concentration in the liver of old animals correlated positively with the changes of GPx activity. Preventive administration of selenopyran (9- phenyl-simmetrical octa-hydroselenoxanthene) to old animals reduced the oxidative stress intensity. Animals of all age groups showed higher selenium concentration in the tissues and the increase in the selenium-dependent GPx activity.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Erieg A. Mohamed ◽  
Despina M. Bordean ◽  
Isidora Radulov ◽  
Răzvan F. Moruzi ◽  
Călin I. Hulea ◽  
...  

Background. Medications to reduce oxidative stress are preventing cellular damage associated with hyperlipidemia. In this regard, statins (e.g., atorvastatin) act primarily by decrease in low-density lipoprotein-c but, in the last decade, hepatotoxicity, associated with liver injuries in the next months after treatments’ initiation, was reported. In this case, associated phytotherapy can be a solution. Purpose. To investigate the antioxidant potential and response to free radicals, in the case of hyperlipidemic rats treated with atorvastatin. Sea buckthorn (Hippophae rhamnoides) and a grape extract (antioxivita) efficiency in the oxidative stress were investigated, also being ascertained the rats’ organs cytoarchitecture. Methods. Eighty-four hyperlipidemic Wistar rats were divided into seven groups and orally treated as follows: ATS, atorvastatin (20 mg/kg·bw); ATS + Hr, atorvastatin + H. rhamnoides; ATS + Aox, atorvastatin + grape extract; Hr, H. rhamnoides; and Aox, grape extract (both as 100 mg/kg·bw). HFD and Control received high fat diet and normal fodder only. After two and six months, respectively, rats were euthanized and the heart, liver, and kidneys were gathered. The tissue samples were prepared by homogenization of 0.5 g tissue, in ethanol, kept for 48 hours at 4°C–10°C and then filtered, in order to assess organs’ cytoarchitecture and the TAC’s values (by using cupric ion reducing antioxidant capacity (CUPRAC) assay). The test tubes were incubated, at room temperature, for 30 minutes, and then analyzed using a spectrophotometer at 450–650 nm. Results. The statistics (ANOVA) revealed that sea buckthorn diminished notably (p<0.001) the oxidative stress in the heart, liver, and kidney. After six months, the TAC’s reduced levels for the heart were significant (p<0.001) in ATS + Aox. In the case of histology, the liver’s cytoarchitecture in ATS revealed abnormal cytoarchitecture. In ATS + Hr, ATS + Aox, Hr, and Aox, cell regeneration improved in different stages, especially for ATS + Hr and ATS + Aox, in comparison with HFD, which exhibited fat degeneration. Kidney’s cytoarchitecture revealed cellular healing, especially in ATS + Hr and ATS + Aox.


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