Filipendula ulmaria extracts attenuate cisplatin-induced liver and kidney oxidative stress in rats: In vivo investigation and LC-MS analysis

2017 ◽  
Vol 99 ◽  
pp. 86-102 ◽  
Author(s):  
Jelena Katanić ◽  
Sanja Matić ◽  
Eva-Maria Pferschy-Wenzig ◽  
Nadine Kretschmer ◽  
Tatjana Boroja ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Filipendula Ulmaria ◽  
Ms Analysis ◽  
Liver And Kidney

Oxidative stress as a mechanism of combined OTA and CTN toxicity in rat plasma, liver and kidney

2018 ◽  
Vol 38 (4) ◽  
pp. 434-445 ◽  
Author(s):  
D Rašić ◽  
V Micek ◽  
MS Klarić ◽  
M Peraica
Keyword(s):  
Oxidative Stress ◽  
Rat Plasma ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Lower Plasma ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Liver And Kidney ◽  
Gpx Activity

Ochratoxin A (OTA) and citrinin (CTN) commonly coexist in grains. Aiming to evaluate oxidative stress in OTA + CTN toxicity, male Wistar rats were orally treated with two doses of OTA (0.125 and 0.250 mg kg−1 of body weight (b.w.)), CTN (2 mg kg−1 of b.w.) and resveratrol (RSV; 20 mg kg−1 of b.w.) and combined daily during 3 weeks. Protein carbonyl concentrations were measured in kidneys and liver; catalytic activity of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) level in plasma, kidneys and liver, while malondialdehyde (MDA) concentration was measured in plasma, kidneys, liver and urine. Mycotoxin treatment significantly increased MDA concentration in plasma and kidney and decreased SOD activity in the liver. Rats treated with CTN and OTA125 + CTN had lower plasma GPx activity. Concentration of GSH in the kidney and protein carbonyls in the kidney and liver as well as GPx activity in the kidney and liver, SOD activity in the kidney and CAT activity in the liver were not affected. Protective effect of RSV was observed on GSH in the kidney and plasma and MDA in the kidney, plasma and urine. Oxidative stress is involved in OTA + CTN toxicity in vivo because such treatment affects parameters of oxidative stress, particularly in plasma. RSV can reduce but not overcome oxidative stress induced by combined OTA and CTN treatment.

In Vivo Biocompatibility Studies of Nano TiO2 Materials

2009 ◽  
Vol 79-82 ◽  
pp. 389-392 ◽  
Author(s):  
Wei Han ◽  
Yue Dan Wang ◽  
Yu Feng Zheng
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Catalase Activity ◽  
Histopathological Changes ◽  
Vacuolar Degeneration ◽  
Tio2 Nanomaterials ◽  
Liver And Kidney ◽  
Different Dimensions ◽  
And Oxidative Stress

TiO2 nanomaterials with different dimensions(zero and one), sizes(20nm, 50nm and 100nm in diameter) and crystal structures(100% rutile, 100% anatase and combination of 20% rutile and 80% anatase) were confected to suspensions and ointment with varied concentrations and evaluated in animal model (Balb-c mouse). These mouse were divided into various groups randomly, with suspension intraperitoneally injected or ointment transdermally daubed. Heart, lung, liver and kidney were collected and prepared to HE sample after one week. Spectrophotometry was applied to study total antioxide capability and catalase activity of blood and tissues. It has been shown that all TiO2 nanomaterial groups had no effect on lives’ morphology and oxidative stress, with no obvious histopathological changes observed in heart, lung, liver and kidney, and these tissues presented no vacuolar degeneration, necrosis edema, engorgement and inflammation.

scholarly journals Cerium Oxide Nanoparticles in Lung Acutely Induce Oxidative Stress, Inflammation, and DNA Damage in Various Organs of Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Mohamed A. Fahim ◽  
Badreldin H. Ali
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Health Concern ◽  
Fuel Additive ◽  
Limited Information ◽  
Pulmonary Exposure ◽  
Multiple Organs ◽  
Liver And Kidney ◽  
Necrosis Factor

CeO2 nanoparticles (CeO2 NPs) which are used as a diesel fuel additive are emitted in the particulate phase in the exhaust, posing a health concern. However, limited information exists regarding the in vivo acute toxicity of CeO2 NPs on multiple organs. Presently, we investigated the acute (24 h) effects of intratracheally instilled CeO2 NPs in mice (0.5 mg/kg) on oxidative stress, inflammation, and DNA damage in major organs including lung, heart, liver, kidneys, spleen, and brain. Lipid peroxidation measured by malondialdehyde production was increased in the lungs only, and reactive oxygen species were increased in the lung, heart, kidney, and brain. Superoxide dismutase activity was decreased in the lung, liver, and kidney, whereas glutathione increased in lung but it decreased in the kidney. Total nitric oxide was increased in the lung and spleen but it decreased in the heart. Tumour necrosis factor-α increased in all organs studied. Interleukin- (IL-) 6 increased in the lung, heart, liver, kidney, and spleen. IL-1β augmented in the lung, heart, kidney, and spleen. Moreover, CeO2 NPs induced DNA damage, assessed by COMET assay, in all organs studied. Collectively, these findings indicate that pulmonary exposure to CeO2 NPs causes oxidative stress, inflammation, and DNA damage in multiple organs.

scholarly journals In vivo Assessment of Combined Effects of Glibenclamide and Losartan in Diabetic Rats

2018 ◽  
Vol 28 (2) ◽  
pp. 178-185 ◽  
Author(s):  
Moureq R. Alotaibi ◽  
Amal J. Fatani ◽  
Ahmed T. Almnaizel ◽  
Mohammed M. Ahmed ◽  
Hatem M. Abuohashish ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Antihypertensive Agents ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Histological Structure ◽  
Antioxidant Enzyme Activities ◽  
Necrosis Factor Alpha ◽  
Liver And Kidney

Objective: Diabetic complications involve multiple pathological pathways, including hyperglycemia-induced oxidative stress and inflammation. Combination therapy is usually employed to improve treatment outcomes and to lower potential adverse effects. In this study, we evaluated the effects of antidiabetic and antihypertensive agents, glibenclamide (GLI) and losartan (LT), on diabetes mellitus (DM)-associated metabolic changes in rats. Materials and Methods: Streptozotocin-induced diabetic animals were orally treated with GLI 5 mg/kg and/or LT 25 mg/kg for 4 weeks. Blood glucose, insulin, aspartate aminotransferase, alanine aminotransferase, urinary creatinine, and urea levels were measured. Serum, liver, and kidney values of inflammatory markers, such as interleukin-1β, tumor necrosis factor alpha, and interleukin-6 were assessed, along with lipid peroxidation products (e.g., thiobarbituric acid reactive substances), endogenous antioxidants (e.g., glutathione), as well as antioxidant enzyme activities (e.g., catalase, superoxide dismutase, and glutathione peroxidase). Finally, histological changes in liver and kidney tissues were evaluated. Results: DM markedly induced systemic, hepatic, and renal inflammation and lowered antioxidant defense mechanisms. Treatment of diabetic rats with either GLI or LT significantly improved liver and kidney functions and histological structure. Moreover, both medications reduced signs of oxidative stress and inflammation in blood, liver, and kidney samples. Combining GLI and LT showed similar protective potential against systemic, hepatic, and renal oxidative stress and inflammation. Conclusion: Adding LT to GLI therapy revealed prospective antioxidant and anti-inflammatory action, while no synergistic or additive effects were observed.

scholarly journals Activity of sEH and Oxidant Status during Systemic Bovine Coliform Mastitis

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 812
Author(s):  
Vengai Mavangira ◽  
Matthew J. Kuhn ◽  
Angel Abuelo ◽  
Christophe Morisseau ◽  
Bruce D. Hammock ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ex Vivo ◽  
Mammary Tissue ◽  
Coliform Mastitis ◽  
Tissue Homogenates ◽  
Liver And Kidney ◽  
Propene Oxide ◽  
Oxidant Status ◽  
And Oxidative Stress

Bovine coliform mastitis presents treatment challenges because of systemic inflammation and oxidative stress. Soluble epoxide hydrolase (sEH) is a promising therapeutic target in conditions characterized by inflammation and oxidative stress but has not been evaluated in cattle. We compared sEH activity and oxidant status in healthy Holstein dairy cows to those with systemic coliform mastitis (n = 5/group) using complementary approaches. First, the activity of sEH on [3H]-trans-diphenyl-propene oxide (tDPPO) was assessed ex vivo using tissue homogenates (mammary, liver, and kidney). Second, the concentrations of sEH substrates and metabolites in plasma, milk, and urine were determined as an index of in vivo sEH activity. Oxidant status was assessed in serum and milk. Data were analyzed by non-parametric methods. Metabolism of tDPPO was greater in mammary tissues from cows with coliform mastitis compared to controls. In contrast, ratios of sEH substrates and metabolites predicted lower sEH activity in cows with coliform mastitis than controls. Milk oxidant status showed greater prooxidant levels in coliform mastitis cows. Cows with coliform mastitis exhibit increased sEH activity in mammary tissue; at the same time, milk oxidant status is increased. Future studies should characterize sEH activity and oxidant status patterns and explore therapies targeting sEH during coliform mastitis.

scholarly journals Protective effect of Ruta Chalepensis L. extract on oxidative stress and liver-kidney function induced by polymicrobial sepsis in rats

2014 ◽  
Vol 10 (1) ◽  
pp. 2146-2161
Author(s):  
Mohamed Kacem ◽  
Gaëlle Simon ◽  
Aïda Elleuch ◽  
Fatma Makni Ayadi ◽  
Tahia Boudawara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Ethanolic Extract ◽  
Pathological Examination ◽  
Enzymatic Antioxidants ◽  
Ruta Chalepensis ◽  
Systemic Inflammatory Disease ◽  
Liver And Kidney

Sepsis, a systemic inflammatory disease developed after an infectious insult and remains the major cause of death in intensive care units. The aim of this study was to examine the protective effect of the ethanolic extract of Ruta chalepensis L. (ERC) against oxidative stress and liver-kidney functions in cecal and ligation puncture (CLP) rats. In vitro, the results showed that ERC rich in phenolic compounds possessed important antioxidant activity. In vivo, CLP-induced oxidative stress evidenced by the increase of the TBARS and decrease in the enzymatic antioxidants (SOD, CAT, GPX) in liver and kidney. Moreover, CLP induced liver-kidney toxicities showed by an increase in the ALT, AST, PAL, LDH, BUN and creatinine in the plasma. However, the administration of ERC to CLP-rats prevents all these disorders. Positive action of ERC was confirmed by histo-pathological examination. Therefore this study suggests that ERC could be a potential therapeutic agent for sepsis treatment.

scholarly journals Ultrasound-Induced Destruction of Nitric Oxide–Loaded Microbubbles in the Treatment of Thrombus and Ischemia–Reperfusion Injury

2022 ◽  
Vol 12 ◽  
Author(s):  
Zenghui Liang ◽  
Huafang Chen ◽  
Xuehao Gong ◽  
Binbin Shi ◽  
Lili Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acoustic Cavitation ◽  
Liver And Kidney ◽  
Underlying Mechanisms

Objectives: Early recanalization of large vessels in thromboembolism, such as myocardial infarction and ischemic stroke, is associated with improved clinical outcomes. Nitric oxide (NO), a biological gas signaling molecule, has been proven to protect against ischemia–reperfusion injury (IRI). However, the underlying mechanisms remain to be explored. This study investigated whether NO could mitigate IRI and the role of NO during acoustic cavitation.Methods:In vivo, thrombi in the iliac artery of rats were induced by 5% FeCl3. NO-loaded microbubbles (NO-MBs) and ultrasound (US) were used to treat thrombi. B-mode and Doppler US and histological analyses were utilized to evaluate the thrombolysis effect in rats with thrombi. Immunohistochemistry, immunofluorescence, and western blotting were conducted to investigate the underlying mechanisms of NO during acoustic cavitation. In vitro, hypoxia was used to stimulate cells, and NO-MBs were employed to alleviate oxidative stress and apoptosis.Results: We developed NO-MBs that significantly improve the circulation time of NO in vivo, are visible, and effectively release therapeutic gas under US. US-targeted microbubble destruction (UTMD) and NO-loaded UTMD (NO + UTMD) caused a significant decrease in the thrombus area and an increase in the recanalization rates and blood flow velocities compared to the control and US groups. We discovered that UTMD induced NO generation through activation of endothelial NO synthase (eNOS) in vivo. More importantly, we also observed significantly increased NO content and eNOS expression in the NO + UTMD group compared to the UTMD group. NO + UTMD can mitigate oxidative stress and apoptosis in the hind limb muscle without influencing blood pressure or liver and kidney functions. In vitro, NO-MBs alleviated oxidative stress and apoptosis in cells pretreated with hypoxia.Conclusion: Based on these data, UTMD affects the vascular endothelium by activating eNOS, and NO exerts a protective effect against IRI.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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