Redox and apoptotic potential of novel ruthenium complexes in the rat blood and heart

2020 ◽  
Author(s):  
Katarina Mihajlovic ◽  
Isidora Milosavljevic ◽  
Jovana Jeremic ◽  
Maja Savic ◽  
Jasmina Sretenovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Ruthenium Complexes ◽  
Redox Status ◽  
Heart Tissue ◽  
Control Group ◽  
Albino Rats ◽  
Oxidative Stress Biomarkers ◽  
Tissue Samples ◽  
Relative Expression

Ruthenium(II) complexes offer the potential for lower toxicity compared to platinum(II) complexes. Our study aimed to compare cardiotoxicity of [Ru(Cl-tpy)(en)Cl][Cl], [Ru(Cl-tpy)(dach)Cl][Cl], [Ru(Cl-tpy)(bpy)Cl][Cl], cisplatin and saline through assessment of redox status and relative expression of apoptosis-related genes. A total of 40 Wistar albino rats were divided into five groups. Ruthenium groups received intraperitoneally single dose of complexes (4 mg/kg/week) for 4-weeks period; cisplatin group received cisplatin (4 mg/kg/week) and control group received saline (4 mL/kg/week) in the same manner as ruthenium groups. In collected blood and heart tissue samples, spectrophotometrically determination of oxidative stress biomarkers was performed. The relative expression of apoptosis-related genes (Bcl-2, Bax, and caspase-3) in hearts was examined by RT-PCR. Our results showed that systemic and cardiac pro-oxidative markers (TBARS and NO2-) were significantly lower in ruthenium groups compared to cisplatin group, while concentrations of antioxidative parameters (CAT, SOD, and GSSG) were significantly higher. Ruthenium administration led to significantly lower gene expression of Bax and caspase-3 compared to cisplatin-treated rats, while Bcl-2 remained unchanged. Applied ruthenium complexes have less pronounced potential for induction of oxidative stress-mediated cardiotoxicity compared to cisplatin. These findings may help for future studies that should clarify the mechanisms of cardiotoxicity of ruthenium-based metallodrugs.

scholarly journals The Antioxidant Effect of Curcumin and Rutin on Oxidative Stress Biomarkers in Experimentally Induced Periodontitis in Hyperglycemic Wistar Rats

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1332
Author(s):  
Gilda M. Iova ◽  
Horia Calniceanu ◽  
Adelina Popa ◽  
Camelia A. Szuhanek ◽  
Olivia Marcu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Diabetic Rats ◽  
Gingival Tissue ◽  
Control Group ◽  
Albino Rats ◽  
Oxidative Stress Biomarkers ◽  
Significant Difference ◽  
The Impact ◽  
Experimentally Induced

Background: There is a growing interest in the correlation between antioxidants and periodontal disease. In this study, we aimed to investigate the effect of oxidative stress and the impact of two antioxidants, curcumin and rutin, respectively, in the etiopathology of experimentally induced periodontitis in diabetic rats. Methods: Fifty Wistar albino rats were randomly divided into five groups and were induced with diabetes mellitus and periodontitis: (1) (CONTROL)—control group, (2) (DPP)—experimentally induced diabetes mellitus and periodontitis, (3) (DPC)—experimentally induced diabetes mellitus and periodontitis treated with curcumin (C), (4) (DPR)—experimentally induced diabetes mellitus and periodontitis treated with rutin (R) and (5) (DPCR)—experimentally induced diabetes mellitus and periodontitis treated with C and R. We evaluated malondialdehyde (MDA) as a biomarker of oxidative stress and reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG and catalase (CAT) as biomarkers of the antioxidant capacity in blood harvested from the animals we tested. The MDA levels and CAT activities were also evaluated in the gingival tissue. Results: The control group effect was statistically significantly different from any other groups, regardless of whether or not the treatment was applied. There was also a significant difference between the untreated group and the three treatment groups for variables MDA, GSH, GSSG, GSH/GSSG and CAT. There was no significant difference in the mean effect for the MDA, GSH, GSSG, GSH/GSSG and CAT variables in the treated groups of rats with curcumin, rutin and the combination of curcumin and rutin. Conclusions: The oral administration of curcumin and rutin, single or combined, could reduce the oxidative stress and enhance the antioxidant status in hyperglycemic periodontitis rats.

Hexagonal boron nitride nanoparticles trigger oxidative stress by modulating thiol/disulfide homeostasis

2021 ◽  
pp. 096032712110028
Author(s):  
F Kar ◽  
İ Söğüt ◽  
C Hacıoğlu ◽  
Y Göncü ◽  
H Şenturk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Boron Nitride ◽  
Hexagonal Boron Nitride ◽  
Chemical Properties ◽  
Heart Tissue ◽  
Albino Rats ◽  
Dependent Manner ◽  
Tissue Samples ◽  
Boron Nitride Nanoparticles

Background: Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP’s dosage and biochemical mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN NPs for the first time. Methods: hBN NPs at concentrations varying between 50–3200 µg/kg was administered by intravenous injection to Wistar albino rats (n = 80) divided into seven dosage and control groups. Blood and tissue samples were taken after 24 hours. Results: Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dose-dependently. However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically. Conclusion: The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by modulating thiol/disulfide homeostasis in rats at higher concentrations

Pregabalin Ameliorates Lipopolysaccharide-Induced Pancreatic Inflammation in Aged Rats

2019 ◽  
Vol 19 (8) ◽  
pp. 1141-1147 ◽  
Author(s):  
Ozlem Ozmen ◽  
Senay Topsakal
Keyword(s):  
Caspase 3 ◽  
Pancreatic Tissue ◽  
Control Group ◽  
Albino Rats ◽  
Histopathological Analysis ◽  
Aged Rats ◽  
Tissue Samples ◽  
Glucose Levels ◽  
Amyloid A ◽  
Group I

Objective: The aim of this study was to examine pancreatic pathology and the prophylactic effects of pregabalin in lipopolysaccharide (LPS) induced sepsis model in aged rats. Methods: Twenty-four female, one-year-old, Wistar Albino rats were assigned to three groups; Group I (control), Group II (study group: 5mg/kg LPS intraperitoneal, single dose) and Group III(treatment group: 5mg/kg LPS+30 mg/kg oral pregabalin one hour before LPS). Animals were sacrificed by exsanguination 6 hours after LPS administration. Blood and pancreatic tissue samples were collected for biochemical, pathological, and immunohistochemical analyses. Results: LPS caused increases in serum amylase and lipase level but led to a reduction in glucose levels. Following histopathological analysis, numerous neutrophil leucocyte infiltrations were observed in vessels and pancreatic tissues. Increased caspase-3 expression was observed in both the endocrine and exocrine pancreas in the LPS group. Similarly, IL-6, caspase-3 (Cas-3), inducible nitric oxide synthase (iNOS), granulocyte colony-stimulating factor (G-CSF) and serum amyloid-A (SAA) expressions were increased by LPS. Pregabalin improved biochemical, histopathological, and immunohistochemical findings. Conclusion: This study showed that LPS causes pathological findings in the pancreas, but pregabalin has ameliorative effects in aged rats with sepsis. Cas-3, IL-6, iNOS, G-CSF, and SAA all play pivotal roles in the pathogenesis of LPS-induced pancreatic damage.

scholarly journals EXPRESSION OF APELIN IS RELATED TO OXIDATIVE DAMAGE IN HEART TISSUE OF RATS DURING CHRONIC SYSTEMIC HYPOXIA

2019 ◽  
Vol 1 (2) ◽  
pp. 68-75
Author(s):  
H R Helmi ◽  
Frans Ferdinal ◽  
Ani Retno Prijanti ◽  
Sri Widia A Jusman ◽  
Frans D Suyatna
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Heart Tissue ◽  
Male Rats ◽  
Heart Weight ◽  
Control Group ◽  
Sprague Dawley ◽  
Relative Expression ◽  
Beneficial Effects ◽  
Systemic Hypoxia

Background: Chronic systemic hypoxia is severe environmental stress for the heart and might lead to the development of heart failure. Apelin is an endogenous peptide that has been shown to have various beneficial effects on cardiac function. Apelin appears to have a role to play in the ventricular dysfunction and maintaining the performance of the heart.Objectives: In the present study we want to investigate the adaptive response of heart tissue to chronic systemic hypoxia and the correlation with apelin expression and oxidative stress in rat. Methods: An experimental study was performed using 28 Sprague-Dawley male rats, 8 weeks of age. Rats were divided into 7 groups 4 each, namely control group; normoxia (O2 atmosphere) and the treatment group of hypoxia (8% O2) for 6 hours; 1;3;5;7 and 14 days respectively. Body weight and heart weight were measured at each treatment. Ventricular thickness was measured by caliper, Apelin mRNA was measured using real-time qRT-PCR with Livak formula and malondialdehyde (MDA) level was used to assess oxidative stress due to cardiac tissue hypoxia.Results: Macroscopic exams showed hypertrophy at day 7th. The relative expression of Apelin mRNA in hypoxic heart is decreased at the beginning and then increased, starting from day-7 to day-14. The MDA levels were significantly increased from day-7 and were strongly correlated with relative expression Apelin.Conclusion:  It is concluded that the increase of Apelin expression is related to oxidative stress in heart tissue of rats during chronic systemic hypoxia.

In vivo effects of intravenous lipid emulsion on lung tissue in an experimental model of acute malathion intoxication

2018 ◽  
Vol 34 (2) ◽  
pp. 110-118 ◽  
Author(s):  
Murat Uysal ◽  
Serhat Karaman
Keyword(s):  
Oxidative Stress ◽  
Lung Tissue ◽  
Lipid Emulsion ◽  
Caspase 3 ◽  
Control Group ◽  
Albino Rats ◽  
Sod Activity ◽  
Expression Levels ◽  
Intravenous Lipid Emulsion ◽  
Group I

Malathion can be ingested, inhaled, or absorbed through the skin, but acute toxicity is maximized when administered orally. Intravenous lipid emulsion (ILE) treatment is used as a new therapeutic method in cases of systemic toxicity caused by some lipid soluble agents. This study aimed to examine the potential treatment effect of ILE on rat lung tissue in a toxicokinetic model of malathion exposure. Twenty-one adult Wistar albino rats were randomly divided into three equal groups. The groups were organized as group I (control), group II (malathion), and group III (malathion + ILE treatment). Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were evaluated in lung tissues. Immunohistochemical and Western blot analyses were performed to determine the bax, bcl-2, and caspase-3 expression levels. Tissue GSH-Px and SOD activities were decreased and MDA levels were increased in the malathion group. ILE administration increased GSH-Px and SOD activity and decreased MDA levels compared to the malathion group. Furthermore, expression of bax, bcl-2, and caspase-3 significantly increased in the malathion group, and ILE infusion reduced these expression levels. The present study revealed that acute oral malathion administration increased oxidative stress and apoptosis in the lung tissue of rats. ILE infusion prevented oxidative stress and decreased the deleterious effects of malathion. Taken together, the findings of our study suggest that lipid emulsion infusion has treatment efficacy on malathion-induced lung toxicity.

scholarly journals Lipopolysaccharide Prompts Oxidative Stress and Apoptosis in Rats’ Testicular Tissue

2018 ◽  
Vol 1 (3) ◽  
pp. 20-31 ◽  
Author(s):  
Amal A Halawa ◽  
Mohamed A El-Adl ◽  
Mohamed F Hamed ◽  
Ahmed Z Balboula ◽  
Mohammed A Elmetwally
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Caspase 3 ◽  
Reproductive Toxicity ◽  
Testicular Tissue ◽  
Seminiferous Tubules ◽  
Control Group ◽  
Albino Rats ◽  
Histopathological Analysis ◽  
Total Antioxidant

Lipopolysaccharide (LPS) is a component of the outer membrane of gram negative bacteria. LPS challenging allows switching transcription of proinflammatory cytokines on via over stimulation of Toll-like receptors (TLRs) signaling pathway with subsequent pathogenic inflammatory response. We investigated the possible reproductive toxicity of LPS in male Wister albino rats. Oxidative stress markers, antioxidant status and caspase-3 activity were analyzed in testicular tissues of rats exposed to either saline or LPS (4 mg/kg BW, ip; 0.18 of the LD50). The samples were collected at 6 h and 72 h after injection of LPS. A significant reduction in testicular reduced glutathione (GSH), glutathione-S-transferase (GST) and superoxide dismutase (SOD) was observed at 72 h compared to control group. Total antioxidant capacity was decreased at 6 h with additional significant reduction at 72 h. Catalase activity was reduced significantly at both 6 and 72 h. Malondialdehyde (MDA) was increased (P ≤ 0.05) in LPS injected rats without variation between 6 and 72 h. A significant increase in nitric oxide (NO) was observed at 72 h after injection. A time-dependent increase in LPS-treated groups was observed in the concentration of caspase-3.Histopathological analysis revealed degenerative changes and necrosis of seminiferous tubules after 6 h with further accumulation of eosinophilic edematous transudate in its lumen after 72 h. In conclusion, by increasing time of exposure, LPS induced lipid peroxidation, oxidative stress, reduced testicular antioxidant capacity and encouraged testicular apoptosis which could be possible mechanisms for impairment of testicular function.

scholarly journals Effect of N-acetylcysteine on pulmonary cell death in a controlled hemorrhagic shock model in rats

2012 ◽  
Vol 27 (8) ◽  
pp. 561-565 ◽  
Author(s):  
Paulo Fernandes Saad ◽  
Karen Ruggeri Saad ◽  
Luiz Dantas de Oliveira Filho ◽  
Sueli Gomes Ferreira ◽  
Marcia Kiyomi Koike ◽  
...  
Keyword(s):  
Cell Death ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Caspase 3 ◽  
Control Group ◽  
Albino Rats ◽  
Shock Model ◽  
Tissue Samples ◽  
Ringer’S Lactate ◽  
Hemorrhagic Shock Model

PURPOSE: To evaluate the effect of N-acetylcysteine (NAC) combined with fluid resuscitation on pulmonary cell death in rats induced with controlled hemorrhagic shock (HS). METHODS: Two arteries (MAP calculation and exsanguination) and one vein (treatments) were catheterized in 22 anesthetized rats. Two groups of male albino rats were induced with controlled HS at 35mmHg MAP for 60 min. After this period, the RL group was resuscitated with Ringer's lactate and the RL+NAC group was resuscitated with Ringer's lactate combined with 150mg/Kg NAC. The control group animals were cannulated only. The animals were euthanized after 120 min of fluid resuscitation. Lung tissue samples were collected to evaluate the following: histopathology, TUNEL and imunohistochemical expression of caspase 3. RESULTS: RL showed a greater number of cells stained by TUNEL than RL + NAC, but there was no change in caspase 3 expression in any group. CONCLUSION: N-acetylcysteine associate to fluid resuscitation, after hemorrhagic shock, decreased cell death attenuating lung injury.

Influence of eugenol on oxidative stress biomarkers in the liver of carrageenan-induced arthritis rats

2018 ◽  
Vol 30 (2) ◽  
pp. 185-193 ◽  
Author(s):  
Stephen Adeniyi Adefegha ◽  
Sunday I. Oyeleye ◽  
Bathlomew M. Okeke ◽  
Ganiyu Oboh
Keyword(s):  
Oxidative Stress ◽  
Control Group ◽  
Albino Rats ◽  
Spontaneous Movement ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Reduced Body ◽  
Behavioral Studies ◽  
Group I ◽  
Elevated Lipid

Abstract Background Eugenol is the foremost constituent of clove oil and widely distributed in many plants. It possesses many pharmaceutical applications, including antioxidant, anti-inflammatory, and anti-tumorigenic properties, among others. This study evaluates the influence of eugenol on oxidative stress biomarkers in the liver of carrageenan-induced arthritis (CIA) rats. Methods Sixty albino rats were randomly divided into 10 (n=6) groups. Group I is the control group that received saline solution orally. Groups II and VII rats received 2.5 mg/kg of eugenol orally (EUG-2.5). Rats in groups III/VIII and IV/IX received 5 and 10 mg/kg of eugenol orally (EUG-5 and EUG-10), respectively. Groups V and X received 0.2 mg/kg of dexamethasone (DEX-0.2) orally. Groups VI to X were injected with 1% carrageenan intra-articularly. Behavioral studies were conducted after 21 days of treatment. Thereafter, the animals were sacrificed, and the livers were isolated and used for biochemical analysis. Results Reduced body weight in arthritic rats was recorded compared to normal controls. Reduced tibiofemoral joint edema and increased spontaneous movement were observed in CIA rats with decreased superoxide dismutase, catalase, reduced glutathione (GSH), glutathione peroxidase, and GSH S-transferase activities compared with the normal control group. Increased endogenous enzyme activities and decreased elevated lipid peroxidation were also observed after eugenol treatment. Conclusion Eugenol ameliorates carrageenan-induced oxidative stress in the liver of arthritic rats.

scholarly journals Effects of mesenchymal stem cell and amnion membrane transfer on prevention of pericardial adhesions

2020 ◽  
Vol 45 (4) ◽  
pp. 405-414
Author(s):  
Mehmet Kabalci ◽  
Mustafa Sahin ◽  
Zeynep Pekcan ◽  
Mehmet Zengin ◽  
Mehmet Tolga Dogru ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Postoperative Adhesion ◽  
Control Group ◽  
Albino Rats ◽  
Tissue Samples ◽  
Positive Effects ◽  
Membrane Transfer ◽  
Amnion Membrane ◽  
Wistar Albino Rats ◽  
Pericardial Adhesions

AbstractBackgroundTo investigate and compare the antiadhesive/antifibrotic effects of mesenchymal stem cells (MSC) and amnion membrane transfer (AMT) in a rat model.Material and methodsThree experimental and sham groups were formed using 30 Wistar-Albino rats. AMT and MSC were applied to the related groups. The control group was not treated. After 12 weeks follow-up, intracardiac blood and cardiac-pericardiac tissue samples were taken. The severity of adhesions and fibrosis were scored macroscopically and microscopically with Hematoxylin/Eosin and Masson’s trichrome staining. TNF-α, TGF-β, IL-1, PDGF, FGF, VEGF and Caspase-3 levels were measured with the ELISA method.ResultsSevere adhesions were observed in the AMT and control groups, but no adhesion was present in the MSC group. Pericardial thickness, increased vascularity, fibrosis, and collagen accumulation were similar between control and AMT groups, but were less in Sham and MSC groups. Between MSC and AMT groups, only Caspase-3 level was different, which is an apoptosis marker.ConclusionThe positive effects of MSC on adhesion, which we achieved in our study, suggest that it may prevent adhesion. AMT did not provide a positive effect. The correlation of Caspase-3 with postoperative adhesion/fibrosis should be examined in more detail.

Antioxidant enzyme activities and lipid peroxidation products in heart tissue of subacute and subchronic formaldehyde-exposed rats: a preliminary study

2006 ◽  
Vol 22 (3) ◽  
pp. 117-124 ◽  
Author(s):  
Mukaddes Güleç ◽  
Ahmet Songur ◽  
Semsettin Sahin ◽  
Oguz A Ozen ◽  
Mustafa Sarsilmaz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Heart Tissue ◽  
Cardiac Cells ◽  
Control Group ◽  
Albino Rats ◽  
Antioxidant Enzyme Activities ◽  
Tbars Level ◽  
Control Groups ◽  
Sod Activity

Objective: The aim of this experimental study was to evaluate the oxidant/antioxidant status and lipid peroxidation in the heart of rats exposed to formaldehyde (FA) inhalation for four weeks (subacute) or 13 weeks (subchronic) continuously. Methods and results: Sixty Wistar albino rats were divided into six groups randomly (ten in each group). The first and second groups were used as subacute and subchronic control groups. FA gas was generated from paraformaldehyde and pumped to a closed glass chamber. Rats were exposed to atmosphere containing 10 and 20 ppm FA (8 h/day, five days per week) during a four and 13 weeks period. After heart tissues were obtained and homogenized, thiobarbituric acid-reactant substances (TBARS) and nitric oxide (NO) levels, as well as superoxide dismutase (SOD) and catalase (CAT) activities, were measured. There were statistically significant findings in SOD and CAT activities in the study groups compared to the control group. Heart tissue SOD level was increased in the group exposed to subacute 10 and 20 ppm FA inhalation compared to the control group (P≤0.011 and ≤0.0001). In addition, heart tissue SOD level was increased in the group exposed to subchronic 10 and 20 ppm FA inhalation compared to the corresponding control group (P≤0.001). On the other hand, there were statistically significant decreases in CAT activity in subacute 10 and 20 ppm groups compared to the corresponding control group (P≤0.012 and ≤0.039, respectively). Although not significant, TBARS levels were increased in both subacute 10 ppm (P=0.100) and subchronic 20 ppm (P=0.053) groups compared to their corresponding control groups. Tissue NO levels were unchanged upon FA inhalation. In the correlation analyses, a meaningful relationship between SOD and CAT activities in subchronic 10 ppm group (r=-0.685, P≤0.029); SOD activity and TBARS level in subchronic 20 ppm group (r=-0.675, P≤0.032); and CAT activity and NO level in subchronic 20 ppm group (r=-0.810, P≤0.005) were found. Conclusion: From the findings of our study, it can be interpreted that subacute and subchronic FA inhalation may stimulate oxidative stress and thus, some secondary toxic effects in cardiac cells and tissue. This increase in the oxidative stress could not induce lipid peroxidation in the membranous structure of cardiac cells. An increased SOD enzyme activity was thought to be secondary to decreased CAT activity, as a compensation mechanism, preventing heart tissue from destruction induced by FA.

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