Effect of dimethyl sulfoxide on gentamicin-induced nephrotoxicity in rats

2001 ◽  
Vol 20 (4) ◽  
pp. 199-203 ◽  
Author(s):  
B H Ali ◽  
H M Mousa
Keyword(s):  
Dimethyl Sulfoxide ◽  
Thiobarbituric Acid ◽  
Hepatic Function ◽  
Protective Role ◽  
Free Radical Scavenger ◽  
Kidney Cortex ◽  
Radical Scavenger ◽  
Tbars Level ◽  
Sod Activity ◽  
Plasma Urea

Nephrotoxicity of gentamicin (GM) has been suggested to be mediated by the generation of reduced oxygen metabolites. The present study investigated the possible protective role of the free radical scavenger dimethyl sulfoxide (DMSO) on some indices of GM nephrotoxicity in rats. The antibiotic was injected intramuscularly (i.m.) at a dose of loo mg/kg for six consecutive days, either with or without treatment with DMSO (12.5%, 25% or 50% in saline) at an intraperitoneal (i.p.) dose of 2 ml/kg 4 days before GM, and concomitantly with GM treatment thereafter. DMSO (25% in saline) was also given as above to rats treated with GM at i.m. doses of 25, 50 or 100 mg/kg for six consecutive days. GM caused dose-dependent significant increases in the concentrations of urea and creatinine in plasma, and in thiobarbituric acid reactive substances (TBARS) level in the kidney cortex and also caused significant decreases in the concentrations of reduced glutathione (GSH) and superoxide dismutase (SOD) activity. In GM-treated rats, DMSO dose-dependently lowered the elevated plasma urea and creatinine concentrations, and the rise in cortical TBARS. It also restored the levels of GSH and SOD activity to near normal. DMSO (25%) was effective in completely preventing the development of signs of nephrotoxicity of G (50 mg/kg). Treatment of the rats with DMSO alone, at any of the above doses, did not alter significantly any of the renal or hepatic function tests studied, and did not appear to adversely affect the kidney or liver histology. However, the efficacy and safety of DMSO require further studies. It is suggested that DMSO has potential protective effect against GM nephrotoxicity in rats.

scholarly journals Possible Protective Role of Melatonin in Pediatric Infectious Diseases and Neurodevelopmental Pathologies

2020 ◽  
Vol 10 (01) ◽  
pp. e104-e109
Author(s):  
Antonio Molina-Carballo ◽  
Antonio Emilio Jerez-Calero ◽  
Antonio Muñoz-Hoyos
Keyword(s):  
Endothelial Cell ◽  
Free Radical ◽  
Chronic Administration ◽  
Protective Role ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Energetic Metabolism ◽  
Beneficial Effects ◽  
Molecular Crosstalk

AbstractMelatonin, produced in every cell that possesses mitochondria, acts as an endogenous free radical scavenger, and improves energetic metabolism and immune function, by complex molecular crosstalk with other intracellular compounds. There is greatly increasing evidence regarding beneficial effects of acute and chronic administration of high melatonin doses, in infectious, developmental, and degenerative pathologies, as an endothelial cell and every cell protectant.

scholarly journals Naringenin Release to Biomembrane Models by Incorporation into Nanoparticles. Experimental Evidence Using Differential Scanning Calorimetry

Surfaces ◽  
2021 ◽  
Vol 4 (4) ◽  
pp. 295-305
Author(s):  
Cristina Torrisi ◽  
Marco Di Guardia ◽  
Francesco Castelli ◽  
Maria Grazia Sarpietro
Keyword(s):  
Differential Scanning Calorimetry ◽  
Heart Tissue ◽  
Protective Role ◽  
Delivery Systems ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Drug Bioavailability ◽  
Cell Level ◽  
Scanning Calorimetry ◽  
Beneficial Effects

Naringenin (4′,5,7-trihydroxyflavanone-7-rhamnoglucosideor naringenin-7-rhamnoglucoside), a flavonoid present in large quantities in citrus, has different beneficial effects on human health as an antioxidant, free radical scavenger, anti-inflammatory, carbohydrate metabolism promoter, and immune system modulator. Different studies have shown that this substance also has a hypoglycemic and antihypertensive effect, reduces cholesterol and triglycerides, and plays an important protective role in the heart tissue; moreover, it provides neuroprotection against various neurological disorders such as Parkinson’s disease and unpredictable chronic stress-induced depression. Despite these advantages, Naringenin is poorly absorbed, and the small percentage absorbed is rapidly degraded by the liver, as a result losing its activity. Several approaches have been attempted to overcome these obstacles, among them, nanotechnology, with the use of Drug Delivery Systems (DDS) as Solid Lipid Nanoparticles (SLN) and Nanostructured Lipid Carriers (NLC). DDS can, in fact, improve the drug bioavailability. The aim of this study was to develop and characterize SLN and NLC containing Naringenin and to evaluate the ability of these nanoparticles to release Naringenin at the cell level using biomembrane models represented by Multilamellar Vesicles (MLV). These studies were performed using Differential Scanning Calorimetry, a powerful technique to detect the interaction of drugs and delivery systems with MLV. It was shown that Naringenin could be better incorporated into NLC with respect to SLN and that Naringenin could be released by NLC into the biomembrane model. Therefore, suggesting the administration of Naringenin loaded into nanoparticles could help avoid the disadvantages associated with the use of the free molecule.

Protective Role of Melatonin and Coenzyme Q10 in Ochratoxin A Toxicity in Rat Liver and Kidney

2007 ◽  
Vol 26 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Emine Sutken ◽  
Erinc Aral ◽  
Filiz Ozdemir ◽  
Sema Uslu ◽  
Ozkan Alatas ◽  
...  
Keyword(s):  
Protective Effect ◽  
Ochratoxin A ◽  
Coenzyme Q ◽  
Kidney Tissue ◽  
Treated Group ◽  
Protective Role ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Liver And Kidney

Melatonin (MEL) and coenzyme Q10 (CoQ10) both display antioxidant and free radical scavenger properties. In the present study, the effect of MEL and CoQ10 on the oxidative stress and fibrosis induced by ochratoxin A (OTA) administration in rats was investigated. Rats were divided into five equal groups, each consisting of seven rats: (1) controls; (2) OTA-treated rats (289 μg/kg/day); (3) OTA+MEL–treated rats (289 μg/kg/day OTA + 10 mg/kg/day MEL); and (4) OTA+CoQ10–treated rats (289 μg/kg/day OTA +1 mg/100 g/day body weight (bw) CoQ10). After 4 weeks of treatment, the level of malondialdehyde (MDA), glutathione peroxidase (GPx), and hydroxyproline (Hyp) were measured in the homogenates of liver and kidney. In the OTA-treated group, the levels of MDA and Hyp in both liver and kidney were significantly increased when compared with the levels of control, whereas GPx activities decreased. In OTA+MEL–treated rats, the levels of MDA and Hyp in both liver and kidney were significantly decreased when compared with the levels of OTA-treated rats; however; GPX activities increased. In the OTA+CoQ10–treated group, the levels of MDA and Hyp were decreased when compared with the levels of OTA-treated rats, whereas GPx activities increased. In the OTA+CoQ 10–treated group, the levels of MDA, Hyp, and GPx were not significantly changed in kidney when compared with OTA-treated group. MEL has a protective effect against OTA toxicity through an inhibition of the oxidative damage and fibrosis both liver and kidney. Although CoQ10 has protective effect against OTA toxicity in liver tissue, it has no effect in kidney tissue.

Enalapril and captopril enhance antioxidant defenses in mouse tissues

1997 ◽  
Vol 272 (2) ◽  
pp. R514-R518 ◽  
Author(s):  
E. M. de Cavanagh ◽  
C. G. Fraga ◽  
L. Ferder ◽  
F. Inserra
Keyword(s):  
Antioxidant Defenses ◽  
Heart Weight ◽  
Kidney Cortex ◽  
Radical Scavenger ◽  
Sod Activity ◽  
Kidney Medulla ◽  
Radical Scavenger Activity ◽  
Mouse Tissues ◽  
Scavenger Activity ◽  
Captopril Treatment

This study was conducted to investigate a possible systemic effect of angiotensin-converting enzyme inhibitors (ACEi) on tissue antioxidant defenses. CF1 mice (4-mo-old females) were administered either water (control) or water containing enalapril (20 mg/l) or captopril (50 mg/l) during 11 wk. Neither enalapril nor captopril treatment had an effect on body mass or brain, kidney, or heart weight relative to controls. CuZn-superoxide dismutase (SOD) activity was increased by enalapril treatment in kidney medulla (27%), heart (24%), and erythrocytes (19%) and by captopril treatment in kidney medulla (43%) and heart (54%) relative to controls. Mn-SOD and catalase activities were unaffected by either treatment. Enalapril, but not captopril treatment, increased Se-glutathione peroxidase activity in renal medulla (19%). Nonenzymatic antioxidant defenses, evaluated by tert-butyl hydroperoxide-initiated chemiluminescence (HICL), were enhanced in kidney cortex (48%) by enalapril and in brain by enalapril (44%) or captopril (36%) treatment relative to controls. As evaluated in vitro by HICL and thiobarbituric acid-reactive substances formation, captopril had a free radical scavenger activity, whereas neither enalapril nor lisinopril was effective. These results suggest that ACEi may protect tissues from oxidative damage by increasing enzymatic and nonenzymatic antioxidant defenses.

scholarly journals Mitigation of cisplatin induced nephrotoxicity by casticin in male albino rats

2023 ◽  
Vol 83 ◽  
Author(s):  
N. Ehsan ◽  
M. U. Ijaz ◽  
A. Ashraf ◽  
S. Sarwar ◽  
A. Samad ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Free Radical Scavenger ◽  
Control Group ◽  
Albino Rats ◽  
Radical Scavenger ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Group 2 ◽  
Kidney Injury Molecule 1

Abstract Cisplatin (CP) is a commonly used, powerful antineoplastic drug, having numerous side effects. Casticin (CAS) is considered as a free radical scavenger and a potent antioxidant. The present research was planned to assess the curative potential of CAS on CP persuaded renal injury in male albino rats. Twenty four male albino rats were distributed into four equal groups. Group-1 was considered as a control group. Animals of Group-2 were injected with 5mg/kg of CP intraperitoneally. Group-3 was co-treated with CAS (50mg/kg) orally and injection of CP (5mg/kg). Group-4 was treated with CAS (50mg/kg) orally throughout the experiment. CP administration substantially reduced the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione S-transferase (GST), glutathione reductase (GSR), glutathione (GSH) content while increased thiobarbituric acid reactive substances (TBARS), and hydrogen peroxide (H2O2) levels. Urea, urinary creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, albumin and creatinine clearance was significantly reduced in CP treated group. The results demonstrated that CP significantly increased the inflammation indicators including nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity and histopathological damages. However, the administration of CAS displayed a palliative effect against CP-generated renal toxicity and recovered all parameters by bringing them to a normal level. These results revealed that the CAS is an effective compound having the curative potential to counter the CP-induced renal damage.

scholarly journals S-allyl Cysteine, a Garlic Compound, Produces an Antidepressant-Like Effect and Exhibits Antioxidant Properties in Mice

2020 ◽  
Vol 10 (9) ◽  
pp. 592
Author(s):  
Elizabeth Ruiz-Sánchez ◽  
José Pedraza-Chaverri ◽  
Omar N. Medina-Campos ◽  
Perla D. Maldonado ◽  
Patricia Rojas
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Forced Swim Test ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Antidepressant Effect ◽  
Radical Scavenger ◽  
Oxidative Stress Markers ◽  
Sod Activity ◽  
Stress Markers

Depression is a psychiatric disorder, and oxidative stress is a significant mechanism of damage in this mood disorder. It is characterized by an enhancement of oxidative stress markers and low concentrations of endogenous antioxidants, or antioxidants enzymes. This suggests that antioxidants could have an antidepressant effect. S-allyl cysteine (SAC) is a compound with antioxidant action or free radical scavenger capacity. The purpose of the current research was to evaluate the antidepressant-like effect as well as the antioxidant role of SAC on a preclinical test, using the Porsolt forced swim test (FST). SAC (30, 70, 120, or 250 mg/kg, ip) was administered to male BALB/c mice daily for 17 days, followed by the FST at day 18. Oxidative stress markers (reactive oxygen species, superoxide production, lipid peroxidation, and antioxidant enzymes activities) were analyzed in the midbrain, prefrontal cortex, and hippocampus. SAC (120 mg/kg) attenuated the immobility scores (44%) in the FST, and protection was unrelated to changes in locomotor activity. This antidepressant-like effect was related to decreased oxidative stress, as indicated by lipid peroxidation and manganese-superoxide dismutase (Mn-SOD) activity in the hippocampus. SAC exerts an antidepressant-like effect that correlated, in part, with preventing oxidative damage in hippocampus.

scholarly journals Oxidant-Antioxidant Balance in the Blood of Patients with Chronic Obstructive Pulmonary Disease After Smoking Cessation

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Alina Woźniak ◽  
Dariusz Górecki ◽  
Michał Szpinda ◽  
Celestyna Mila-Kierzenkowska ◽  
Bartosz Woźniak
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Smoking Cessation ◽  
Pulmonary Disease ◽  
Thiobarbituric Acid ◽  
Chronic Obstructive ◽  
Study Group ◽  
Tbars Level ◽  
Sod Activity ◽  
Obstructive Pulmonary Disease

The effect of smoking cessation on the oxidative stress in patients with chronic obstructive pulmonary disease (COPD) was assessed. We recruited 73 smokers with COPD (study group), whose blood was analysed before smoking cessation, after the 1st, 2nd, and 3rd months of abstinence, 35 healthy nonsmokers (Control I), and 35 smokers with COPD (Control II). Blood was taken once in Control I and 4 times (every month) in Control II. In the study group conjugated dienes (CDs) level in plasma and erythrocytes before smoking cessation was 3 and 6.5 times higher than in Control I, respectively (P<0.001), while thiobarbituric acid-reactive substances (TBARS) level was 89% (P<0.001) and 51% higher (P<0.01), respectively. Superoxide dismutase (SOD) activity was 40% higher (P<0.05) while glutathione peroxidase (GPx) was 41% lower (P<0.001) than in Control I. In Control II, the similar differences as compared to Control I were observed throughout the study. Smoking cessation resulted in decrease of CDs, TBARS, and SOD and GPx increase, with no changes in catalase and vitamins A and E. COPD is accompanied by oxidative stress. A three-month tobacco abstinence facilitated restoring the oxidant-antioxidant balance systemically, but it did not affect spirometric parameters.

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

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