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

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.

2020 ◽  
Vol 10 (01) ◽  
pp. e104-e109
Author(s):  
Antonio Molina-Carballo ◽  
Antonio Emilio Jerez-Calero ◽  
Antonio Muñoz-Hoyos

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.


2007 ◽  
Vol 26 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Emine Sutken ◽  
Erinc Aral ◽  
Filiz Ozdemir ◽  
Sema Uslu ◽  
Ozkan Alatas ◽  
...  

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.


2001 ◽  
Vol 20 (4) ◽  
pp. 199-203 ◽  
Author(s):  
B H Ali ◽  
H M Mousa

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.


1985 ◽  
Vol 1 (3) ◽  
pp. 249-251
Author(s):  
I. Kosugi ◽  
K. Tajimi ◽  
K. Okada

Reduced glytathione (GSH) is the tripeptide of glycine, cysteine and glutamic acid and is widely distributed in the body. FSH has been reported to comprise at least 90% of the nonprotein sulfhydryl (NPSH). Although the role of GSH in the tissue has not been clearly established, it is known to be a cofactor for enzymes, a substrate in detoxifications, and a free radical scavenger.Several investigators have reported that the level of NPSH, mainly GSH, in the tissue was decreased in several types of shock and that exogenous administration of GSH has beneficial effects on shock (1,2). This study was designed to evaluate the effects of GSH on the survival rate in mice and the hepatic energy metabolism in rats after administration of endotoxin. These results were compared with those of methylprednisolone sodium succinate (MP), since many investigators have reported that the large doses of glucocorticoid have beneficial effects in several types of shock in experimental animals and in man (3,4).


2009 ◽  
Vol 9 ◽  
pp. 109-117 ◽  
Author(s):  
Marina K. Abuladze ◽  
Victor M. Sokhadze ◽  
Emma N. Namchevadze ◽  
E. Kiziria ◽  
Leila V. Tabatadze ◽  
...  

Differential scanning calorimetry (DSC) was applied to estimate the impact of the toxic oxidant potassium permanganate (PM) on the intracellular structural and functional alterations at whole cell level using soil bacteriaArthrobacter oxydansas a model culture. Differential scanning calorimetry (DSC) was applied in order to estimate the impact of the toxic oxidant potassium permanganate (PM) on the intracellular structural and functional alterations at the whole cell level using the soil bacteria Arthrobacter oxydans as a model culture. We compared the total melting heat and the temperature of DNA-protein complex (DNP) melting at the PM application prior to the calorimetry measurement and after 24-h exposure at the concentration range 0.02–1.4 mM. The initial oxidative effect caused changes in the pattern of the whole cell melting spectra (mainly at the temperature range 56–78°C), the decrease of Tmax°C DNP melting, and did not influence significantly the total heat of bacterial melting at different concentrations of PM. The prolonged effect of permanganate up to 24 h was characterized by a biphasic dose-dependent response to stress estimated by the DSC technique and the colony-forming assay. The low doses of PM (0.02 and 0.2 mM) stimulated cell proliferation, and increased the total whole cell melting heat and the temperature of DNP melting. The toxic effect of PM up to 0.04 mMreduced cell viability, changed the character of multipeaked thermograms, and lowered the total melting heat and the temperature of DNP melting in a concentration-dependent manner. This study presents the DSC method for evaluating and monitoring the effects of exposure to potential human and environmental toxicants.


2018 ◽  
Vol 105 (3) ◽  
pp. 233-246 ◽  
Author(s):  
IC Chiş ◽  
D Baltaru ◽  
A Dumitrovici ◽  
A Coseriu ◽  
BC Radu ◽  
...  

Background Exposure to high altitude in hypobaric hypoxia (HH) is considered to be a physiological oxidative/nitrosative stress. Quercetin (Que) is an effective antioxidant and free radical scavenger against oxidative/nitrosative stress. Aims The aim of this study was to investigate the cardioprotective effects of Que in animals exposed to intermittent HH (IHH) and therefore exposed to oxidative/nitrosative stress. Materials and methods Wistar albino male rats were exposed to short-term (2 days) or long-term (4 weeks; 5 days/week) IHH in a hypobaric chamber (5,500 m, 8 h/day, 380 mmHg, 12% O2, and 88% N2). Half of the animals received natural antioxidant Que (body weight: 30 mg/kg) daily before each IHH exposure and the remaining rats received vehicle (carboxymethylcellulose solution). Control rats were kept under normobaric normoxia (Nx) and treated in a corresponding manner. One day after the last exposure to IHH, we measured the cardiac hypoxia-induced oxidative/nitrosative stress biomarkers: the malondialdehyde (MDA) level and protein carbonyl (PC) content, the activity of some antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)], the nitrite plus nitrate (NOx) production, and the inducible nitric oxide synthase (iNOS) protein expression. Results Heart tissue MDA and PC levels, NOx level, and iNOS expression of IHH-exposed rats had increased, and SOD and CAT activities had decreased compared with those of the Nx-exposed rats (control groups). MDA, CP, NOx, and iNOS levels had decreased in Que-treated IHH-exposed rats compared with IHH-exposed rats (control groups). However, Que administration increased SOD and CAT activities of the heart tissue in the IHH-exposed rats. Conclusion HH exposure increases oxidative/nitrosative stress in heart tissue and Que is an effective cardioprotective agent, which further supports the oxidative cardiac dysfunction induced by hypoxia.


Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska

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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