scholarly journals α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Mariola Herbet ◽  
Magdalena Izdebska ◽  
Iwona Piątkowska-Chmiel ◽  
Monika Gawrońska-Grzywacz ◽  
Dorota Natorska-Chomicka ◽  
...  

Chronic exposure to stress factors contributes to the development of depression by generating excess of reactive oxygen species which leads to oxidative stress and inflammatory processes. The aim of the study was to assess the potential protective properties of α-tocopherol supplementation on the rats exposed to chronic variable stress (CVS). Male Wistar rats (50-55 days old, weighing 200-250 g) were divided into three groups (n=10): control, stressed, and stressed and receiving (+)-α-tocopherol solution in a dose of 100 mg/kg/day. Rats in the stressed groups were exposed to CVS for 40 days. Markers of redox disorders (glutathione reduced and oxidized levels, GSH/GSSG ratio, glutathione peroxidase, glutathione reductase activities, total antioxidant status, and lipid peroxidation) and inflammatory response (IL-1β, IL6, and TNF-α) were determined in the blood. Additionally, molecular biomarkers of depression (expression of Fkbp5 and Tph2) were studied in hippocampus. The biochemical analysis was inconclusive about the presence of oxidative stress in the blood of rats exposed to CVS. However, changes in all parameters suggest presence of redox equilibrium disorders. Similarly, activation of inflammatory processes was observed as a result of CVS. Molecular effects of environmental stress in hippocampus were also observed. Generally, α-tocopherol ameliorated redox equilibrium disorders, tempered inflammatory response, and protected from changes in determined molecular markers of depression.

Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.


2020 ◽  
Vol 245 (14) ◽  
pp. 1260-1267
Author(s):  
Sylwia Dzięgielewska-Gęsiak ◽  
Dorota Stołtny ◽  
Alicja Brożek ◽  
Małgorzata Muc-Wierzgoń ◽  
Ewa Wysocka

Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r =  0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.


2017 ◽  
Vol 68 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Mahmoud M. Said ◽  
Marwa M. Abd Rabo

AbstractAluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1protein) and 5-HT (2.13±0.27 ng mg-1tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1protein) and Casp-3 (3.80±0.37 ng mg-1protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.


2018 ◽  
Vol 16 (2) ◽  
Author(s):  
Caleb Shitsuka ◽  
Flávia Kazue Ibuki ◽  
Fernando Neves Nogueira ◽  
Fausto Medeiros Mendes ◽  
Marcelo Bönecker

ABSTRACT Objective To evaluate oxidative stress in saliva of children with dental erosion as compared to children with no erosion. Methods One single examiner, trained and prepared to make diagnosis of dental erosion according to the Basic Erosive Wear Examination index, selected 40 children aged 4 to 6 years, who attended a pediatric dentistry prevention clinic. Two groups were formed - one comprising children with dental erosion (n=22), and another with no dental erosion (n=18). The quantity of dental biofilm was verified using the Simplified Index of Oral Hygiene, and unstimulated saliva was collected for biochemical analyses. The following were assessed in saliva: flow rate, buffering capacity, pH, and total protein concentration. Malondialdehyde levels were also verified to determine oxidative stress and total antioxidant status. Results The quantity of biofilm was smaller in children with mean dental erosion±standard deviation (0.76±0.25), as compared to those with no dental erosion (1.18±0.28). There was no statistical difference in saliva parameters of oxidative stress in children with dental erosion. Conclusion The activity of oxidative stress in saliva did not influence dental erosion process when in its early stages.


Author(s):  
Nur Shafika Mohd Sairazi ◽  
K. N. S. Sirajudeen ◽  
Mustapha Muzaimi ◽  
Mummedy Swamy ◽  
Mohd Asnizam Asari ◽  
...  

Objective: The present study examined the protective effect of tualang honey (TH) against kainic acid (KA)-induced oxidative stress in the cerebellum and brainstem of rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups: Control, KA-treated, TH+KA-treated, and topiramate (TPM, an antiepileptic agent)+KA-treated groups. Rats were pretreated orally with drinking water, TH (1.0 g/kg body weight), or TPM (40 mg/kg body weight), respectively, five times at 12 h intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Oxidative stress markers were analyzed in different brain regions (cerebellum and brainstem) 2 h, 24 h, and 48 h after KA administration.Results: KA caused significant (p<0.05) elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production, impairment of glutathione system, and a significant reduction in the total antioxidant status in the rat cerebellum and brainstem at multiple time-points, as compared to control groups. Pretreatment with TH significantly (p<0.05) reduced the elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production and increasing a reduction in the total antioxidant status in the rat cerebellum and brainstem induced by KA at multiple time-points, as compared to KA only-treated group.Conclusion: Taken together, this study suggests that TH has therapeutic potential in reducing oxidative stress in the cerebellum and brainstem of KA-induced rats via its antioxidant property.


Author(s):  
Prafulla Chandra Tiwari ◽  
Mayank Jain ◽  
Shipra Kartik ◽  
Rajendra Nath ◽  
Rishi Pal

Background: Persistent up regulation of NF-&kappa;B leads to chronic inflammation and subsequent microglial activation and takes neurons towards death by activating death receptor domains and the p53 pathway. Thus, inhibition of NF-&kappa;B may lead to more effective treatment for Parkinson&rsquo;s disease. Therefore, we have used mangiferin, specific inhibitor of NF-&kappa;B in this study. Method: The study utilized male Wistar rats weighing 200-250 gm (n=8 in each group). Stereotactic surgery of rats was done to induce 6-OHDA lesioning in rats. On day 42, rats were subjected to behavioural studies to evaluate effect of mangiferin and their brains were taken out after euthanasia to perform biochemical and molecular studies. Results: Mangiferin significantly increases locomotor parameters in 6-OHDA lesioned rats. It also decreases activity of Cyclooxygenase enzyme which then leads to decrease concentration of inflammatory cytokines. Microglial inflammation was also substantially reduced by reducing MPO concentration. Oxidative stress burden was also reduced after treatment with mangiferin as indicated by increase in Total Antioxidant Capacity, SOD and Catalase and reduction in concentration of MDA. Treatment with mangiferin also reduces burden of oxidative stress by increasing the activity of NRF2/ARE pathway. Activity of Caspase 3 and 9 was also significantly reduced after treatment with mangiferin. Significant decrease in activity of both Cox1 and Cox 2 was also observed. Maximum improvement in all parameters was observed in rats treated with grouping of mangiferin 45mg.kg-1 and levodopa 10mg.kg-1. Treatment with levodopa alone has no significant effect on biochemical and molecular parameters though it significantly improves behavioural parameters. Conclusion and Implications: Results of this study suggest that mangiferin has protective effect in hemi-parkinsonian rats by inhibiting NF-&kappa;B. Current treatment of Parkinson&rsquo;s disease does not target the underlying problem of the disease. Therefore, combination therapy of mangiferin and levodopa can be helpful in better management of Parkison&rsquo;s.


Medicina ◽  
2019 ◽  
Vol 55 (5) ◽  
pp. 150 ◽  
Author(s):  
Marek Paździor ◽  
Małgorzata Kiełczykowska ◽  
Jacek Kurzepa ◽  
Dorota Luchowska-Kocot ◽  
Joanna Kocot ◽  
...  

Background and Objective: Osteoarthritis (OA) is a disorder of the musculoskeletal system resulting in worsening of life condition. The research revealed the involvement of oxidative stress into both OA pathogenesis and the effects of therapeutic agents applied in OA cases. The activities of the most important antioxidant enzymes, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and total antioxidant status (TAS), in blood of the knee OA patients were studied, with the aim of clarifying which enzymatic antioxidants are involved into osteoarthritis (OA)-related oxidative stress and whether any compensatory effects occur. The results were additionally analyzed with regard to gender. Methods: Whole blood SOD (U/mL), plasma GPx (U/L) and CAT (U/mL) activities as well as plasma TAS (mmol/L)) in knee OA patients were investigated. Sixty-seven patients (49 females and 18 males) with primary knee OA were enrolled. The control comprised 21 subjects (10 females and 11 males) free of osteoarthritis or inflammation. Results: TAS was decreased in OA subjects (4.39 ± 0.53 vs. 4.70 ± 0.60), with this effect being more significant in OA females (4.31 ± 0.51 vs. 5.02 ± 0.54). GPx was depressed in all OA patients (518 ± 176 vs. 675 ± 149). In both genders, GPx was decreased, significantly in males (482 ± 185 vs. 715 ± 105). SOD was decreased in all OA patients (109 ± 32 vs. 127 ± 42). CAT showed no difference in all OA subjects vs. control, while in OA females it was depleted (20.2 (11.6–31.6) vs. 38.5 (27.9–46.6)) and in OA men it increased (26.9 (23.3–46.5) vs. 14.0 (7.0–18.6)). Conclusions: The obtained results suggest that in men some compensatory mechanisms towards OA-related oxidative stress occurred. Based on the obtained data, the introduction of antioxidant supplements into OA therapy could be suggested with further research concerning the choice of agents.


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