scholarly journals Effects of Safranal on Tissue Oxidative Stress in Sub-Chronic Thinner-Addicted Rats

2020 ◽  
Vol 71 (1) ◽  
pp. 1997
Author(s):  
M. DÜZ ◽  
A. F. FIDAN
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Total Antioxidant Capacity ◽  
Reduced Glutathione ◽  
Control Group ◽  
Albino Rats ◽  
Total Antioxidant ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

The present study was carried out to determine the effects of sub-chronic thinner addiction on the oxidant-antioxidant balance and oxidative stress on certain tissues and the possible protective effect of safranal against thinner toxication in rats. Adult male Wistar albino rats were randomly divided into four groups of 10 animals each as follows: control (C), safranal (S), thinner (T) and thinner+safranal (T+S). The control group received 1cc saline by gastric gavage. Safranal was administered to S and T+S groups by using gastric gavage at a dose of 100 mg/kg/day and volume of 0.1 mL/kg/day. Thinner inhalation was applied to T and T+S groups in a container with NaOH tablets twice a day. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NOx) metabolites, total antioxidant capacity (TAS) and total oxidant capacity (TOS) were determined in liver, lung, brain, kidney and testis tissues of the rats. In the T+S group, it was observed that the MDA levels significantly decreased in all tissues, except the kidney, in comparison to the thinner inhalation group (p = 0.000). When the NOx levels of the T+S group were compared with the levels of the T group, it was concluded that there existed a statistically significant decrease in the NOx levels in alltissues (p = 0.000). In T+S group, it was observed that safranal either eliminated or mitigated oxidative stress that developed in tissues through decreasing MDA and TOS levels and increasing GSH and TAS levels and caused significant decreases in NOX levels in all tissues. As a result, it was determined that safranal, although not uniform for all tissue types, had a protective potential against the damaging effects of oxidative stress caused by sub-chronic thinner inhalation.

scholarly journals Gebe Ratlara uygulanan Akrilamid ve E Vitaminin Plasenta Dokusu Üzerine Olası Etkilerinin Araştırılması

2017 ◽  
Vol 5 (4) ◽  
pp. 349
Author(s):  
Mehmet Erman Erdemli ◽  
Eyüp Altınöz ◽  
Zeynep Aksungur ◽  
Zümrüt Doğan ◽  
Harika Gözükara Bağ ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Total Antioxidant Capacity ◽  
Corn Oil ◽  
Reduced Glutathione ◽  
Control Group ◽  
Vaginal Smear ◽  
Protective Agent ◽  
Pregnant Rats ◽  
Total Antioxidant

Investigate the changes that occur in the placenta tissues of pregnant rats that were administered acrylamide (AA) and vitamin E as a protective agent during pregnancy. Thirty rats that were proven positive for pregnancy with vaginal smear test were randomly distributed into control, corn oil, vitamin E, acrylamide and vitamin E + acrylamide groups. Pregnant rats were decapitated on the 20th day of the experiment. Malondialdehyde (MDA), reduced glutathione (GSH), total antioxidant capacity (TAS), total oxidant capacity (TOS) and Xanthine oxidase (XO) levels were measured in placenta tissues. It was determined that acrylamide application during pregnancy statistically significantly increased MDA, TOS and XO levels and reduced GSH and TAS levels in the placenta tissue of pregnant rats when compared to all other groups, and GAS and TAS levels statistically significantly increased in vitamin E administered group when compared to all other groups and TOS and XO levels were decreased to control group levels. It was observed that orally administered AA changed the antioxidant / oxidant equilibrium favoring the oxidants by increasing MDA, XO and TOS levels in pregnant rats and caused oxidative stress, while vitamin E administration returned the antioxidant / oxidant equilibrium back to normal levels, preventing oxidative stress induced toxicity.

scholarly journals Carvacrol attenuates cyclophosphamide-induced oxidative stress in rat kidney

2017 ◽  
Vol 95 (7) ◽  
pp. 844-849 ◽  
Author(s):  
Sibel Gunes ◽  
Adnan Ayhanci ◽  
Varol Sahinturk ◽  
Diler Us Altay ◽  
Ruhi Uyar
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Tissue Damage ◽  
Total Antioxidant Capacity ◽  
Rat Kidney ◽  
Control Group ◽  
Antioxidative Effect ◽  
Total Antioxidant ◽  
And Oxidative Stress

Cyclophosphamide (CP) is an antineoplastic drug that induces kidney damage via producing oxidative stress. Carvacrol (CAR) has antioxidative effect and we postulated that it can be protective against CP-induced nephrotoxicity. Six groups (n = 7) of rats (control, 100 mg/kg CP, CP+5 mg/kg CAR, CP+10 mg/kg CAR, 5 mg/kg CAR, and 10 mg/kg CAR) were injected intraperitoneally. Serum malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), creatinine (CRE), total antioxidant capacity (TAC), and total oxidant state (TOS) were measured, and oxidative stress indexes (OSI) were calculated. Kidneys were also analyzed histologically. In CP-alone group MDA, CRE, TOS, and OSI levels increased whereas GSH, SOD, CAT, and TAC levels decreased compared with control group. In CP plus CAR groups, MDA, TOS, and OSI levels decreased whereas GSH, SOD, CAT, and TAC levels increased compared with CP-alone group. However, CRE levels were similar in CP-alone and CP+5 CAR group whereas decreased in CP+10 CAR group. CP+10 CAR group was significantly different in all parameters (except TAC) from CP+5 CAR group. Kidney microscopy was showed lower tissue damage in CP plus CAR groups. In conclusion, 10 mg/kg CAR is more effective than 5 mg/kg CAR in prevention of CP-induced oxidative damage on kidney.

scholarly journals Effects of Thymoquinone on Sperm Parameters, Apoptosis, Testosterone Level, and Oxidative Stress in a Mouse Model of D-Galactose-Induced Aging

2018 ◽  
Vol 24 (3) ◽  
pp. 180-186 ◽  
Author(s):  
Seyedeh Saleheh Attari ◽  
Shabnam Mohammadi ◽  
Alireza Ebrahimzadeh ◽  
Hossein Hosseinzadeh ◽  
Mohammad Soukhtanloo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Antioxidant Capacity ◽  
Testosterone Level ◽  
Total Antioxidant Capacity ◽  
Sperm Parameters ◽  
Control Group ◽  
Significant Difference ◽  
Total Antioxidant ◽  
And Oxidative Stress

Background: The aging process is accompanied by low secretion of sex hormones and testicular apoptosis. The antioxidant properties of thymoquinone (TQ) may prevent the effects of aging. Therefore, in the present study, the effects of different doses of TQ were investigated on sperm parameters, testosterone level, apoptosis, and oxidative stress in a mouse model of D-galactose-induced aging. Methods: In this experimental study, 30 adult male mice were randomly divided into 5 groups. The control group did not receive any injections, while the D-galactose group received an intraperitoneal injection of 300 mg/kg of D-galactose for 42 days. The TQ1-TQ3 groups received intraperitoneal injections of 5, 2.5, and 1.25 mg/kg of TQ plus D-galactose, respectively for 14 days (from the 1st to the 14th day of the experiment). The morphometric analysis, testicular apoptosis examination, and sperm analysis were performed, and testosterone level, total antioxidant capacity, and malondialdehyde level were evaluated on day 42 of the experiment. Data were analyzed using SPSS. Results: Administration of TQ in the TQ1 group caused a significant difference in sperm parameters, compared to the D-galactose group (P<0.05). The lowest amount of positive tunnel cells was related to 5 mg/kg of TQ and the highest to 2.5 mg/kg of TQ. There was no significant difference in the parameters of seminal vesicles, epididymis, prostate, and testis between the groups (P>0.05). The malondialdehyde level were decreased in the TQ1-TQ3 groups, compared to the D-galactose group (P<0.001). On the other hand, the total antioxidant capacity was increased significantly in the TQ1 group, compared to the D-galactose group (P<0.001). Conclusion: Administration of 5 mg of TQ for 14 days improved sperm quality and biochemical parameters, while reducing apoptotic cells of the testes in a mouse model of aging.

Evaluation of Salivary Antioxidants and Oxidative Stress Markers in Male Smokers

2019 ◽  
Vol 22 (7) ◽  
pp. 496-501
Author(s):  
Fatemeh Ahmadi-Motamayel ◽  
Parisa Falsafi ◽  
Hamidreza Abolsamadi ◽  
Mohammad T. Goodarzi ◽  
Jalal Poorolajal
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Cigarette Smoke ◽  
Total Antioxidant Capacity ◽  
The Body ◽  
Total Antioxidant ◽  
The Mean ◽  
And Oxidative Stress

Background: Cigarette smoke free radicals can cause cellular damage and different diseases. All the body fluids have antioxidants which protect against free radicals. Objective: The aim of this study was to evaluate salivary total antioxidant capacity and peroxidase, uric acid and malondialdehyde levels in smokers and a nonsmoking control group. Methods: Unstimulated saliva was collected from 510 males. A total of 259 subjects were current smokers and 251 were non-smokers. The levels of salivary total antioxidant capacity, uric acid, peroxidase and malondialdehyde were measured using standard procedures. Data were analyzed with t test and ANOVA. Results: The smokers were younger and dental hygiene index was higher than healthy nonsmoking controls. The mean total antioxidant capacity in smokers and nonsmokers was 0.13±0.07 and 0.21±011, respectively (P=0.001). Smokers had significantly lower peroxidase and uric acid levels than healthy controls. In addition, the mean malondialdehyde levels in the smokers and nonsmokers were 4.55 ±2.61 and 2.79 ±2.21, respectively (P=0.001). Conclusion: Cigarette smoke produces free radical and oxidative stress, causing many side effects. Salivary antioxidant levels decreased and malondialdehyde levels increased in smokers, indicating the high oxidative stress among smokers compared to nonsmokers. Cigarette smoke had deleterious effects on main salivary antioxidants levels.

scholarly journals NF-κB and FosB mediate inflammation and oxidative stress in the blast lung injury of rats exposed to shock waves

2021 ◽  
Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Shock Waves ◽  
Time Dependent ◽  
Inflammatory Factors ◽  
Control Group ◽  
Dependent Manner ◽  
Total Antioxidant ◽  
Blast Lung Injury ◽  
And Oxidative Stress

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P&lt;0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.

The Association between Oxidative Stress and Cardiac Functions in Infants Born to Preeclamptic Mothers

2018 ◽  
Vol 36 (11) ◽  
pp. 1205-1210
Author(s):  
Didem Arman ◽  
Secil Ercin ◽  
Sevilay Topcuoğlu ◽  
Ayşem Kaya ◽  
Taner Yavuz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Premature Infants ◽  
Stress Index ◽  
Control Group ◽  
Cardiac Functions ◽  
Total Antioxidant ◽  
Echocardiographic Parameters ◽  
Oxidant Status ◽  
The Relationship ◽  
And Oxidative Stress

Objective The present study aimed to assess the global oxidant and antioxidant status in infants born to preeclamptic mothers and their correlation with cardiac functions. Study Design We compared 40 infants born to preeclamptic mothers with 40 premature infants born to normotensive mothers. We assessed the relationship between echocardiographic measurements and total antioxidant capacity (TAC) and total oxidant status (TOS) values. Results In the study group, TAC, TOS, and oxidative stress index (OSI) levels were significantly higher in the cord blood (p = 0.03, 0.04, and 0.039, respectively) than in the control group. We did not observe any correlation between echocardiographic measurements and TAC, TOS, and OSI levels in infants born to preeclamptic mothers. Conclusion Compared with the control group, despite higher TAC levels in infants born to preeclamptic mothers, concurrent elevated OSI levels reveal that the oxidant–antioxidant balance is disturbed in favor of oxidants. Furthermore, the findings of this study suggest that echocardiographic parameters are unaffected by the oxidant status.

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyclosporin A ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Protective Mechanism ◽  
Antioxidant Parameters ◽  
Group 2 ◽  
Wistar Albino Rats

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

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