scholarly journals Protective effects of Celosia argentea Linn. Vitamin E and dexamethasone on radiation-induced damage on the developing rat cerebellum

2019 ◽  
Vol 8 (2) ◽  
pp. 1647-1661 ◽  
Author(s):  
Love Chioma Kanu ◽  
Olatunde Owoeye ◽  
Innocent Ohiorenuan Imosemi ◽  
Adelofolarin Obanishola Malomo
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Gamma Radiation ◽  
Rat Brain ◽  
Control Group ◽  
Rat Cerebellum ◽  
Group I ◽  
Celosia Argentea ◽  
Radiation Induced ◽  
Developing Rat

The potential neuroprotective effect of aqueous extract of Celosia argentea Linn (AECA), Vitamin E (Vit E) and Dexamethasone (Dexa) on radiation-induced damage on the developing rat cerebellum was studied. Forty-two female rats weighing between 147 g and 222 g were randomized into six groups (N=7). Control group – Group I, Irrad group – Group II, AECA group – Group III, AECA + Irrad group – Group IV, Vit E + Irrad group – Group V and Dexa+ Irrad group – Group VI. Rats were mated and pregnant rats were exposed to 2.5 Gy gamma radiation on gestation day 7. The administration of 400 mg/kg of AECA, 500 mg/kg of Vit E and 0.005 ml/rat of Dexa started from gestation day 1 till postnatal day 28. Postpartum, 5 pups from each group were exposed to behavioural and biochemical tests and then sacrificed. Brain tissue fixed in 10% formalin, processed by paraffin wax method was stained with H&E and Cresyl violet stains for histology. Radiation significantly (p<0.05) reduced gross, behavioural, histological and histomorphometric parameters, while eliciting oxidative stress relative to control group on post-natal days 7, 14, 21 and 28. Treatment with AECA, Vit E and Dexa with radiation significantly (p<0.05) reduced most of the alterations induced by radiation in the various parameters. This study confirmed development of oxidative stress in rat pups using single dose 2.5 Gy gamma-irradiation. The antioxidant properties of AECA and Vit E and the anti-inflammatory property of Dexa were able to mitigate the alterations in the developing rat brain parameters.Key words: Gamma-radiation, neuroprotective, plant products, rat brain.

scholarly journals THE EFFECT OF INTERMITTENT HYPOBARIC HYPOXIA ON OXIDATIVE STRESS STATUS AND ANTIOXIDANT ENZYMES ACTIVITY IN RAT BRAIN

2019 ◽  
Vol 1 (2) ◽  
pp. 46-51 ◽  
Author(s):  
Syarifah Dewi ◽  
Wawan Mulyawan ◽  
Septelia Inawati Wanandi ◽  
Mohamad Sadikin
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Antioxidant Enzyme ◽  
Hypobaric Hypoxia ◽  
Specific Activity ◽  
Barometric Pressure ◽  
Control Group ◽  
Exposure Group ◽  
Group I ◽  
Oxidative Stress Status

Background: High altitude can cause hypobaric hypoxia (HH), resulted from the lower barometric pressure and hence partial pressure of oxygen. Hypoxia can lead to a lot of deleterious molecular and cellular changes, such as generation of free radicals or reactive oxygen species (ROS). Increasing of ROS can cause oxidative stress if the antioxidant enzyme does not increase simultaneously. Oxidative damage in brain has toxic effect on cognitive functions.Objective: In this study, we investigate effect of acute intermittent HH on oxidative stress and antioxidant enzyme activity in rat brain.Method: Wistar rats divided into 5 groups, consisting control group and four experimental groups which treated to HH. Rats were exposed to simulated HH equivalent to 35.000 feet in hypobaric chamber for 1 minute, repeated once a week.Results: Level of malondialdehyde and carbonyl in rat brain under acute HH increased at HH exposure (group I) compare to control group. These levels decreased afterward at intermittent HH exposure (group II-IV). Specific activity of superoxide dismutase (SOD) shows increasing level at intermittent HH exposure, especially group IV was increasing of SOD level significantly. The increasing pattern of specific activity of catalase was inversely from SOD pattern, but it still has higher activity in intermittent HH compare to control group.Conclusion: Brain tissue seems to be able to perform an adequate adaptive response to hypobaric hypoxia after the training, shown by its significantly decreased MDA and carbonyl level and also increased specific activity of SOD and catalase.

Nephrotoxicity and its prevention by catechin in ferric nitrilotriacetate promoted oxidative stress in rats

2004 ◽  
Vol 23 (3) ◽  
pp. 137-143 ◽  
Author(s):  
Kanwaljit Chopra ◽  
Devinder Singh ◽  
Vikas Chander
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Renal Dysfunction ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Morphological Alterations ◽  
Group Iii ◽  
Ferric Nitrilotriacetate ◽  
Group I ◽  
Rats And Mice

Intraperitoneal injection of ferric nitrilotriacetate (Fe-NTA) to rats and mice results in iron-induced free radical injury and cancer in kidneys. This study was designed to investigate the effect of catechin, a bioflavonoid with antioxidant potential, on Fe-NTA-induced nephrotoxicity in rats. Four groups were employed in the present study. Group I served as control group, Group II animals received Fe-NTA (8 mg iron/kg body weight i.p.), Group III animals were given 40 mg/kg catechin p.o. twice a day for 4 days and on the 5th day Fe-NTA was challenged, and Group IV animals received catechin alone for 4 days. Renal function was assessed by measuring plasma creatinine and blood urea nitrogen. The oxidative stress was measured by renal malondialdehyde levels, reduced glutathione levels and by enzymatic activity of catalase, glutathione reductase and superoxide dismutase. One hour after a single intraperitoneal (i.p.) injection of Fe-NTA (8 mg iron/kg), a marked deterioration of renal architecture, renal function and severe oxidative stress was observed. Pretreatment of animals with catechin markedly attenuated renal dysfunction, reduced elevated thiobarbituric acid reacting substances (TBARS), restored the depleted renal antioxidant enzymes and normalized the renal morphological alterations. These results clearly demonstrate the role of oxidative stress and its relation to renal dysfunction, and suggest a protective effect of catechin on Fe-NTA-induced nephrotoxicity in rats.

Effects of Manganese (Mn) on the Developing Rat Brain: Oxidative-Stress Related Endpoints

2002 ◽  
Vol 23 (2) ◽  
pp. 169-175 ◽  
Author(s):  
Sarah Weber ◽  
David C. Dorman ◽  
Lawrence H. Lash ◽  
Keith Erikson ◽  
Kent E. Vrana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Brain Oxidative Stress ◽  
Developing Rat

scholarly journals Changes in oxidation-antioxidation function on the thymus of chickens infected with reticuloendotheliosis virus

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Dahan Yang ◽  
Chenhui Zhao ◽  
Meixi Zhang ◽  
Shujun Zhang ◽  
Jie Zhai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Control Group ◽  
Reticuloendotheliosis Virus ◽  
Antioxidative Function ◽  
Group I ◽  
Antioxidant Function ◽  
Thymus Atrophy ◽  
The Status ◽  
Specific Pathogen

Abstract Background Reticuloendotheliosis virus (REV) is a retrovirus that causes severe immunosuppression in poultry. Animals grow slowly under conditions of oxidative stress. In addition, long-term oxidative stress can impair immune function, as well as accelerate aging and death. This study aimed to elucidate the pathogenesis of REV from the perspective of changes in oxidative-antioxidative function following REV infection. Methods A total of 80 one-day-old specific pathogen free (SPF) chickens were randomly divided into a control group (Group C) and an REV-infected group (Group I). The chickens in Group I received intraperitoneal injections of REV with 104.62/0.1 mL TCID50. Thymus was collected on day 1, 3, 7, 14, 21, 28, 35, and 49 for histopathology and assessed the status of oxidative stress. Results In chickens infected with REV, the levels of H2O2 and MDA in the thymus increased, the levels of TAC, SOD, CAT, and GPx1 decreased, and there was a reduction in CAT and Gpx1 mRNA expression compared with the control group. The thymus index was also significantly reduced. Morphological analysis showed that REV infection caused an increase in the thymic reticular endothelial cells, inflammatory cell infiltration, mitochondrial swelling, and nuclear damage. Conclusions These results indicate that an increase in oxidative stress enhanced lipid peroxidation, markedly decreased antioxidant function, caused thymus atrophy, and immunosuppression in REV-infected chickens.

New and safe experimental model of radiation-induced neurovascular histological changes for microsurgical research

2016 ◽  
Vol 51 (2) ◽  
pp. 124-137
Author(s):  
Sergi Barrera-Ochoa ◽  
Irene Gallardo-Calero ◽  
Andrea Sallent ◽  
Alba López-Fernández ◽  
Ramona Vergés ◽  
...  
Keyword(s):  
Side Effects ◽  
Experimental Model ◽  
Experimental Studies ◽  
Neurovascular Bundle ◽  
Control Group ◽  
Sprague Dawley ◽  
Histological Changes ◽  
Group I ◽  
Radiation Induced

The aim is to create a new and safe experimental model of radiation-induced neurovascular histological changes with reduced morbidity and mortality for use with experimental microsurgical techniques. Seventy-two Sprague–Dawley rats (250–300 g) were divided as follows: Group I: control group, 24 rats clinically evaluated during six weeks; Group II: evaluation of acute side-effects (two-week follow-up period), 24 irradiated (20 Gy) rats; and Group III: evaluation of subacute side-effects (six-week follow-up period), 24 irradiated (20 Gy) rats. Variables included clinical assessments, weight, vascular permeability (arterial and venous), mortality and histological studies. No significant differences were observed between groups with respect to the variables studied. Significant differences were observed between groups I vs II–III regarding survival rates and histological changes to arteries, veins and nerves. Rat body weights showed progressive increases in all groups, and the mortality rate of the present model is 10.4% compared with 30–40% in the previous models. In conclusion, the designed model induces selective changes by radiotherapy in the neurovascular bundle without histological changes affecting the surrounding tissues. This model allows therapeutic experimental studies to be conducted, including the viability of microvascular and microneural sutures post radiotherapy in the cervical neurovascular bundle.

scholarly journals Sulforaphane-Mediated Nrf2 Activation Prevents Radiation-Induced Skin Injury through Inhibiting the Oxidative-Stress-Activated DNA Damage and NLRP3 Inflammasome

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1850
Author(s):  
Jinlong Wei ◽  
Qin Zhao ◽  
Yuyu Zhang ◽  
Weiyan Shi ◽  
Huanhuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Western Blotting ◽  
Nlrp3 Inflammasome ◽  
Fibrous Tissue ◽  
Mouse Skin ◽  
Control Group ◽  
Skin Injury ◽  
Antioxidant Genes ◽  
Radiation Induced

This article mainly observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI). In addition, we will discuss the mechanism of SFN’s protection on RISI. The RISI model was established by the irradiation of the left thigh under intravenous anesthesia. Thirty-two C57/BL6 mice were randomly divided into control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group. At eight weeks after irradiation, the morphological changes of mouse skin tissues were detected by H&E staining. Then, the oxidative stress and inflammatory response indexes in mouse skin tissues, as well as the expression of Nrf2 and its downstream antioxidant genes, were evaluated by ELISA, real-time PCR, and Western blotting. The H&E staining showed the hyperplasia of fibrous tissue in the mouse dermis and hypodermis of the IR group. Western blotting and ELISA results showed that the inflammasome of NLRP3, caspase-1, and IL-1β, as well as oxidative stress damage indicators ROS, 4-HNE, and 3-NT, in the skin tissues of mice in the IR group were significantly higher than those in the control group (p < 0.05). However, the above pathological changes declined sharply after SFN treatment (p < 0.05). In addition, the expressions of Nrf2 and its regulated antioxidant enzymes, including CAT and HO-1, were higher in the skin tissues of SFN and IR/SFN groups, but lower in the control and IR groups (p < 0.05). SFN may be able to suppress the oxidative stress by upregulating the expression and function of Nrf2, and subsequently inhibiting the activation of NLRP3 inflammasome and DNA damage, so as to prevent and alleviate the RISI.

scholarly journals Effects of Propolis Extract Supplementation during Pregnancy on Stress Oxidative and Pregnancy Outcome: Levels of Malondialdehyde, 8-Oxo-2′-Deoxogunosine, Maternal Body Weight, and Number of Fetuses

2021 ◽  
Vol 31 (3) ◽  
pp. 156
Author(s):  
Joko Wahyu Wibowo ◽  
Minidian Fasitasari ◽  
Siti Thomas Zulaikhah
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Pregnancy Outcomes ◽  
Feeding Tube ◽  
Control Group ◽  
Maternal Body ◽  
Control Group Design ◽  
Pregnant Rats ◽  
Propolis Extract ◽  
Group I

<p>Oxidative stress is related to pregnancy complications that could increase maternal and infant mortality. This study aimed to determine the effect of propolis extract supplementation during pregnancy on oxidative stress level and pregnancy outcomes utilizing Malonedealdehyde (MDA) and 8-Oxo-2′-Deoxogunosine (8-OHdG) levels, maternal body weight, and the average number of fetuses as the parameters. The study was conducted by using a posttest only control group design on 24 pregnant Wistar rats, which were divided into four groups. Group I was control, Group II-IV were the treatment groups given propolis extract of 1.8mg, 3.6mg, and 7.2mg/200gBW/day, respectively. The standard feed given was AIN93G dose of 20g/day and distilled water ad libitum. Propolis extract was given using a gastric feeding tube every morning for 20 days. At the end of the treatment, body weight was meisured and blood collected for assessed MDA and 8-OHdG levels  by ELISA method  and then we performed abdominal surgery to count number of fetuses. The result are there were decreasing level of MDA and 8-OHDG by administration of propolis significantly (p&lt;0.05) group: I: 2,04±0,091, II: 1,55±0,067, III: 1,05±0,176, IV: 0,73±0,075 (mmol/mL) (p=0.001); 8 OHdG level (ng/mL) group I: 10,02±0,403, II: 8,60±0,078, III: 7,89±0,051, IV: 7,53±0,063 (p=0,001). Average of maternal body weight (g) were increased: group I: 228,33±3,93, II: 237,17±4,36, III: 244,83±4,02, IV: 248,00±5,76 (p=0,001) and Average number of fetuses tend to increased as well, group I : 8,5±0,05, II: 7,8±0,41, III: 9,5±1,05, IV: 9,6±0,52 (p=0,02). The conclusion of this research are supplementation of propolis extract in pregnant rats can reduce oxidative stress and improve pregnancy outcomes.</p>

scholarly journals The effect of vitamin C on Endosulfan-induced oxidative stress parameters in prepubertal rats

Biomedicine ◽  
2020 ◽  
Vol 39 (2) ◽  
pp. 333-338
Author(s):  
Kalaivani Manokaran ◽  
Vasanthalaxmi Krishnananda Rao ◽  
Nilima . ◽  
Manjula Shimoga Durgoji Rao ◽  
Sucheta Prasanna Kumar
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Wistar Rats ◽  
Statistical Significance ◽  
Treated Group ◽  
Reproductive Organs ◽  
Protective Role ◽  
Control Group ◽  
Group I ◽  
Testicular Weight

Introduction and Aim: Oxidative stress plays a very important role in endosulfan-induced toxic effects on reproductive organs. Vitamin C is a potent antioxidant which plays an important role in decreasing oxidative stress. The present study was aimed to investigate the protective role of vitamin C against endosulfan-induced testicular toxicity in Wistar rats. To investigate a protective effect of vitamin C against endosulfan induced toxicity on biochemical changes. Materials and Methods: Seventy male neonatal Wistar rats were divided into  seven groups. The group  I was taken as the control group, the endosulfan-treated were grouped into II (3 mg/kg body weight (BW) and group III (6 mg/kg BW), Group IV (9 mg/kg BW) and Group V (12 mg/kg BW). Group VI (9 mg/kg BW) and group VII (12 mg/kg BW) were pretreated with vitamin C (20 mg/kg BW) for 60 days. After  the experimental procedures, the testicular weight, lactate dehydrogenase (LDH) enzyme and testosterone in plasma, LDH, steroidogenic enzymes 3?-HSD and 17?-HSD in testis were evaluated. One-way ANOVA was used to determine the statistical significance. Results: Significant improvement in the testicular weight (P<0.05) , LDH (P<0.05) levels both in plasma and testis, increase in testosterone(P<0.001) and steroidogenic enzyme levels(P<0.001) was observed in the group pretreated with vitamin C treated group when compared to the endosulfan treated group. Conclusion: Vitamin C decreases the toxic effect of endosulfan on testis. The present action might be  due to its antioxidative properties.

scholarly journals Hydroethanolic Extract of Defatted Buchholzia coriacea Seeds Alleviates Tamoxifen-Induced Hepatic Triglyceride Accumulation, Inflammation and Oxidative Distress in Rat

Medicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 1
Author(s):  
Ayokanmi Ore ◽  
Abideen Idowu Adeogun ◽  
Oluseyi Adeboye Akinloye
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Liver Injury ◽  
Hepatic Function ◽  
Protein Carbonyls ◽  
Control Group ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Group I ◽  
Hydroethanolic Extract

Background: Tamoxifen (TMX) has proven to be effective in the prevention and treatment of breast cancer. However, long-term use of TMX is associated with hepatic steatosis, oxidative liver injury and hepatocarcinoma. Buchholzia coriacea seeds (BCS) have been widely applied in traditional medicine due to their nutritional and therapeutic potentials. This study investigates the protective effect of hydroethanolic extract of (defatted) B. coriacea seeds (HEBCS) against TMX–induced hepatotoxicity in rats. Methods: Thirty-six (36) male albino rats were divided into six groups (n = 6/group). Group I served as control. Group II received 50 mg/kg/day TMX orally (p.o.) (TMX) for 21 days, group III received TMX plus 125 mg/kg/d HEBCS p.o. (HEBCS 125) for 21 days, group IV received TMX plus 250 mg/kg/d HEBCS p.o. (HEBCS 250) for 21 days and rats in group V and VI received HEBCS 125 and HEBCS 250 respectively for 21 days. Results: Compared with the control, TMX caused a significant increase (p < 0.05) in serum hepatic function biomarkers: alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase by 57%, 60% and 68% respectively. TMX also caused a significant increase in hepatic triglycerides level by 166% when compared with control and a significant decrease in serum HDL-cholesterol level by 37%. Compared with control, hepatic marker of inflammation, tumour necrosis factor alpha (TNF-α) increased significantly by 220%, coupled with significant increase in expression of interleukin 6 and cyclooxygenase 2. There was also significant increase in levels of Biomarkers of oxidative stress, nitric oxide, malondialdehyde and protein carbonyls in the TMX group by 89%, 175% and 114% respectively when compared with the control. Hepatic antioxidants, reduced glutathione (GSH) level and activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) decreased significantly in the TMX group by 35%, 67%, 41%, 59% and 53% respectively when compared with the control. However, HEBCS at 250 mg/kg significantly protected against TMX–induced hepatotoxicity by decreasing hepatic triglyceride content, serum hepatic function biomarkers, hepatic inflammation and oxidative stress with significant improvement in hepatic antioxidant system. Histopathological findings show that HEBCS alleviate TMX–induced hepatocyte ballooning. Conclusions: Current data suggest that HEBCS protected against TMX–induced hepatotoxicity in rats. HEBCS may be useful in managing TMX–induced toxicities in breast cancer patients. It may also be helpful against other forms of liver injury involving steatosis, inflammation, free radicals, and oxidative damage.

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