• Journal of Animal Reproduction and Biotechnology
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• v.34 no.2
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• pp.86-92
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• 2019

The aim of this study was to investigate effects of hyaluronidase during IVM on oocyte maturation, oxidative stress status, expression of cumulus expansion-related (PTX, pentraxin; GJA1, gap junction protein alpha 1; PTGS2, prostaglandin-endoperoxide synthase 2) and fatty acid metabolism-related (FADS1, delta-6 desaturase; FADS2, delta-5 desaturase; PPARα, peroxisome proliferator-activated receptor-alpha) mRNA, and embryonic development of porcine oocytes. The cumulus-oocyte complexes (COCs) were incubated with 0.1 mg/mL hyaluronidase for 44 h. Cumulus expansion was measured at 22 h after maturation. At 44 h after maturation, nuclear maturation, intracellular glutathione (GSH) and reactive oxygen species (ROS) levels were measured. Gene expression in cumulus cells was analyzed using real time PCR. The cleavage rate and blastocyst formation were evaluated at Day 2 and 7 after insemination. In results, expansion of cumulus cells was suppressed by treatment of hyaluronidase at 22 h after maturation. Intracellular GSH level was reduced by hyaluronidase treatment (p < 0.05). On the other hand, hyaluronidase increased ROS levels in oocytes (p < 0.05). Only PTGS2 mRNA was enhanced in COCs by hyaluronidase (p < 0.05). Population of oocytes reached at metaphase II stage was higher in control group than hyaluronidase treated group (p < 0.05). Both of cleavage rate and blastocyst formation were higher in control group than hyaluronidase group (p < 0.05). Our present results showed that developmental competence of porcine oocytes could be reduce by hyaluronidase via inducing oxidative stress during maturation process and it might be associated with prostaglandin synthesis. Therefore, we suggest that suppression of cumulus expansion of COCs could induce oxidative stress and decrease nuclear maturation via reduction of GSH synthesis and it caused to decrease developmental competence of mammalian oocytes.

• The Journal of Korean Physical Therapy
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• v.22 no.6
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• pp.65-70
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• 2010

Purpose: Exercise has been shown to be a simple and economical therapeutic modality that may be considered as an effective aid for diabetic mellitus. For example, exercise training increases insulin sensitivity in type 2 diabetes. But we found no reported of how exercise affect type 1 diabetes. This study investigated the impact of aerobic and graduated treadmill exercise regimens on body weight, glucose and insulin concentrations, lipid profiles, and oxidative stress indicators in rats with streptozotocin (STZ) induced diabetes. Glycosylated hemoglobin ($HbA_{1c}$) was determined as an indicator of glucose control during exercise. Methods: In our study, a total of 40 rats were used. Three groups of 10 rats each were given STZ to induce diabetes. The remaining 10 rats became the normal group. After 28 days we determined biochemical parameters such as glucose, glycosylated hemoglobin ($HbA_{1c}$), insulin concentration, serum total cholesterol (TC), triglycerides (TG), and high-density lipoprotein (HDL). Superoxide dismutase (SOD) and catalase activities were also measured. Results: Concentrations of blood glucose and $HbA_{1c}$ in the moderated exercise groups were significantly decreased after 28 days compared with the control group (p<0.05). There was a significant reduction in serum TC and TG in the experimental groups. The activity of SOD increased significantly by 17.70% and 48.25% respectively. Conclusion: These results indicate that physical training and exercise training affects body weight, fasting blood glucose, $HbA_{1c}$, insulin, lipid profiles, and antioxidant status in rats with streptozotocin-induced diabetes. We suggest that graduated treadmill exercise may have therapeutic, preventative, and protective effects against diabetes mellitusby improving glycemic control, oxidant defenses, and lipid metabolism.

• Parasites, Hosts and Diseases
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• v.50 no.4
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• pp.375-377
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• 2012

Malaria is still a leading cause of morbidity and mortality. The increase in lipid peroxidation reported in malaria infection and antioxidant status may be a useful marker of oxidative stress during malaria infection. The aim of this study was to investigate the role of antioxidant enzymes against toxic reactive oxygen species in patients infected with Plasmodium vivax and healthy controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were determined in 91 P. vivax patients and compared with 52 controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were $8.07{\pm}2.29$ nM/ml, $2.69{\pm}0.33$ U/ml, and $49.6{\pm}3.2$ U/g Hb in the patient group and $2.72{\pm}0.50$ nM/ml, $3.71{\pm}0.47$ U/ml, and $62.3{\pm}4.3$ U/g Hb in the control group, respectively. Malondialdehyde levels were found statistically significant in patients with vivax malaria higher than in healthy controls (P<0.001). On the other hand, superoxide dismutase and glutathione peroxidase activities were found to be significantly lower in vivax malaria patients than in controls (P<0.05). There was an increase in oxidative stress in vivax malaria. The results suggested that antioxidant defense mechanisms may play an important role in the pathogenesis of P. vivax.

• Molecular & Cellular Toxicology
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• v.4 no.4
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• pp.360-365
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• 2008

In the last several years, studies on the association of oxidative stress damage with exposure in the work place have been conducted. Xenobiotics create an imbalance of the homeostasis between oxidant molecules and antioxidant defense. By monitoring oxidative stress biomarkers, information was obtained on damages induced by oxidative stress and the toxicity of xenobiotics. In the present study, a Job Exposure Matrix (JEM) was constructed using the data from the Working Environment Measurement (WEM) of painters in the shipyard industry from the past 3 years to assess the exposure status. Additionally, by measuring the concentration of urinary malondialdehyde (MDA), the effect of lipid peroxidation was examined. The subjects consisted of 68 workers who were exposed to mixed organic solvents in the painting process and 25 non-exposure controls. The exposure indices of the exposure groups were significantly different (sprayer: 0.83, touchup: 0.54, assistant: 0.13, P<0.05). The urinary MDA concentration of the exposure group was 48.60${\pm}$ 39.23 ${\mu}mol$/mol creatinine, which was significantly higher than 18.03${\pm}$16.33 ${\mu}mol$/mol creatinine of the control group (P<0.05). From the multiple regression analysis of urinary MDA, the regression coefficient for exposure grade was statistically significant. In future studies, evaluation of the antioxidant levels of subjects should be performed simultaneously with quantitative exposure measurements.

• Food Science and Biotechnology
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• v.16 no.6
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• pp.967-974
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• 2007

The present work is aimed to evaluate the protective effect of glutathione-enriched Saccharomyces cerevisiae FF-8 strain on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity and oxidative stress in rats. The activities of liver markers (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase), lipid peroxidative index (thiobarbituric acid-reactive substances), and the antioxidant status (reduced glutathione) were used to monitor those protective roles of FF-8 strain. The liver marker enzymes in plasma and the lipid peroxidation in the liver were increased when $CCl_4$ was treated but these were significantly decreased by FF-8 strain treatment. The hepatic concentration of glutathione in the current glutathione-enriched FF-8 strain fed animal was approximately twice as high as the normal, but this was slightly increased in response to $CCl_4$ plus glutathione-enriched FF-8 strain. The increased liver triglyceride concentration due to the $CCl_4$ treatment was significantly decreased by FF-8 strain and the reduced level reached to that of normal group. Administration of FF-8 strain in normal rat did not show any signs of harmful effects. Therefore, the current findings suggest that FF-8 strain could be an effective antioxidant with no or negligible side-effects and it might be useful for the purpose of protection treatment of hepatotoxicity and oxidative stress in $CCl_4$-treatment in rat.

• BMB Reports
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• v.38 no.3
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• pp.300-306
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• 2005

Tamoxifen citrate is an anti-estrogenic drug used for the treatment of breast cancer. It showed a degree of hepatic carcinogenesis, when it used for long term as it can decrease the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in liver rat cells leading to liver injury. In this study, a model of liver injury in female rats was done by intraperitoneal injection of tamoxifen in a dose of 45 mg/kg body weight for 7 successive days. This model produced a state of oxidative stress accompanied with liver injury as noticed by significant declines in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) in a dose of 200 mg/kg body weight daily for 10 successive days, resulted in alleviation of the oxidative stress status of tamoxifen-intoxicated liver injury in rats as observed by significant increments in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases; sGPT and sGOT levels. The administration of DDB before tamoxifen intoxication (as protection) is more little effective than its curative effect against tamoxifen-induced liver injury. The data obtained from this study speculated that DDB can mediate its biochemical effects through the enhancement of the antioxidant enzyme activities and reduced glutathione level as well as decreasing lipid peroxides.

• Preventive Nutrition and Food Science
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• v.19 no.1
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• pp.19-26
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• 2014

Increased consumption of fresh vegetables that are high in polyphenols has been associated with a reduced risk of oxidative stress-induced disease. The present study aimed to evaluate the antioxidant effects of spinach in vitro and in vivo in hyperlipidemic rats. For measurement of in vitro antioxidant activity, spinach was subjected to hot water extraction (WE) or ethanol extraction (EE) and examined for total polyphenol content (TPC), oxygen radical absorbance capacity (ORAC), cellular antioxidant activity (CAA), and antigenotoxic activity. The in vivo antioxidant activity of spinach was assessed using blood and liver lipid profiles and antioxidant status in rats fed a high fat-cholesterol diet (HFCD) for 6 weeks. The TPC of WE and EE were shown as $1.5{\pm}0.0$ and $0.5{\pm}0.0mg$ GAE/g, respectively. Increasing the concentration of the extracts resulted in increased ORAC value, CAA, and antigenotoxic activity for all extracts tested. HFCD-fed rats displayed hyperlipidemia and increased oxidative stress, as indicated by a significant rise in blood and liver lipid profiles, an increase in plasma conjugated diene concentration, an increase in liver thiobarbituric acid reactive substances (TBARS) level, and a significant decrease in manganese superoxide dismutase (Mn-SOD) activity compared with rats fed normal diet. However, administration of 5% spinach showed a beneficial effect in HFCD rats, as indicated by decreased liver TBARS level and DNA damage in leukocyte and increased plasma conjugated dienes and Mn-SOD activity. Thus, the antioxidant activity of spinach may be an effective way to ameliorate high fat and cholesterol diet-induced oxidative stress.

• Toxicological Research
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• v.35 no.1
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• pp.13-24
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• 2019

Numerous ethnomedicinal uses have been attributed to different parts of Annona senegalensis (ASE), including its uses as food and food additives. The present study investigated toxicological and antioxidant effects of 28 days administration of ethanol extracts of ASE stem bark to Wistar strain albino rats. Acute toxicity test was done to determine lethal dose in Wistar rats while sub-acute toxicity test was conducted on rats divided into four groups (A - control, B - 50 mg/kg, C - 100 mg/kg, D - 150 mg/kg, respectively and treated for 28 days. Oxidative stress markers in liver and kidney as well as hepatic succinate dehydrogenase activity in the mitochondrial and post mitochondrial fractions (PMF) were evaluated. The $LD_{50}$ value of ASE was > 2,000 mg/kg. White blood cell counts gradually increased, but red blood cell counts and haematocrits level decreased significantly (p < 0.05) by about 50%. Liver enzymes in the serum and mitochondrial succinate dehydrogenase activity increased significantly (p < 0.05). Superoxide dismutase and catalase activities also increased in liver mitochondria and PMF while malondialdehyde (MDA) and reduced glutathione levels increased only in the PMF. Furthermore, only MDA levels increased significantly in the kidney after 28 days extract administration. Histopathological examination showed hepatic necrosis and no obvious signs of nephrotoxicity. Anona senegalensis is relatively safe, but prolonged ingestion could induce oxidative stress and impair ATP synthesis through the modulation of the activity of mitochondrial succinate dehydrogenase.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.2
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• pp.131-137
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• 2021

Aging is the process spontaneously occurred in living organisms. Cardiac fibrosis is a pathophysiological process of cardiac aging. Mangiferin is a well-known C-glucoside xanthone in mango leaves with lots of beneficial properties. In this study, rat model of cardiac fibrosis was induced by injected with 150 mg/kg/d D-galactose for 8 weeks. The age-related cardiac decline was estimated by detecting the relative weight of heart, the serum levels of cardiac injury indicators and the expression of hypertrophic biomakers. Cardiac oxidative stress and local inflammation were measured by detecting the levels of malondialdehyde, enzymatic antioxidant status and proinflammatory cytokines. Cardiac fibrosis was evaluated by observing collagen deposition via masson and sirius red staining, as well as by examining the expression of extracellular matrix proteins via Western blot analysis. The cardiac activity of profibrotic TGF-β1/p38/MK2 signaling pathway was assessed by measuring the expression of TGF-β1 and the phosphorylation levels of p38 and MK2. It was observed that mangiferin ameliorated D-galactose-induced cardiac aging, attenuated cardiac oxidative stress, inflammation and fibrosis, as well as inhibited the activation of TGF-β1/p38/MK2 signaling pathway. These results showed that mangiferin could ameliorate cardiac fibrosis in D-galactose-induced aging rats possibly via inhibiting TGF-β/p38/MK2 signaling pathway.

• Clinical and Experimental Reproductive Medicine
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• v.49 no.4
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• pp.277-284
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• 2022

Objective: Oxidative stress is a key player in the development of idiopathic male infertility (IMI), and various antioxidants have been used for the treatment of IMI with inconsistent results. Coenzyme Q10 (CoQ10) is a cofactor and an antioxidant that may improve semen parameters and reduce oxidative stress in patients with idiopathic oligoasthenospermia (OA). Therefore, this study aimed to explore the effect of CoQ10 on semen parameters and antioxidant markers in patients with idiopathic OA. Methods: Fifty patients with idiopathic OA and 35 fertile controls were enrolled in this prospective controlled study. All participants underwent a comprehensive fertility assessment. All patients received CoQ10 (300 mg/day) orally once daily for 3 months. Semen parameters, seminal CoQ10 levels, reactive oxygen species (ROS) levels, total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were measured in patients and controls at the start of the study and after 3 months. Results: Treatment with CoQ10 resulted in increased sperm progressive motility (p<0.05), total motility (p<0.01), seminal TAC (p<0.01), SOD (p<0.05), GPx (p<0.001), and seminal CoQ10 (p<0.001) levels and reduced ROS (p<0.01) in patients as compared to baseline. Sperm concentration and motility were also significantly correlated with antioxidant measures and seminal CoQ10 levels (r=0.38-0.57). Conclusion: CoQ10 therapy (300 mg/day for 3 months) improved sperm motility and seminal antioxidant markers in patients with idiopathic OA. Therefore, CoQ10 could be a promising treatment for patients with idiopathic infertility and may improve their fertility potential.