Protective effects of erdosteine on rotenone-induced oxidant injury in liver tissue

2004 ◽  
Vol 20 (6-10) ◽  
pp. 141-147 ◽  
Author(s):  
Alpaslan Terzi ◽  
Mustafa Iraz ◽  
Semsettin Sahin ◽  
Atilla Ilhan ◽  
Nuri Idiz ◽  
...  

Rotenone, an insecticide of botanical origin, causes toxicity through inhibition of complex I of the respiratory chain in mitochondria. This study was undertaken to determine whether rotenone-induced liver oxidant injury is prevented by erdosteine, a mucolytic agent showing antioxidant properties. There were four groups of Male Wistar Albino rats: group one was untreated as control; the other groups were treated with erdosteine (50 mg/kg per day, orally), rotenone (2.5 mg/mL once and 1 mL/kg per day for 60 days, i.p.) or rotenone plus erdosteine, respectively. Rotenone treatment without erdosteine increased xanthine oxidase (XO) enzyme activity and also increased lipid peroxidation in liver tissue P < 0.05). The rats treated with rotenone plus erdosteine produced a significant decrease in lipid peroxidation and XO activities in comparison with rotenone group PB / 0.05). Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group PB / 0.05). There was no significant difference in nitric oxide (NO) level between groups. There were negative correlations between CAT activity and malondialdehyde (MDA) level (r= -0.934, P <0.05) with between CAT and SOD activities (r= -0.714, P <0.05), and a positive correlation between SOD activity and MDA level (r= 0.828, P <0.05) in rotenone group. In the rotenone plus erdosteine group, there was a negative correlation between XO activity and NO level in liver tissue (r= -0.833, P -0.05). In the light of these findings, erdosteine may be a protective agent for rotenone-induced liver oxidative injury in rats.

Author(s):  
B. A. Mba ◽  
C. S. Alisi ◽  
A. C. Ene

Aim: The aim of this study is to evaluate the antioxidant properties and protective effects of aqueous anti-ulcer drug (AQAUD) against aspirin-induced gastric ulcer in albino rats. Methods: In this study, 30 male albino rats were divided into 5 groups of 6 each. Rats in group I served as normal control and received food and water. Animals in group II received food and water in addition to aspirin (400 mg/kg.b.wt) orally on the 14th day. Rats in groups III, IV and V received “AQAUD” (250 mg/kg.b.wt), (500 mg/kg.b.wt) and Omeprazole (20 mg/kg.b.wt) respectively for 14 days and aspirin (400 mg/kg.b.wt) orally on the 14th day. In vitro antioxidant property of “AQAUD” was assessed by its nitric oxide and hydroxyl radicals scavenging properties. The ulcer protective effect of “AQAUD” was assessed by determining the free and total acidity, ulcer index and % protection in the stomach content. The antioxidant potential in animals was evaluated by determining the concentrations of malondialdehyde and reduced glutathione. Superoxide dismutase and catalase activities were assayed in the stomach homogenates to further assess antioxidant potential. Total phenolics and flavonoid compounds were quantified to know the antioxidant content. Histopathological assessment of the gastric mucosa was used to assess the protective potentials of “AQAUD”. Data were analyzed using Statistical Package for Social Science (SPSS) version 21. Results: The results revealed that free acidity and ulcer indexes were significantly (p<0.05) reduced by “AQAUD”. There was a significant decrease in SOD activity of the stomach homogenates when compared to the aspirin group, with values for “AQAUD” 250 mg/kg.b.wt and “AQAUD” 500 mg/kg b.wt as 37.24±5.39ux10-2/mg protein and 23.64±2.91ux10-2/mg protein respectively. Result of acute toxicity testing showed that “AQAUD” is generally safe up to 5000 mg/kg b.wt. Conclusion: The results revealed that treatment with aspirin caused loss of gland architecture with erosion of epithelial layer, but AQAUD treatment ameliorated the effect of aspirin administration. The study revealed that “AQAUD” has considerable antioxidant potentials and can effectively protect against gastric ulcers.


2018 ◽  
Vol 103 (5-6) ◽  
pp. 260-269
Author(s):  
Yasemin Burcu Ustun ◽  
Cengiz Kaya ◽  
Ersin Koksal ◽  
Yunus Atalay ◽  
Ziya Yilmaz ◽  
...  

Objective: Hepatic ischemia and reperfusion (IR) injury is the most important cause of cellular death and hepatic dysfunction following liver transplantation and resection. Our aim in this study is to reveal the early stage effects of thyroid hormone levels on hepatic IR injury that effectively act on cellular homeostasis. Methods: Forty-six male Wistar albino rats were divided into 6 groups as follows: euthyroid-sham (n = 8), euthyroid with IR injury (n = 8), hyperthyroid-sham (n = 7), hyperthyroid with IR injury (n = 7), hypothyroid-sham (n = 8), and hypothyroid with IR injury (n = 8). After 90 minutes of partial hepatic ischemia, 90 minutes of reperfusion was applied. Liver tissue malondialdehyde (MDA) levels, catalase (CAT), glutathion peroxidase, and superoxide dismutase (SOD) enzyme activities were measured. Hepatic tissue was immunohistochemically analyzed. Results: MDA levels of liver tissue were analyzed, and hepatic MDA levels in the hyper-IR group were found to be significantly lower (P = 0.002) than those of the hypo-IR and euthyroid-IR groups. Serum CAT levels did not differ between control groups, whereas CAT values in the hyper-IR group were detected to be significantly lower than in the euthyroid-IR and hypothyroid-IR groups (P = 0.003). However, levels of SOD and glutathione peroxidase (GPX) were not affected by the functional state of the thyroid. No statistically significant difference was seen in the results of the histopathologic evaluation and immunohistochemical staining of the liver tissue. Conclusion: The administration of thyroid hormone within a short time before IR injury may have protective effects.


2016 ◽  
Vol 94 (3) ◽  
pp. 278-286 ◽  
Author(s):  
Dalia H. El-Kashef ◽  
Asmaa E. El-Kenawi ◽  
Mona Abdel Rahim ◽  
Ghada M. Suddek ◽  
Hatem A. Salem

The present study was designed to explore the possible protective effects of agmatine, a known nitric oxide (NO) synthase inhibitor, against gentamicin-induced nephrotoxicity in rats. For this purpose, we quantitatively evaluated gentamicin-induced renal structural and functional alterations using histopathological and biochemical approaches. Furthermore, the effect of agmatine on gentamicin-induced hypersensitivity of urinary bladder rings to acetylcholine (ACh) was evaluated. Twenty-four male Wistar albino rats were randomly divided into 3 groups, namely control, gentamicin (100 mg/kg, i.p.), and gentamicin plus agmatine (40 mg/kg, orally). At the end of the study, all rats were sacrificed and then blood and urine samples and kidneys were taken. Administration of agmatine significantly decreased kidney/body mass ratio, serum creatinine, lactate dehydrogenase (LDH), renal malondialdehyde (MDA), myeloperoxidase (MPO), NO, and tumor necrosis factor-alpha (TNF-α) while it significantly increased creatinine clearance and renal superoxide dismutase (SOD) activity when compared with the gentamicin-treated group. Additionally, agmatine ameliorated tissue morphology as evidenced by histological evaluation and reduced the responses of isolated bladder rings to ACh. Our study indicates that agmatine administration with gentamicin attenuates oxidative-stress associated renal injury by reducing oxygen free radicals and lipid peroxidation, restoring NO level and inhibiting inflammatory mediators such as TNF-α.


2015 ◽  
Vol 3 (1) ◽  
pp. 41-47
Author(s):  
Nirjala Laxmi Madhikarmi ◽  
Kora Rudraiah Siddalinga Murthy

INTRODUCTION: The present study evaluated the modulatory effects of diphenylhydrazine induced experimental wistar albino rats and also to assess various biochemical parameters in whole blood and red blood cell lysate.MATERIALAND METHODS: Twenty male albino rats weighing 180-200 gm were selected for the study and divided in two groups; ten phenylhydrazine dihydrochloride (PHZ) induced anemia and ten healthy control. Thiobarbituric acid reactive substances and lipid hydroperoxide were measured as lipid peroxidation parameter. The antioxidant vitamins A, C and E and enzymatic antioxidants; catalase, glutathione peroxidase and superoxide dismutase were also assessed.RESULTS: Phenylhydrazine induced anemic rats showed a significant increase in the lipid peroxidation and decrease in the antioxidants as compared to healthy rats.CONCLUSION: The study concludes that phenylhydrazine induced experimental anemic albino rats showed increased oxidative stress than compared with healthy albino rats.Journal of Universal College of Medical Sciences Vol. 3, No. 1, 2015: 41-47 


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Kannappan Poornima ◽  
Palanisamy Chella Perumal ◽  
Velliyur Kanniappan Gopalakrishnan

This study is an attempt to evaluate the hepatoprotective activity ofTabernaemontana divaricataagainst DEN and Fe NTA induced liver necrosis in rats. Ethanolic extract of the whole plant ofTabernaemontana divaricataat doses of 200 and 400 mg/kg body weight and 5-fluorouracil (standard drug) was orally administered to male Wistar Albino rats once daily for 24 weeks, simultaneously treated with the carcinogen DEN and Fe NTA. In simultaneously treated animals, the plant extract significantly decreased the levels of uric acid, bilirubin, AST, ALT, and ALP in serum and increased the levels of liver marker enzymes in liver. Treatment with the extracts resulted in a significant increase in the levels of antioxidants accompanied by a marked reduction in the levels of malondialdehyde when compared to DEN and Fe NTA treated group. When compared with 200 mg/kg bw rats, 400 mg/kg bw rats and 5-fluorouracil treated rats showed better results in all the parameters. The histopathological studies confirmed the protective effects of extract against DEN and Fe NTA induced liver necrosis. Thus, it could be concluded that the use ofTabernaemontana divaricataextract in the treatment of carcinogen induced hepatic necrosis.


2015 ◽  
Vol 93 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Chandrabose Sureka ◽  
Thiyagarajan Ramesh ◽  
Vavamohaideen Hazeena Begum

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.


2018 ◽  
Vol 53 (4) ◽  
pp. 293-298
Author(s):  
S. Salehi ◽  
MR. Bayatiani ◽  
P. Yaghmaei ◽  
S. Rajabi ◽  
MT. Goodarzi ◽  
...  

Ionizing radiation interacts with biomolecules to produce free radicals, which can damage all components of the cell. The aim of this study was to evaluate the protective effects of different doses of resveratrol against X-ray-induced damage in male rat. The animals were divided into five groups, each composed of six rats: two groups as control groups received saline or ethanol (ethanol in saline, 25%, V/V as a vehicle). Two groups received resveratrol (5 and 10 mg/kg.bwt) for 30 days before X-ray exposure. One group received X-ray. The rats were sacrificed 24 h after the last exposure, blood samples were collected and serum level of malondialdehyde (MDA), total antioxidant capacity (TAC), and the activities of superoxide dismutase (SOD) and catalase (CAT) were measured by spectrophotometric method. X-ray irradiation significantly increased the levels of MDA and decreased TAC as well as SOD activity as compared with control groups. Furthermore, resveratrol pretreatment led to remarkable decrease in MDA concentration and increase in the activities of SOD and CAT as well as TAC compared to those of controls. Our results revealed antioxidant properties of resveratrol and suggest it as a potent radioprotector to ameliorate X-irradiation induced damage in the body.


2009 ◽  
Vol 79 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Chaturvedi

In the present study, protective effects of bitter melon (Momordica charantia) extract on lipid peroxidation induced by immobilization stress in rats have been assessed. Graded doses of extract (50, 100, and 150 mg/kg body weight) were administered orally to rats subjected to immobilization stress for two hours for seven consecutive days. Stress was applied by keeping the rats in a cage where no movement was possible. After seven days, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substances, reduced glutathione, and catalase. In vitro effects of M. charantia extract on lipid peroxidation in liver homogenate of normal, control, and rats pretreated with extract were carried out against cumene hydroperoxide-induced lipid peroxidation. Results reveal that in vivo M. charantia inhibited stress-induced lipid peroxidation by increasing the levels of reduced glutathione and activities of catalase. These results were further supported by in vitro results. In vitro inhibition of lipid peroxidation was indicated by low levels of thiobarbituric acid in the liver homogenate from pretreated rats and normal rats when incubated with both cumene hydroperoxide and extract. Inhibition was also noted in the homogenate where the rats were pretreated but the mixture contained no extract. Thus this plant provides protection by strengthening the antioxidants like reduced glutathione and catalase. Inclusion of this plant in the daily diet would be beneficial.


2010 ◽  
Vol 3 (4) ◽  
pp. 254-261 ◽  
Author(s):  
Mohamed M. Sayed-Ahmed ◽  
Abdulaziz M. Aleisa ◽  
Salim S. Al-Rejaie ◽  
Abdulaziz A. Al-Yahya ◽  
Othman A. Al-Shabanah ◽  
...  

Hepatocellular carcinoma accounts for about 80–90% of all liver cancer and is the fourth most common cause of cancer mortality. Although there are many strategies for the treatment of liver cancer, chemoprevention seems to be the best strategy for lowering the incidence of this disease. Therefore, this study has been initiated to investigate whether thymoquinone (TQ),Nigella sativaderived-compound with strong antioxidant properties, supplementation could prevent initiation of hepatocarcinogenesis-induced by diethylnitrosamine (DENA), a potent initiator and hepatocarcinogen, in rats. Male Wistar albino rats were divided into four groups. Rats of Group 1 received a single intraperitoneal (I.P.) injection of normal saline. Animals in Group 2 were given TQ (4 mg/kg/day) in drinking water for 7 consecutive days. Rats of Group 3 were injected with a single dose of DENA (200 mg/kg, I.P.). Animals in Group 4 were received TQ and DENA. DENA significantly increased alanine transaminase (ALT), alkaline phosphatase (ALP), total bilirubin, thiobarbituric acid reactive substances (TBARS) and total nitrate/nitrite (NOx) and decreased reduced glutathione (GSH), glutathione peroxidase (GSHPx), glutathione-s-transferase (GST) and catalase (CAT) activity in liver tissues. Moreover, DENA decreased gene expression of GSHPx, GST and CAT and caused severe histopathological lesions in liver tissue. Interestingly, TQ supplementation completely reversed the biochemical and histopathological changes induced by DENA to the control values. In conclusion, data from this study suggest that: (1) decreased mRNA expression of GSHPx, CAT and GST during DENA-induced initiation of hepatic carcinogenesis, (2) TQ supplementation prevents the development of DENA-induced initiation of liver cancer by decreasing oxidative stress and preserving both the activity and mRNA expression of antioxidant enzymes.


2015 ◽  
Vol 6 ◽  
Author(s):  
Goktas Hatice ◽  
Bacanli Merve ◽  
Aydin Sevtap ◽  
Taner Gokce ◽  
Sahin Tolga ◽  
...  

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