scholarly journals Synergistic Effect of Quercetin and α-Lipoic Acid on Aluminium Chloride Induced Neurotoxicity in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Sooad Saud Al-Otaibi ◽  
Maha Mohamad Arafah ◽  
Bechan Sharma ◽  
Abdullah Salih Alhomida ◽  
Nikhat Jamal Siddiqi

Objectives. The present study was carried out to study the protective effects of quercetin and α-lipoic acid alone and in combination against aluminum chloride induced neurotoxicity in rats. Materials and Methods. The study consisted of eight groups, namely, Group 1: control rats, Group 2: rats receiving aluminium chloride 7 mg/kg body weight intraperitoneal route (i.p) for two weeks, Group 3: rats receiving quercetin 50 mg/kg body weight i.p. for two weeks, Group 4: rats receiving quercetin 50 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks, Group 5: rats receiving α-lipoic acid 20 mg/kg body weight i.p. for two weeks, Group 6: rats receiving lipoic acid 20 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks, Group 7: rats receiving α-lipoic acid 20 mg/kg body weight and quercetin 50 mg/kg body weight i.p. for two weeks, and Group 8: rats receiving α-lipoic acid 20 mg/kg body weight and quercetin 50 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks. The animals were killed after 24 hours of the last dose by cervical dislocation. Results. Aluminium chloride treatment of rats resulted in significant increases in lipid peroxidation, protein carbonyl levels, and acetylcholine esterase activity in the brain. This was accompanied with significant decreases in reduced glutathione, activities of the glutathione reductase, and superoxide dismutase. Pretreatment of AlCl3 exposed rats to either quercetin or α-lipoic acid also restored altered lipid peroxidation and superoxide dismutase to near normal levels. Quercetin or α-lipoic acid pretreatment of AlCl3 exposed rats improved the protein carbonyl and reduced glutathione, glutathione reductase, and acetylcholine esterase activities in rat brains towards normal levels. Combined pretreatment of AlCl3 exposed rats with quercetin and α-lipoic acid resulted in a tendency towards normalization of most of the parameters. Conclusions. Quercetin and α-lipoic acid complemented each other in protecting the rat brain against oxidative stress induced by aluminium chloride.

2000 ◽  
Vol 78 (4) ◽  
pp. 447-453 ◽  
Author(s):  
F Liu ◽  
T B Ng

Male Sprague-Dawley rats were randomly divided into four groups. Two of the groups received a single intraperitoneal injection of melatonin and 5-methoxytryptamine (5 mg/kg body weight), respectively, at 9 PM. One group received an intraperitoneal injection of 5-methoxytryptophol (5 mg/kg body weight) at 9 AM. The remaining group received alcoholic saline (vehicle) and served as the control. All rats were sacrificed 90 min after injection and the livers, kidneys, and brains were dissected. The activities of superoxide dismutase, catalase, and glutathione reductase in the organs were measured. It was found that both melatonin and 5-methoxytryptamine were approximately equipotent in enhancing the activities of superoxide dismutase and glutathione reductase in the kidney and liver, while 5-methoxytryptophol displayed a weaker effect. Both melatonin and 5-methoxytryptamine augmented the level of reduced glutathione in the kidney and liver, while 5-methoxytryptophol did so only in the kidney. All three pineal indoles increased the activity of superoxide dismutase and lowered the ratio of oxidized to reduced glutathione in the brain.Key words: pineal indoles, catalase, superoxide dismutase, glutathione reductase.


10.5219/1375 ◽  
2020 ◽  
Vol 14 ◽  
pp. 836-846
Author(s):  
Olena Shatynska ◽  
Oleksandr Tokarskyy ◽  
Petro Lykhatskyi ◽  
Olha Yaremchuk ◽  
Iryna Bandas ◽  
...  

The purpose of the current study was to evaluate the protective properties of dietary magnesium supplementation on pancreatic tissue of rats with alloxan-induced diabetes mellitus. Twenty-five male Wistar rats were split into five groups (control, diabetes, diabetes with 100 mg Mg daily, diabetes with 250 mg Mg daily, diabetes with 500 mg Mg daily) with feeding supplementation starting on day 1, diabetes induction on day 21, and animal sacrifice on day 30. Fasting glucose in blood serum was measured on days 21, 25, 27, and day 30. Glucose metabolism enzymes, namely, lactate dehydrogenase and glucose-6-phosphate dehydrogenase, were measured in pancreatic tissue upon the sacrifice, as well as lipid peroxidation, antioxidant system protective enzymes (catalase and superoxide dismutase), and glutathione system components (glutathione reductase, glutathione peroxidase, and glutathione reduced). Pearson correlation coefficients showed strong negative correlation between serum glucose (control and diabetic animals) and glucose metabolism enzymes, catalase, superoxide dismutase, glutathione peroxidase in pancreatic tissue (r >-0.9, p <0.05), moderate negative correlation with reduced glutathione (r = -0.79, p <0.05), moderate positive correlation with lipid peroxidation index (r = +0.67, p <0.05), weak correlation with glutathione reductase (r = -0.57, p <0.05). Magnesium supplementation slowed down diabetes onset considering fasting glucose levels in rats (p <0.05), as well as partially restored investigated dehydrogenase levels in the pancreas of rats comparing to diabetes group (p <0.05). The lipid peroxidation index varied between treatments showing the dose-dependent influence of Mg2+. Magnesium supplementation partially restored catalase and superoxide dismutase activities in pancreatic tissue, as well as glutathione peroxidase and reduced glutathione levels (p <0.05), while glutathione reductase levels remained unaffected (p >0.05). The obtained results suggested a model, where magnesium ions may have a possible protective effect on pancreatic tissue against the negative influence of alloxan inside β cells of the pancreas.


2016 ◽  
Vol 36 (1) ◽  
pp. 42-50 ◽  
Author(s):  
Adil Mehraj Khan ◽  
Satyavan Rampal ◽  
Naresh Kumar Sood

The effect of 21 days of repeated oral administration of levofloxacin and enrofloxacin both alone and in combination with meloxicam, on the oxidative balance in blood was evaluated in rabbits. Rabbits were randomly allocated to six groups of four animals each. Control group was gavaged 5% dextrose and 2% benzyl alcohol. Three groups were exclusively gavaged meloxicam (0.2 mg/kg body weight o.d.), levofloxacin hemihydrate (10 mg/kg body weight b.i.d 12 h), and enrofloxacin (20 mg/kg body weight o.d.), respectively. Two other groups were co-gavaged meloxicam with levofloxacin hemihydrate and enrofloxacin, respectively. A reduction ( p < 0.05) of reduced glutathione levels was observed in groups treated with meloxicam both alone and in combination with levofloxacin, whereas an increase ( p < 0.01) in the levels of this antioxidant was observed in the groups treated with enrofloxacin. The activities of enzymes, glutathione peroxidase and superoxide dismutase, were induced ( p < 0.05) in levofloxacin-alone treated group. Superoxide dismutase was also induced ( p < 0.05) in meloxicam-alone treated group and inhibited ( p < 0.05) in enrofloxacin-meloxicam co-treated group. The activity of catalase was non-significantly different between various groups. Enrofloxacin-treated groups had higher ( p < 0.01) lipid peroxidation than control and levofloxacin-alone treated groups. Elevated lipid peroxidation was also observed in the groups treated with meloxicam both alone and in combination with levofloxacin ( p < 0.05). In conclusion, these drugs have potential to induce oxidative imbalance, however, compared to levofloxacin, more oxidative damage is produced by enrofloxacin and meloxicam.


2018 ◽  
Vol 8 (6-s) ◽  
pp. 48-52
Author(s):  
B. Sabari Senthil ◽  
V.K. Kalaichelvan ◽  
A. Kottai Muthu

Objective: The objective of the present study was to investigate the Evaluation of In vivo antioxidant activity of Ethanolic extract of root of Smilax zeylanica(EESZ) on Aluminium Chloride Induced apoptosis suppressing oxidative stress  in Wistar rats. Materials and Methods: The ethanolic extract from the roots of S. china by hot continuous percolation method. The rats were divided into 5 groups and each group consists of 6 animals. Rats were treated with EESC for 150 and 300 mg/ kg of body weight and piracetam, 0.5 mg/ kg of body weight for 14 successive days after inducing oxidative stress  with aluminium chloride (100 mg/ kg of body weight) for 60 days. The lipid peroxidation level (TBARS) and antioxidant activities like Superoxide dismutase (SOD), Catalase (CAT) and reduced Glutathione (GSH) were estimated in rats. Results: AlCl3 induced rats showed increased the TBARS and decreased the antioxidant enzymes like Superoxide dismutase (SOD), Catalase (CAT) and reduced Glutathione (GSH) when compared with the control group. The EESZ at higher dose 300 mg/ kg of body weight animals were significantly (P < 0.001) reduced the TBARS and increased the anti oxidant enzymes Superoxide dismutase (SOD), Catalase (CAT) and reduced Glutathione (GSH) when compared with the AlCl3 treated group Conclusion: Findings of the present study revealed that Ethanolic extract from roots of Smilax zeylanica  may be used as a significant source of natural antioxidant, which might be helpful in preventing the progress of various oxidative stresses.                    Keywords: S. zeylanica, antioxidant, ethanolic extract, TBARS, rats.


2002 ◽  
Vol 21 (12) ◽  
pp. 675-680 ◽  
Author(s):  
K Ramanathan ◽  
B S Balakumar ◽  
C Panneerselvam

Arsenic is an ubiquitous element in the environment causing oxidative burst in the exposed individuals leading to tissue damage. Antioxidants have long been known to reduce the free radical-mediated oxidative stress. Therefore, the present study was designed to determine whether supplementation of a-tocopherol (400 mg/kg body weight) and ascorbic acid (200 mg/kg body weight) to arsenic-intoxicated rats (100 ppm in drinking water) for 30 days affords protection against the oxidative stress caused by the metalloid. The arsenic-treated rats showed elevated levels of lipid peroxide, decreased levels of non-enzymatic antioxidants and activities of enzymatic antioxidants. Administration of a-tocopherol and ascorbic acid to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, reduced glutathione, ascorbic acid and a-tocopherol and so do the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal. These findings suggest thata-tocopherol and ascorbic acid prevent LPO and protect the antioxidant system in arsenic-intoxicated rats.


2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  

We report the effect of cross-sex hormonal replacement on antioxidant enzymes from rat retroperitoneal fat adipocytes. Eight rats of each gender were assigned to each of the following groups: control groups were intact female or male (F and M, resp.). Experimental groups were ovariectomized F (OvxF), castrated M (CasM), OvxF plus testosterone (OvxF + T), and CasM plus estradiol (CasM + E2) groups. After sacrifice, retroperitoneal fat was dissected and processed for histology. Adipocytes were isolated and the following enzymatic activities were determined: Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR). Also, glutathione (GSH) and lipid peroxidation (LPO) were measured. In OvxF, retroperitoneal fat increased and adipocytes were enlarged, while in CasM rats a decrease in retroperitoneal fat and small adipocytes are observed. The cross-sex hormonal replacement in F rats was associated with larger adipocytes and a further decreased activity of Cu-Zn SOD, CAT, GPx, GST, GR, and GSH, in addition to an increase in LPO. CasM + E2exhibited the opposite effects showing further activation antioxidant enzymes and decreases in LPO. In conclusion, E2deficiency favors an increase in retroperitoneal fat and large adipocytes. Cross-sex hormonal replacement in F rats aggravates the condition by inhibiting antioxidant enzymes.


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 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.


PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9232
Author(s):  
Sarah Albogami ◽  
Aziza Hassan ◽  
Nibal Ahmed ◽  
Alaa Alnefaie ◽  
Afnan Alattas ◽  
...  

Background Little is known regarding the toxic and therapeutic doses of amygdalin. Treatment regimens and schedules can vary between humans and animal models, and there have been reports of cyanide toxicity due to amygdalin use. Objective The aim of this study was to evaluate the effect of different doses of amygdalin on antioxidant gene expression and suppression of oxidative damage in mice. Methods Forty adult male mice were divided randomly into four groups (n = 10) as follows and treated orally for two weeks: a control group treated with saline solution, a group treated with amygdalin at 200 mg/kg body weight, a group treated with amygdalin at 100 mg/kg body weight, and a group treated with amygdalin at 50 mg/kg body weight. Liver and testis samples were collected for gene expression, biochemical and histopathological analyses. Results The mice treated with medium-dose amygdalin (100 mg/kg) showed upregulated mRNA expression of glutathione peroxidase (P < 0.01) and superoxide dismutase (P < 0.05) and significantly decreased lipid peroxidation (P < 0.05) in hepatic and testicular tissues compared to those in the untreated groups (controls), with mild histopathological effects. The mice treated with high-dose of amygdalin (200 mg/kg) showed downregulated mRNA expression of glutathione peroxidase and superoxide dismutase (P < 0.01) and significantly increased lipid peroxidation (P < 0.05) in both hepatic and testicular tissues compared to those in the untreated groups (controls), with an apparent effect at the histopathological level. No effects were observed in the mice treated with low-dose amygdalin (50 mg/kg) at the gene, protein and histopathological level. Conclusion Low-and medium-dose amygdalin did not induce toxicity in the hepatic and testicular tissues of male mice, unlike high-dose amygdalin, which had a negative effect on oxidative balance in mice. Therefore, amygdalin at a moderate dose may improve oxidative balance in mice.


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