Preventive effect of aminoguanidine compared to vitamin E and C on cisplatin-induced nephrotoxicity in rats

Atasayar, Suna; Gürer-Orhan, Hande; Orhan, Hilmi; Gürel, Bora; Girgin, Gözde; Özgüneş, Hilâl

doi:10.1016/j.etp.2008.04.016

Cited by 75 publications

(71 citation statements)

References 38 publications

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“…10 Aminoguanidine has been shown to protect against the tissue damage associated with periodontitis by reducing nitric oxide production and oxidative stress, and increasing glutathione content. 11 In a very recent study, 12 aminoguanidine has been shown to reduce cisplatin induced nephrotoxicity due to its antioxidant effect. In another recent study, 13 aminoguanidine has been shown to increase the endogenous antioxidant defence mechanism in rats and protect the animals from radiation-induced lung toxicity.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Abraham

Rabi

Selvakumar

2008

Cell Biochemistry & Function

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Cyclophosphamide (CP) is an antineoplastic agent that is used for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) is a major dose limiting side effect of CP. Recent studies show that aminogaunidine, an inhibitor of inducible nitric oxide synthase is a potent antioxidant and prevents changes caused by oxidative stress such as depletion of antioxidant activity and tissue injury. The purpose of the study is to investigate the effect of aminoguanidine on parameters of oxidative stress, antioxidant enzymes and bladder injury caused by CP. Adult male rats were randomly divided into four groups. Control rats were administered saline; the AG control group received 200 mg/kg body wt of aminoguanidine; The CP group received a single injection of CP at the dose of 150 mg/kg body wt intraperitoneally. The CP þAG group received aminoguanidine (200 mg/kg body wt) intraperitoneally 1 h before the administration of CP. The rats were sacrificed 16 h after CP/saline administration. The bladder was used for light microscopic studies and biochemical studies. The markers of oxidative damage including protein carbonyl content, protein thiol, malondialdehyde and conjugated dienes were assayed in the homogenates along with the activities of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase and glutathione S transferase. In the bladders of CP treated rats edema of lamina propria with epithelial and sub-epithelial hemorrhage was seen. All the parameters of oxidative stress that were studied were significantly elevated in the bladders of CP treated rats. The activities of the antioxidant enzymes were significantly lowered in the bladders of CP treated rats. Aminoguanidine pretreatment prevented CP-induced oxidative stress, decrease in the activities of anti-oxidant enzymes and reduced bladder damage. The results of the present study suggest the antioxidant role for aminoguanidine in CP-induced bladder damage.

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Section: Introductionmentioning

confidence: 99%

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Abraham

Rabi

Selvakumar

2008

Cell Biochemistry & Function

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“…Reduced form of glutathione prevent the cellular content from attack to the toxic effects of lipid peroxidation (Shelly et al, 2009). Normally, GSH can bind with superoxide and hydroxyl radical (Atasayar et al, 2009). The results obtained may provide evidence that APM intake enhances generation of oxidative stress in rat by altering the glutathione ratio status.…”

Section: Discussionmentioning

confidence: 99%

Impact of Aspartame Consumption on Neurotransmitters in Rat Brain

Baothman¹,

Moselhy²,

Al-Shehri³

et al. 2017

Afr J Tradit Complement Altern Med

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Background: Aspartame (APM), a common artificial sweetener, has been used for diabetic subjects and body weight control for a long time. The goal of the present study was to evaluate the impact of APM consumption on neurotransmitters and oxidative stress in rat's brain. Materials and Methods: Four groups of male Wistar albino rats was used: Group1, control (Rats fed on normal diet). Group 2: Rats were received aspartame (50 mg/kg b w). Group3: Rats were received aspartame (75 mg/kg b w). Group 4: Rats were received aspartame (125 mg/kg b w). Five rats were decapitated after 10, 20, 30 and 40 days from start of experiment. Blood and brain tissue were collected for biochemical analysis. Biochemical analysis of brain tissue includes neurotransmitters (Acetylcholine, epinephrine, norepinephrine, γ-aminobutyric acid and serotonin). Serum for determination of lipid peroxidation (MDA), reduced glutathione and superoxide dismutase (SOD). Results: the data obtained showed that antioxidant activities (SOD and GSH) were reduced significantly (p<0.001) while malondialdhyde (MDA) level was increased compared with control. Brain neurotransmitters levels (serotonin, GABA and dopamine) were reduced significantly compared with control (p<0.001, <0.01) after consumption of APM. However, the level of acetylcholine and norepinephrine increased in rats fed AMP compared with control (p<0.001). The effect of APM is dose dependent. Conclusion: Consumption of APM for a long time increased oxidative stress in brain tissue and disruption in neurotransmitters that affect physiological functions.

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“…[39][40][41][42] There are many studies which have demonstrated the involvement of oxidative stress, lipid peroxidation and mitochondria dysfunction in CP-induced liver toxicity. [41][42][43][44][45] A mechanism by which CP exerts its cytotoxicity is through the generation of reactive oxygen species (ROS). 45,46 The administration of CP causes an increase in lipid peroxide levels and a decrease in the activity of antioxidant defense enzymes, as well as in the concentrations of nonenzymatic components of Anti oxidative stress that prevent, or protect against, lipid peroxidation in the tissues 47 .It is accepted that both correlate to oxidative stress and cause an imbalance between the generation of oxygen derived radicals and the organism's antioxidant potential.…”

Section: Discussionmentioning

confidence: 99%

“…[41][42][43][44][45] A mechanism by which CP exerts its cytotoxicity is through the generation of reactive oxygen species (ROS). 45,46 The administration of CP causes an increase in lipid peroxide levels and a decrease in the activity of antioxidant defense enzymes, as well as in the concentrations of nonenzymatic components of Anti oxidative stress that prevent, or protect against, lipid peroxidation in the tissues 47 .It is accepted that both correlate to oxidative stress and cause an imbalance between the generation of oxygen derived radicals and the organism's antioxidant potential. 48 Supplementation of the antioxidant vitamin E has been reported to inhibit lipid peroxide in various conditions such as CP-induced nephrotoxicity and hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

The preventive effect of bismuth and vitamin E combination on cisplatin hepatotoxicity in cancer patients

Mowlood

2012

ZJMS

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Background and objectives:The objective of this study was to explore the optimal combination of agents with their doses used along with cisplatin for the protection of hepatotoxicity. Methods: This experiment was carried out on a patients suffering from different solid types of tumor divided into two groups: cisplatin group receiving cisplatin in a dose of 90 mg/ m² body surface area(BSA) and the therapy group receiving cisplatin in a dose of 90 mg/m² BSA and bismuth subcitrate (200mg/day) with vitamin E (400mg/day). Ten healthy subjects were taken as a control group.Total serum bilirubin (TSB), serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT) and alkaline phosphatase (ALP) were tested for the assessments of liver function. Results: The level of TSB, GPT, GOT and ALP in healthy subjects did not changed significantly with respect to baseline value along the entire period of the study ; while cisplatin group showed a sustain and significant elevation in TSB, GPT, GOT and ALP level in comparison with baseline along the entire period of the study, P<0.05. Meanwhile, the hepatotoxic effect of cisplatin was shown to be slightly but however significantly decreased in patients received bismuth-vitamin E therapy (P<0.05) along the entire period of the study. Conclusion: Bismuth and vitamin E combination play a beneficial role for prevention of cisplatin hepatotoxicity. The potentiated actions for prevention of cisplatin hepatotoxicity could be achieved via combined use of these agents .

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Preventive effect of aminoguanidine compared to vitamin E and C on cisplatin-induced nephrotoxicity in rats

Cited by 75 publications

References 38 publications

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Impact of Aspartame Consumption on Neurotransmitters in Rat Brain

The preventive effect of bismuth and vitamin E combination on cisplatin hepatotoxicity in cancer patients

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