Protective role of melatonin in cyclosporine A-induced oxidative stress in rat liver

Rezzani, Rita; Buffoli, Barbara; Rodella, Luigi Fabrizio; Stacchiotti, Alessandra; Bianchi, Rossella

doi:10.1016/j.intimp.2005.03.021

Cited by 65 publications

(66 citation statements)

References 53 publications

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“…Various antioxidants such as melatonin (Rezzani et al 2005), lycopene (Atessahin et al 2006), lipoic acid (Amudha et al 2006) and green tea (Mohamadin et al 2005) have been investigated for their potential effects to prevent the side effects of toxic substances. There is another type of antioxidants, flavonoids, which are richly found in fruits and vegetables.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

et al. 2015

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D-Galactosamine (D-GalN), which is an established experimental toxin, primarily causes liver injury by the generation of free radicals and depletion of UTP nucleotides. D-GalN intoxication also induces renal dysfunction thus, renal failure is often associated with the end-stage of the liver damage. We have investigated both preventive and curative effects of ellagic acid (EA) in this study. EA treatment at a gavage dose of 20 mg/kg body weight was administered before and after intraperitoneal (i.p.) injection of D-GalN at a dose of 750 mg/kg. Tissue and blood samples of animals were collected for morphological and biochemical evaluations. Our study results suggest that EA treatment both prior to and after the toxin administration successfully altered the toxic effects on the rats. Moreover, pre-treatment of EA was more protective than post-treatment indicated by histopathological and biochemical values. In conclusion, EA treatment both before and after D-GalN intoxication could protect kidney tissues against D-GalN induced oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

et al. 2015

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“…Hepatotoxicity induced by CsA administration is widely reported in literature (Wolf et al 1997, Durak et al 2004, Hagar 2004, Rezzani 2004, 2005a, 2006, Kurus et al 2008, Bohmer et al 2011. There are two possible mechanisms of CsAinduced hepatotoxicity: (1) due to an excess of free radical production during CsA metabolism in the liver; or (2) CsA may impair the antioxidant defense (Durak et al 2004).…”

Section: Discussionmentioning

confidence: 99%

“…There are two possible mechanisms of CsAinduced hepatotoxicity: (1) due to an excess of free radical production during CsA metabolism in the liver; or (2) CsA may impair the antioxidant defense (Durak et al 2004). Rezzani et al (2005a) suggested that the oxidative stress induced by CsA is associated with the imbalance of free oxygen radical production and the antioxidant defense system. The increase of CsA-associated oxidative (2004) observed, in the rabbits' liver, severe hydropic degeneration in parenchymal cells after treatment with CsA (25mg/kg/day, orally during 10 days).…”

Section: Discussionmentioning

confidence: 99%

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The effects of Cyclosporin A and Heteropterys tomentosaon the rat liver

Freitas

Almeida

Monteiro

et al. 2015

An. Acad. Bras. Ciênc.

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Cyclosporin A (CsA) is a widely employed immunosuppressive drug that is associated with several side effects, among then hepatotoxicity. Heteropterys tomentosa is a Brazilian plant efficient in reducing damage caused by CsA on the rat testis and prostate. The aim of this study was to evaluate the effect of CsA and H. tomentosa (administered isolated or simultaneously) on the liver of Wistar rats. The animals were treated daily with water (control), CsA (15mg/kg/day), H. tomentosa infusion or CsA+H. tomentosa, for 21 or 56 days. The treatments did not alter liver morphology or cause fibrosis. H. tomentosa administered for 21 days increased the number of hepatocyte nuclei and Kupffer cell volumetric proportion. After 56 days of treatment, H. tomentosa administration did not alter the parameters analyzed. Biochemical plasma dosages and liver stereology showed impairment caused by CsA-treatment after 21 days; these results were not observed after 56 days of treatment. The simultaneous treatment with CsA and H. tomentosa for 21 or 56 days did not alleviate nor accentuate CsA hepatic effects. The present study showed that the 21 days treatment with CsA caused more alteration to the liver than the 56 days treatment; this could be related to hepatic recovery after the long term treatment.

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“…Grp75 has been implicated in various biological processes of human cells (13) and has been shown to respond to numerous forms of stress, including ischemia (15), glucose deprivation (16), oxidative injury (22) and drug resistance (23). In addition, data from previous studies have shown that the treatment of IR led to the upregulation of the Grp75 protein (17,18).…”

Section: Discussionmentioning

confidence: 99%

Glucose-regulated protein 75 overexpression attenuates ionizing radiation-mediated injury in PC12 cells by inducing the expression of topoisomerase IIα

Guo

Yang

et al. 2012

Molecular Medicine Reports

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Abstract. Glucose-regulated protein 75 (Grp75), also known as mortalin/mthsp70/PBP74, is a member of the heat-shock protein 70 (HSP70) family. Grp75 is known to protect cells from stress-induced injury. Previous studies have shown that the expression of Grp75 is upregulated by a low dose of ionizing radiation (IR). To evaluate the protective role of Grp75 on cell proliferation in response to IR, Grp75 was overexpressed in a rat adrenal pheochromocytoma cell line (PC12). It was revealed that Grp75 overexpression desensitized PC12 cells to IR-mediated cell injury. In addition, the expression of topoisomerase IIα (Topo IIα) was downregulated in PC12 cells following γ-ray IR. The effect of Grp75 overexpression on Topo IIα expression was examined. It was revealed that Grp75 overexpression reversed the inhibitory effect of IR on Topo IIα expression. In conclusion, the data indicated that Grp75 overexpression attenuates IR-induced injury in PC12 cells by maintaining the expression of Topo IIα. IntroductionIonizing radiation (IR) induces a variety of cellular responses at clinically relevant doses. MCF-7 cells were arrested at the G1 and G2 phases of the cell cycle and MDA-MB231 cells were arrested at the G2 phase in response to IR (1,2). It has been demonstrated that X-rays at extremely low doses, between 1-5 cGy, stimulate cell proliferation, whereas at doses >1 Gy, IR is lethal to cells (3). Topoisomerase IIα (Topo IIα), a nuclear enzyme involved in a number of cellular processes, is necessary for eukaryotic survival. Topo IIα is significant in the replication and repair of DNA and takes part in chromosome condensation and segregation during mitosis (4). Previous studies have demonstrated that DNA Topo IIα expression levels correlate with chromatid radiosensitivity (5). Topo IIα has also been shown to play a significant role in male mouse meiosis and its activity is required at the metaphase-anaphase transition of the two meiotic divisions for proper chromosome disjunction (6,7). The expression of Topo IIα changes periodically during cell growth and therefore, Topo IIα is thought to be a marker of cell proliferation (8-10). Topo IIα expression is affected by numerous environmental factors, including heat-shock and IR. It has been reported that, if the activity of Topo IIα is restrained or the distribution of Topo IIα in cells changes as the result of genetic mutations, the aneuploid ratio of the cells increases (11,12).Grp75, a member of the HSP70 family, is involved in multiple functions that are required to maintain cell metabolism, including the stress response, cell proliferation and differentiation (13). Previous studies have demonstrated that Grp75 levels appear to correlate with mitochondrial activity and biogenesis (14) and that Grp75 expression is induced by cerebral ischemia (15), glucose deprivation (16) and low doses of IR (17). The gene expression of Grp75 in HT29 and MCF-7 cells was upregulated following exposure to IR (17,18). To investigate the potential link between the expression of Grp75 and Topo I...

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Protective role of melatonin in cyclosporine A-induced oxidative stress in rat liver

Cited by 65 publications

References 53 publications

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

Protective effects of ellagic acid in d-galactosamine-induced kidney damage in rats

The effects of Cyclosporin A and Heteropterys tomentosaon the rat liver

Glucose-regulated protein 75 overexpression attenuates ionizing radiation-mediated injury in PC12 cells by inducing the expression of topoisomerase IIα

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