In vitro effect of manganese chloride exposure on energy metabolism and oxidative damage of mitochondria isolated from rat brain

Zhang, Fanglin; Xu, Zhenbo; Gao, Jian; Xu, Bin; Deng, Yu

doi:10.1016/j.etap.2008.04.003

Cited by 126 publications

(76 citation statements)

References 38 publications

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“…The amount of MDA formed in each of the samples was assessed through measuring the absorbance of the supernatant at 532 nm with an ELISA reader (Tecan, Rainbow Thermo, Austria). Tetrametoxypropane (TEP) was used as standard and MDA content was expressed as nmol/mg protein (17).…”

Section: Measurement Of Lipid Peroxidationmentioning

confidence: 99%

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Koohsari

Shaki

Jahani

2016

Braz. arch. biol. technol.

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Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METHinduced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.

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Section: Measurement Of Lipid Peroxidationmentioning

confidence: 99%

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Koohsari

Shaki

Jahani

2016

Braz. arch. biol. technol.

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“…Several mechanisms of Mn neurotoxicity have been proposed, including the disruption of mitochondrial metabolism [20], induction of oxidative stress [21], and alteration of iron homeostasis [22]. In this study, the pathogenesis of manganism is considered to involve excessive release of Glu.…”

Section: Discussionmentioning

confidence: 99%

“…After 5-min room temperature incubation (20 • C), chloroform was added for phase separation. The upper aqueous phase was collected and the RNA was precipitated by mixing with isopropyl alcohol.…”

Section: Reverse Transcription-polymerase Chain Reactionmentioning

confidence: 99%

Manganese exposure alters the expression of N‐methyl‐d‐aspartate receptor subunit mRNAs and proteins in rat striatum

Deng

2010

J Biochem & Molecular Tox

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Manganese is one of the ubiquitous environmental pollutants that can induce an indirect excitotoxicity caused by altered glutamate (Glu) metabolism. The present study has been carried out to investigate the effect of Mn on the expression of N-methyl-d-aspartate receptor (NR) subunit mRNAs and proteins in rat striatum when rats were in manganism. The rats were divided randomly into four groups of six males and six females each: control group (group 1) and 8, 40, and 200 micromol/kg Mn-treated groups (groups 2-4). The control group rats were subcutaneously (s.c.) injected with normal saline. Manganese-treated rats were s.c. injected with respectively 8, 40, and 200 micromol/kg of MnCl(2) . 6H(2)O in normal saline. The administration of MnCl(2) . 6H(2)O for 4 weeks significantly increased Mn concentration in the striatum. With the increase in administered MnCl(2) dosage, Glu concentration and cell apoptosis rate increased significantly. The relative intensity of NR2A mRNA decreased significantly in 8 micromol/kg Mn-treated rats. However, relative intensities of NR1 and NR2B mRNAs decreased significantly in 40 micromol/kg Mn-treated rats. Similarly, the relative intensity of NR2A protein showed a significant decrease in 40 micromol/kg Mn-treated rats whereas those of NR1 and NR2B decreased significantly in 200 micromol/kg Mn-treated rats. Therefore, the expression of NR2A mRNA and protein were much more sensitive to Mn than that of NR1 and NR2B. In conclusion, the results suggested that Mn induced nerve cell damage by increasing extracellular Glu level and altered expression of NR subunit mRNAs and proteins in rat striatum.

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“…LPO, as indicated by the formation of malondialdehyde (MDA), was measured according to the method outlined by Zhang et al (21). The suspensions of the mitochondria, which were at a density of 0.5 mg protein/ml, were incubated in 0.25 mL of sulfuric acid (0.05 M) and 0.3 mL of 0.2% TBA.…”

Section: Measurement Of Lpomentioning

confidence: 99%

The Ameliorative Effect of Naringenin on Paraquat-Induced Toxicity in Mitochondria Isolated from Rats

Daneshgar

Rezaeian

Goudarzi

et al. 2016

Jundishapur J Nat Pharm Prod

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Background: Paraquat (PQ) is a dipyridyl herbicide that sustains damage due to redox cycling. An important aspect of PQ toxicity is defined by its interactions with mitochondria. Objectives: This study was designed to evaluate the ability of naringenin (NG) to prevent PQ-induced mitochondrial dysfunction in rat-isolated liver mitochondria. Materials and Methods:To determine the IC50 of PQ , the mitochondrial viability was specified using an MTT assay. Different concentrations of PQ (0, 2.5, 5, and 10 mM) were used, and the IC50 of PQ was assigned as approximately 2 mM. The suspensions of

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In vitro effect of manganese chloride exposure on energy metabolism and oxidative damage of mitochondria isolated from rat brain

Cited by 126 publications

References 38 publications

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Manganese exposure alters the expression of N‐methyl‐d‐aspartate receptor subunit mRNAs and proteins in rat striatum

The Ameliorative Effect of Naringenin on Paraquat-Induced Toxicity in Mitochondria Isolated from Rats

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