Proteomic analysis of rat retina after methanol intoxication

Chen, Jiemin; Zhu, Guangyou; Xia, Wen-Tao; Zhao, Ziqin

doi:10.1016/j.tox.2012.01.002

Cited by 16 publications

(19 citation statements)

References 21 publications

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“…Thirty blood samples (ten samples from group A, group B, and group C resp.) were used to determine methanol concentrations by headspace gas chromatography (GC/HS), as previously described [ 5 ]. Methanol concentrations were calculated from a standard curve produced using GC/HS results from a series of known concentrations of chromatographic grade methanol.…”

Section: Methodsmentioning

confidence: 99%

“…Currently, most studies on methanol intoxication focus on a-wave and b-wave subcomponents in photopic and scotopic environment [ 3 , 4 ]. Our previous research showed that a-wave and b-wave were greatly destroyed upon methanol intoxication [ 5 ]. However, very limited researches on the characters of OPs waves upon methanol poisoning were performed.…”

Section: Introductionmentioning

confidence: 99%

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The Intoxication Effects of Methanol and Formic Acid on Rat Retina Function

Zhou

Chen

et al. 2016

Journal of Ophthalmology

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Objective. To explore the potential effects of methanol and its metabolite, formic acid, on rat retina function. Methods. Sprague-Dawley rats were divided into 3- and 7-day groups and a control. Experimental groups were given methanol and the control group were provided saline by gavage. Retinal function of each group was assessed by electroretinogram. Concentrations of methanol and formic acid were detected by GC/HS and HPLC, respectively. Results. The a and b amplitudes of methanol treated groups decreased and latent periods delayed in scotopic and photopic ERG recordings. The summed amplitudes of oscillatory potentials (OPs) of groups B and C decreased and the elapsed time delayed. The amplitudes of OS1, OS3, OS4, and OS5 of group B and OS3, OS4, and OS5 of group C decreased compared with the control group. The IPI1 of group B and IPI1-4 of group C were broader compared with the control group and the IPI1-4 and ET of group B were broader than group C. Conclusions. Both of scotopic and photopic retinal functions were impaired by methanol poisoning, and impairment was more serious in the 7-day than in the 3-day group. OPs, especially later OPs and IPI2, were more sensitive to methanol intoxication than other eletroretinogram subcomponents.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Intoxication Effects of Methanol and Formic Acid on Rat Retina Function

Zhou

Chen

et al. 2016

Journal of Ophthalmology

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“…It was reported that retinal ATP synthase decreases following methanol intoxication. For example, proteomic analysis of the rat retina revealed that sodium formate induces a marked decrease in the levels of ATP in photoreceptor cells ( 7 , 14 ). A marked decline in the viability of 661W cells following exposure to sodium formate was also observed in the present study.…”

Section: Discussionmentioning

confidence: 99%

Sodium formate induces autophagy and apoptosis via the JNK signaling pathway of photoreceptor cells

Wang

et al. 2015

Molecular Medicine Reports

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Incidents associated with methanol intoxication resulting from the consumption of fake wine occur not infrequently worldwide. Certain individuals are made blind due to methanol poisoning. The present study aimed to investigate the effects of sodium formate exposure on photoreceptor cells (661W cells). The 661W cells were exposed to sodium formate for 6–24 h and cell viability was determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Subsequently, the 661W cells were exposed to 15 or 30 mM sodium formate for 24 h. The level of apoptosis was determined using Hoechst 33342/propidium iodide staining, visualizing the cells under a fluorescence microscope, and annexin V-fluorescein isothiocyanate staining, using flow cytometric analysis. Intracellular reactive oxygen species (ROS) were measured using 2′,7′-dichlorofluorescein diacetate (DCFH-DA) staining, followed by flow cytometric analysis. Autophagy of the 661W cells was measured by monodansylcadaverine staining. The activation of phosphorylated c-Jun N-terminal kinase (p-JNK), B-cell lymphoma (Bcl-2), Bcl-2-associated X protein, cleaved caspase-3, cleaved caspase-9 and microtubule-associated protein 1A/1B-light chain 3 (LC3) was assessed by western blotting. The effects of Z-VAD-fmk (a pan-caspase inhibitor) and SP600125 (a JNK inhibitor) on the viability of the sodium formate-induced 661W cells were determined using an MTT assay. Sodium formate treatment induced a decrease in the viability of the 661W cells in a time- and a dose-dependent manner. In addition, sodium formate at concentrations of 15 or 30 mM markedly increased the level of apoptosis and the ROS levels, as measured by DCFH-DA staining of the 661W cells. Additionally, 661W cells exposed to sodium formate for 24 h exhibited increased levels of p-JNK, Bax, cleaved caspase-3, cleaved caspase-9 and LC3II (the phosphatidylethanolamine-modified form of LC3), although the level of Bcl-2 was decreased. Furthermore, cell cytotoxicity and autophagy were induced upon treatment with sodium formate. Z-VAD-fmk and SP600125 were able to effectively circumvent the effects of sodium formate on cell viability. These results suggested that the cytotoxicity induced by sodium formate induces the activation of the JNK signaling pathway, leading to caspase-dependent apoptosis. Increased levels of autophagy were also observed during the process of 661W cell damage induced by sodium formate.

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“…The mechanism is currently presumed to be formic acid-induced retinal damage from animal models. [4] There are no studies conducted in human for the pathophysiology of methanol optic neuropathy. There was one recent research demonstrating the role of intravenous erythropoietin with oral prednisolone to improve a visual acuity in the patients with optic neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Bilateral putaminal hemorrhages: Serious complication of methanol intoxication

et al. 2013

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Context:Methanol intoxication is a life-threatening condition. Hallmark of clinical presentations include severe wide anion gap metabolic acidosis with very high serum osmolar gap and visual complication.Case Report:We report a case of severe methanol intoxication with bilateral putaminal hemorrhage, an uncommon serious complication. A 56-year-old man presented with altered mental status. Fundus examination showed optic disc edema. Arterial Blood Gas (ABG) revealed severe anion gap metabolic acidosis with osmolal gap. Head computed tomography (CT) showed hypodense lesions in basal ganglia bilaterally. Hemodialysis and intravenous fomepizole were initiated. Serum methanol level was significantly elevated. Unfortunately, patient was lethargic 2 weeks after discharge. Repeated CT of head demonstrated new putaminal hemorrhages.Conclusion:Bilateral putaminal hemorrhage is an uncommon but serious complication in methanol intoxication. Clinicians should have high index of suspicion for putaminal hemorrhage when patients with recent methanol intoxication present with altered mental status.

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Proteomic analysis of rat retina after methanol intoxication

Cited by 16 publications

References 21 publications

The Intoxication Effects of Methanol and Formic Acid on Rat Retina Function

The Intoxication Effects of Methanol and Formic Acid on Rat Retina Function

Sodium formate induces autophagy and apoptosis via the JNK signaling pathway of photoreceptor cells

Bilateral putaminal hemorrhages: Serious complication of methanol intoxication

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