Induction of xanthine oxidase activity, endoplasmic reticulum stress and caspase activation by sodium metabisulfite in rat liver and their attenuation by Ghrelin

Ercan, Sevim; Kencebay, Ceren; Basaranlar, Goksun; Derın, Narin; Aslan, Mutay

doi:10.1016/j.fct.2014.11.021

Cited by 18 publications

(10 citation statements)

References 40 publications

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“…Many studies have demonstrated the inhibitory effect of ghrelin on ERS. By inhibiting ERS, ghrelin protects against injury such as apoptosis both in vivo and in vitro [16][17][18][19][20]. We found the preventive effect of ghrelin on AS.…”

Section: Discussionsupporting

confidence: 52%

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Ghrelin ameliorates atherosclerosis by inhibiting endoplasmic reticulum stress

Chen

et al. 2016

Fundam Clin Pharmacol

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The effects of ghrelin, a peptide hormone, on atherogenesis are mainly beneficial. This study aimed to investigate whether ghrelin ameliorates atherosclerosis (AS) by preventing endoplasmic reticulum stress (ERS). AS was induced by a high-fat diet in ApoE mice. AS lesions in aortas were detected by Oil Red O staining, and the inner diameter and intima-media thickness (IMT) of the abdominal aorta were analyzed by ultrasonography. The protein expression of the ERS markers, 78-kDa glucose-regulated protein, C/EBP homologous protein, and active caspase-12, was detected by Western blot analysis. High-fat diet-fed ApoE mice showed AS lesions and increased aortic IMT. Ghrelin ameliorated these findings. Moreover, the protein expression of ERS markers was upregulated in the AS aorta and downregulated by ghrelin treatment. The above beneficial effects of ghrelin on AS and ERS were blocked by the ERS inducer, tunicamycin. In rat aortic endothelial cells, oxidized low-density lipoprotein and tunicamycin triggered ERS, which could be inhibited by ghrelin pretreatment. These results suggest that ghrelin can ameliorate activation of ERS, which may be the beneficial effect of ghrelin on AS. Ghrelin may be a new target and strategy for prevention and therapy of AS.

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Section: Discussionsupporting

confidence: 52%

“…Ghrelin inhibited ERS protected against ischemia/reperfusion or isoproterenol‐induced heart injury in rats . In addition, ghrelin attenuated the induction of ERS by sodium metabisulfite in rat liver .…”

Section: Introductionmentioning

confidence: 93%

Ghrelin ameliorates atherosclerosis by inhibiting endoplasmic reticulum stress

Chen

et al. 2016

Fundam Clin Pharmacol

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“…During our daily activities, spray-type household products are recognized as the major source of inhalation exposure to chemicals ( Hahn et al, 2010 ; Shim et al, 2013 ), although they are not well studied despite their wide usage. Sodium metabisulfite (Na 2 S 2 O 5 ; SM), also known as disodium salt, sodium pyrosulfite, disodium sulfite, sodium sulfite anhydrous, or sodium disulfite, is an inorganic sulfite used widely as a preservative to combat the proliferation of microorganisms; additionally, it has antioxidant properties in some wines and foods ( Jamieson et al, 1985 ; Ercan et al, 2015 ) and is used as a disinfectant or an antioxidant in cosmetic products and some pharmaceuticals ( Noorafshan et al, 2013 ). SM is a white crystalline or powder solid chemical with a slight sulfur odor and this chemical becomes a corrosive acid when they are mixed with water.…”

Section: Introductionmentioning

confidence: 99%

Potentiation of Sodium Metabisulfite Toxicity by Propylene Glycol in Both in Vitro and in Vivo Systems

Yoo¹,

Lim²,

Kim³

et al. 2018

Front. Pharmacol.

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Many consumer products used in our daily lives result in inhalation exposure to a variety of chemicals, although the toxicities of the active ingredients are not well known; furthermore, simultaneous exposure to chemical mixtures occurs. Sodium metabisulfite (SM) and propylene glycol (PG) are used in a variety of products. Both the cytotoxicity and the sub-acute inhalation toxicity of each chemical and their mixtures were evaluated. Assays for cell viability, membrane damage, and lysosome damage demonstrated that SM over 100 μg/ml induced significant cytotoxicity; moreover, when PG, which was not cytotoxic, was mixed with SM, the cytotoxicity of the mixture was enhanced. Solutions of 1, 5, and 20% SM, each with 1% PG solution, were prepared, and the whole body of rats was exposed to aerosols of the mixture for 6 h/day, 5 days/week for 2 weeks. The rats were sacrificed 1 (exposure group) or 7 days (recovery group) after termination of the exposure. The actual concentration of SM in the low-, medium-, and high-exposure groups was 3.91 ± 1.26, 35.73 ± 6.01, and 80.98 ± 5.47 mg/m3, respectively, and the actual concentration of PG in each group was 6.47 ± 1.25, 8.68 ± 0.6, and 8.84 ± 1.77 mg/m3. The repeated exposure to SM and PG caused specific clinical signs including nasal sound, sneeze, and eye irritation which were not found in SM single exposure. In addition, the body weight of treatment group rats decreased compared to that of the control group rats in a time-dependent manner. The total protein concentration and lactate dehydrogenase activity in the bronchoalveolar lavage fluid (BALF) increased. Histopathological analysis of the lungs, liver, and nasal cavity was performed. Adverse effects were observed in the nasal cavity, with squamous cell metaplasia identified in the front of the nasal cavity in all high-exposure groups, which completely recovered 7 days after exposure was terminated. Whereas inhalation of SM for 2 weeks only reduced body weight in the high-dose group, inhalation of SM and PG mixtures for 2 weeks significantly decreased body weight and induced metaplasia of the respiratory epithelium into squamous cells in the medium- and high-dose groups. In conclusion, PG potentiated the toxicity of SM in human lung epithelial cells and the inhalation toxicity in rats.

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“…In brief, the hippocampal CA1 tissue was carefully isolated from the rat brain (sham group: n = 6; 2VO group: n = 6 per time point) under microscope and homogenized with 1 ml ice-cold lysis buffer supplied with the kit. After centrifugation (10,000 rpm for 15 min) and assessment of protein concentration, the samples were assayed for caspase activity based on the detection of the chromophore p-nitroaniline (pNA) after cleavage from the labeled substrates (Ercan et al, 2015 ). The cleavage of synthetic caspase-3, -8 and -9 were spectrophotometrically detected at 405 nm in a microplate reader.…”

Section: Methodsmentioning

confidence: 99%

The Expression of Hippocampal NRG1/ErbB4 Correlates With Neuronal Apoptosis, but Not With Glial Activation During Chronic Cerebral Hypoperfusion

Hei

Chen

et al. 2018

Front. Aging Neurosci.

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Permanent bilateral common carotid occlusion (2VO) is well-established to investigate the chronic cerebral hypoperfusion (CCH)-induced cognitive deficits. Besides, previous studies suggested that disturbance of Neuregulin1 (NRG1)/ErbB4 signaling is associated with cognitive impairments, as well as neuronal apoptosis and neuroinflammation in CNS. However, the expression pattern of hippocampal NRG1/ErbB4 has not been systematically investigated during CCH. Here, we aim to investigate the temporal changes of hippocampal NRG1/ErbB4 during CCH and their possible relationship with neuronal apoptosis and glial activation. Morris water maze (MWM) and Radial arm water maze (RAWM) tests were used to analyze cognitive impairment in 2VO rats at 28 days post-surgery, and Enzyme-Linked Immunosorbent Assay (ELISA), western blotting and immunostaining were performed at different time points (24 h, 7 days, 14 days, 28 days) to detect the expression pattern of NRG1/ErbB4 and the distribution of ErbB4. Neuronal nuclei (NeuN), NeuN/TUNEL, Iba1 and GFAP immunostaining and caspase activity in hippocampal CA1 subarea were assessed during CCH as well. We found that the expression of NRG1 and phosphorylated ErbB4 (pErbB4)/ErbB4 changed in a time-dependent manner (up-regulated in the acute phase and then decreased in the chronic phase of CCH). Besides, ErbB4-expressed neurons and selective types of GABAergic cells decreased after CCH, but the distribution pattern of ErbB4 remained unchanged. In addition, the expression of hippocampal NRG1/ErbB4 positively correlated with the level of neuronal apoptosis (both NeuN/TUNEL immunostaining and caspase-3 activity), but not with glial activation according to Pearson’s correlation. These findings indicated that hippocampal NRG1/ErbB4 may be involved in the pathogenesis of CCH, especially neuronal apoptosis during CCH.

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Induction of xanthine oxidase activity, endoplasmic reticulum stress and caspase activation by sodium metabisulfite in rat liver and their attenuation by Ghrelin

Cited by 18 publications

References 40 publications

Ghrelin ameliorates atherosclerosis by inhibiting endoplasmic reticulum stress

Ghrelin ameliorates atherosclerosis by inhibiting endoplasmic reticulum stress

Potentiation of Sodium Metabisulfite Toxicity by Propylene Glycol in Both in Vitro and in Vivo Systems

The Expression of Hippocampal NRG1/ErbB4 Correlates With Neuronal Apoptosis, but Not With Glial Activation During Chronic Cerebral Hypoperfusion

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